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Liubov Ben-Nun
The research is composed of two parts: the first studies the family
system of King David, the roots of his family, the development of this
system and its subsystems, the structure and its expansion, the
dynamics of the family, and the relationships between family
members and the external world. The second part examines the
medical record of the King that is the biblical text, evaluating the
most likely diagnoses of the diseases that afflicted the King from the
viewpoint of contemporary medicine.
50th Book.
Published By B.N. Publication House, Israel
First Edition (in Hebrew) 2003
Second Edition 2006
Third Edition 2009
Fourth edition 2015
King David.
Bolognese artist Guercino 17th century.
BIBLICAL EXEGESIS
It should be noted and stressed that this research is
in no way concerned with a discussion of any
interpretations of the Bible by the great commentators
such as Rambam, the sages of the Talmud and the
Mishnah, or interpretation based on knowledge of the
ancient world found in Julius Preuss’ book. The
research is based solely on the actual words on the
verses of the Bible.
CONTENTS
MY VIEW 1
A PERSONAL ACCOUNT 2
PREFACE 2
FOREWORD 3
THE FAMILY LIFE CYCLE 9
THE ROOTS 10
OBED – THE GRANDFATHER OF KING DAVID 10
JESSE'S FAMILY 10
THE BATTLE WITH GOLIATH 10
DAVID AND KING SAUL'S FAMILY 12
KING SAUL 12
JONATHAN 15
DAVID'S FAMILY 15
DAVID, MERAB, AND MICHAL 15
A NEW FAMILY 17
THE KING OF JEHUDA 21
POLYGAMOUS FAMILY 21
THE KING OF ISRAEL 26
THE AFFAIR OF BATHSHEBA 26
UNPROTECTED SEXUAL CONTACTS 27
CONDOMS 36
FAMILY SYSTEM THEORY 39
A NEW COMPOSITION OF THE KING'S FAMILY 41
DEATH OF A NEWBORN SON 41
BIRTH ASPHYXIA 43
LOW/VERY LOW BIRTH WEIGHT 44
PREMATURITY 45
INTRAUTERINE GROWTH RETARDATION 47
PREMATURE RUPTURE OF MEMBRANES 48
CONGENITAL MALFORMATIONS 49
SEPSIS 52
MENINGITIS 53
NECROTISING ENTEROCOLITIS 54
DIARRHEA 55
NEONATAL TETANUS 56
MALARIA 58
MEASLES 59
SYPHILIS 60
RESPIRATORY DISTRESS SYNDROME 62
SUDDEN INFANT DEATH SYNDROME 64
HOME BIRTH 66
SOCIOECONOMIC STATUS 67
THE MOURNING PROCESS 69
FAMILY GROWTH 73
THE WARRIOR 74
DAVID'S SONS THE CHIEF RULERS 74
MEFIVOSHET – A NEW FAMILY MEMBER 74
AMNON 79
EATING DISORDERS 79
ANOREXIA NERVOSA 87
PARTIAL SYNDROMES OF EATING DISORDERS 88
FOOD AVOIDANCE EMOTIONAL DISORDERS 90
PRIMARY DEPRESSION 91
EATING DISORDERS NOT OTHERWISE SPECIFIED 93
CLINICAL PHENOMENON OF SELF-HARM 95
TAMAR AND AMNON 98
SEXUAL ASSAULT 99
EPIDEMIOLOGY 100
RISKY SEXUAL BEHAVIOR 108
INTIMATE PARTNER SEXUAL VIOLENCE 114
SEXUAL ABUSE IN THE WORKPLACE 118
MILITARY SEXUAL TRAUMA 122
CHARACTERISTICS OF SEXUAL ASSAULT 127
INJURIES ASSOCIATED WITH SEXUAL VIOLENCE 135
REPRODUCTIVE HEALTH AND PREGNANCY 139
SEXUALLY TRANSMITTED DISEASES 143
PSYCHOLOGICAL CONSEQUENCES 147
POSTTRAUMATIC STRESS DISORDER 152
SEXUAL ASSAULT CENTRES 155
FAMILY FUNCTIONING 158
AN ANCIENT VICTIM 159
REVENGE 160
MOURNING FOR AMNON 161
ABSALOM 164
CLASSIFICATION OF HEART INJURIES 165
ABSALOM'S REBELLION 166
PENETRATING HEART INJURIES 166
THE RELATIONSHIP BETWEEN ABSALOM AND KING DAVID 168
ABSALOM'S PERSONALITY 170
FAMILY ASSESSMENT 170
MOURNING FOR ABSALOM 171
THE FATE OF CONCUBINES 174
THE GIBEONITES 176
STRESSFUL LIFE EVENTS AND SUBSEQUENT CRISES 178
SUMMARY OF FAMILY LIFE CYCLE 180
THE DISEASES THAT AFFLICTED THE OLD KING 184
THE OLD KING 185
EYE DISEASES 185
THE BIBLICAL DESCRIPTION 187
EPIDEMIOLOGY OF BLINDNESS 188
AGE-RELATED MACULAR DEGENERATION 199
TYPES 201
EPIDEMIOLOGY 202
RISK FACTORS 207
SYMPTOMATOLOGY 209
CATARACT 210
RISK FACTORS 216
SYMPTOMATOLOGY 218
GLAUCOMA 219
TYPES 220
EPIDEMIOLOGY 220
MECHANISMS OF THE DISEASE 224
SYMPTOMATOLOGY 225
DIAGNOSIS 226
OPTIC NEUROPATHY 230
OPTIC ATROPHY 233
REFRACTIVE ERROR 239
OCULAR MANIFESTATIONS OF CANCER 245
OTHER CAUSES 258
THE DISEASE OF THE BONES 268
THE BIBLICAL DESCRIPTION 268
OSTEOPOROSIS 268
TYPES 273
MALE OSTEOPOROSIS 276
CUSHING SYNDROME 277
HYPERTHYROIDSM/HYPOTHYROIDISM 278
ACROMEGALY 281
HYPOGONADISM 285
PRIMARY HYPERPARATHYROIDISM 289
PAGET'S DISEASE 292
LACTASE DEFICIENCY 297
BILIARY CIRRHOSIS 299
WHIPPLE DISEASE 303
CHRONIC OBSTRUCTIVE LUNG DISEASE 306
RHEUMATIC DISEASES 309
RHEUMATOID ARTHRITIS 310
MALNUTRITION 313
MEDICATIONS 315
IDIOPATHIC 318
ONCOHAEMATOLOGICAL DISORDERS 320
MULTIPLE MYELOMA 321
MONOCLONAL GAMMOPATHY OF UNDETERMINED SIGNIFICANCE 327
WALDENSTROM MACROGLOBULINEMIA 328
HEAVY CHAIN DISEASES 330
SMALL LYMPHOCYTE CELL DISORDERS 332
OSTEOMYELOFIBROSIS 335
AMYLOIDOSIS 340
PLASMACYTOMA 346
OTHER MALIGNANT DISEASES 349
LUNG CANCER 349
GASTRIC CARCINOMA 353
COLORECTAL CANCER 356
HEPATOCELLULAR CARCINOMA 359
PANCREATIC CANCER 363
GIANT CELL TUMOR 368
LEPTOMENINGEAL CARCINOMATOSIS 371
RENAL CELL CARCINOMA 372
PROSTATE CANCER 376
BLADDER CARCINOMA 380
METASTATIC BONE DISEASE 384
CLINICAL FEATURES 388
HAS THIS PATIENT CANCER? 394
THE DISEASE THAT CAUSED WEIGHT LOSS 395
INTRODUCTION 395
WEIGHT LOSS AS DESCRIBED IN THE BIBLE 396
CACHEXIA 396
WEIGHT LOSS IN THE ELDERLY 400
PHYSIOLOGICAL ANOREXIA OF AGING 403
PATHOLOGICAL CAUSES OF WEIGHT LOSS 406
THE DISEASE THAT CAUSED CHRONIC WEAKNESS 411
INTRODUCTION 411
WEAKNESS AS DESCRIBED IN THE BIBLE 411
DEFINITION 412
GENERAL WEAKNESS 412
FATIGUE IN CANCER PATIENTS 414
ANEMIA OF CHRONIC DISEASES 418
CANCER-RELATED ANEMIA 421
HYPOTHERMIA 424
INTRODUCTION 424
HYPOTHERMIA AS DESCRIBED IN THE BIBLE 425
ABNORMAL PHYSIOLOGIC MECHANISMS 425
TYPES OF HYPOTHERMIA 426
ENVIRONMENTAL HYPOTHERMIA 427
URBAN HYPOTHERMIA 429
CLINICAL STAGES 430
ADDITIONAL SIGNS 432
WAS THE KING'S TEMPERATURE TAKEN? 432
EKG CHANGES 433
HYPOTHERMIA IN THE KING 433
THERAPY 434
PRESSURE ULCERS 436
SKIN ULCERS AS DESCRIBED IN THE BIBLE 437
DEFINITION 437
MECHANISM OF DEVELOPMENT 438
EPIDEMIOLOGY 440
HOSPITAL COST 443
CLASSIFICATION 443
EUROPEAN PRESSURE ADVISORY PANNEL 443
MAKLEBUST & SIEGGREEN CLASSIFICATION SYSTEM 444
PRESSURE ULCER PAIN 444
MALODOROUS WOUNDS 446
RISK FACTORS FOR PRESSURE ULCERS 449
DIFFERENTIAL DIAGNOSIS 454
ERECTILE DYSFUNCTION 455
INTRODUCTION 455
THE BIBLICAL DESCRIPTION 456
DEFINITION 456
EPIDEMIOLOGY 457
ETIOLOGY 460
KING DAVID'S CASE 467
MENTAL DISORDER 470
INTRODUCTION 470
HISTORICAL BACKGROUND 471
PSYCHIATRIC EPIDEMIOLOGY 472
DEPRESSION 477
CRITERIA FOR MAJOR DEPESSION 483
SUBSTANCE-INDUCED MOOD DISORDER 484
GENERAL MEDICAL CONDITION 485
DYSTHYMIC DISORDER 486
MINOR DEPRESSION 488
STRATEGIES FOR DIAGNOSING DEPRESSION 490
MECHANISM OF DEPRESSION DEVELOPMENT 492
OUTCOME 497
GENERALIZED ANXIETY DISORDER 502
SUMMARY OF MEDICAL RECORD 506
ABBREVATIONS 507
PICTURES 513
1
L. Ben-Nun King David
MY VIEW
A PERSONAL ACCOUNT
When I arrived in Florence and saw the statue of David, I was
thrilled by the wonderful figure, and said to myself: how could a
mortal sculpt such an amazing figure, with such perfection of beauty
that seems to be alive? The sight gave me inspiration to learn more
about this giant character in the Bible, using all aspects of
contemporary medical science.
From the top of the Tower of David in Jerusalem, a symbol of the
rebirth of the Jewish people in the promised land, I set myself the
goal of diagnosing the state of health of King David, a character who
influenced the fate of the Jewish people, but solely according to the
actual text of the biblical verses, with no traditional interpretation,
from the viewpoint of contemporary medicine.
PREFACE
The purpose of this research is to analyze the medical situations and
conditions referred to in the Bible, as we are dealing with a
contemporary medical record.
FOREWORD
Every society is age graded, and every society has a system of
social expectations regarding age of appropriate behavior. The
individual passes through a socially regulated cycle from birth to
death as inexorably as he passes through the biological cycle: a
succession of socially delineated age-statuses, each with its
recognized rights, duties and obligations. There exists a socially
prescribed timetable for the ordering of major life events: a time in
the life span when men and women are expected to marry, a time to
raise children, and a time to retire. Men and women are aware not
only of the social clocks that operate in various areas of their lives,
but also of their own timing with regard to major life events. From
this perspective, time is at least a three-dimensional phenomenon in
charting the course of the life cycles, with historical time, lifetime (or
chronological age) and social time all intricately intertwined (1).
Family is defined as any group of people related either
biologically, emotionally, or legally (2), and is a basic structure of
each society. This structure is the most important small social system
that has survived through generations. During long human history,
the family adapted to the norms of each society, and its functioning
depended on the norms of each specific society.
Man has survived in all societies by belonging to aggregates that
vary in different cultures in their level of organization and
differentiation. It is an inherent and basic human condition that man
survives in groups, and the family is the most enduring social form of
small group. Primitive cultures rely on large groupings with relatively
stable distributions of functions among subgroups. In more complex
societies requiring new survival skills, the social structures and
groupings are more widely differentiated (3).
The family had undergone changes throughout history, that
parallel changes in society and has given up or taken over many of
the functions of protecting and socializing its member's response to
society's needs. Today, many people are wondering what is
happening to the family. People are troubled about many aspects of
current family life, including the divorce rate, reports of widening
child abuse, accounts of violence between spouses, and the
abundance of couples in nontraditional living and social
arrangements – contract marriages, people living in communes, and
4
L. Ben-Nun King David
The aging family involves a shift of roles, with the middle generation
taking on a more central place in the family. Retirement occurs at this
stage. People may adjust well to, or even welcome, retirement when it
is voluntary. Marital problems can arise if the new roles are not worked
out satisfactorily. Couples in the sixth stage tend to be maritally rather
than parentally oriented. The marriage is likely to become more
egalitarian. The couple may continue to have an active and meaningful
sex life. Marital satisfaction is likely to be at its highest point since the
couple’s early years together. Family relationships are still important.
Contact with children tends to be frequent. Strains may result if adult
children move back into the home, however. Women are far more
likely than men to experience the death of a spouse. Both men and
women whose spouses die face a difficult period of adjustment. There
is a loss of identity and a variety of physical and emotional
consequences of bereavement. Many eventually remarry, although
widows are less likely to do so than are widowers. Companionship is
one of the most common reasons that both men and women remarry
after the death of a spouse (5).
In spite of the changes that have occurred in contemporary society,
the function of the family as a system, its pattern of interaction, the
relationships within it, the creation of subsystems within the family,
and the psychosocial problems experienced by family members have
changed little through the ages. Both highly functioning and
dysfunctional families, which have existed since the dawn of human
history, will continue to be part of each society. It is important to study
both ancient families and contemporary families in order to handle
many of the problems found in dysfunctional families.
This study assessed the association between parental style, family
functioning and adolescent well-being, contrasting intact families
with those of changed configuration. The subjects included 801 grade
10 general level teenagers in 11 high schools of a single educational
system. Results indicated that the configuration of the family was not
the key determinant of effectiveness of family functioning. Instead,
the style of parenting turned out to be the main determinant of both
family functioning and well-being of the adolescents. While both
"parents" were judged to have contributed to these outcomes, cross
gender effects were found (6).
This paper investigates how education influences marriage
behavior in the US, West Germany, and former East Germany.
Following family economics, for women a longer education decreases
7
L. Ben-Nun King David
References
1. Neugarten B. Adaptation and the Life Cycle. The Counseling
Psychologist. 1976;6:1.
2. Ramsey CN, Lewis JM. Family structure and functioning. In: Robert E.
Rakel (ed.). Textbook of Family Practice. W. B. Saunders. Philadelphia,
London. Third ed. 1984, pp. 21-40.
3. McDaniel SH, Campbell TL, Seaburn DB. Basic premises of family-
oriented primary care. Family systems concepts. In: McDaniel SH, Campbell
TL, Seaburn DB (eds.). Springer-V, New York, Berlin. 1990, pp. 3-15, 33-39.
4. Cherlin A, Furstenberg Ff Jr. The changing European family: lessons for
the American reader. J Fam Issues. 1988;9:291-7.
5. Lauer RH, Lauer J. Marriage and Family. The Quest for Intimacy.
Available 15 November 2014 at highered.mheducation.com/
sites/0072487747/student _view0/ chapter15.
6. McFarlane AH, Bellissimo A, Norman GR. Family structure, family
functioning and adolescent well-being: the transcendent influence of
parental style. J Child Psychol Psychiatry. 1995;36(5):847-64.
7. Bruderl J, Diekmann A. Education, birth cohort, and marriage age: a
comparative analysis of marriage age in West Germany, East Germany, and
the United States. Z Soziol. 1994;23(1):56-73, 77.
8. Minuchin S. Families and Family Therapy. Cambridge: Harvard
University Press, 1974.
9
L. Ben-Nun King David
THE ROOTS
and his family. He refused the King's proposal to don armor of heavy
metal, preferring to remain in his shepherd's garment, armed with a
mere stick, sling, and smooth stones – weapons with which he was
familiar (1).
During the battle with Goliath ".. David hastened, and ran toward
the army to meet Philistine. And David put his hand in his bag, and
took thence a stone, and slung it, and smote the Philistine in his
forehead, that the stone sunk into his forehead; and he fell upon his
face to the earth" (I Samuel 17:48,49).
Goliath, a terrifying giant from the area of Gat, was slow-moving
and ponderous (1,2-4). It is most likely that Goliath was suffering
from acromegaly. The slowness of Goliath had been attributed to
three phenomena. The first is the heavy weight. In addition to his
vast physical size, Goliath was dressed in a heavy metal suit of armor:
"And he had a helmet of brass upon his head and he was armed with
a coat of mail; and the weight of the coat was five thousand shekels,
it was of brass. And he had graves of brass upon his legs, and a target
of brass between his shoulders. And the staff of his spear was like a
weaver's beam; and his spear's head weighed six hundred shekels of
iron." (17:5-7). The second explanation is that arthropathy and
myopathy frequently appear in the late stages of acromegaly (1,5).
According to Birginer, there is no indication to suspect such
complications. The third theory claims a visual disorder. Goliath was
not blind; he saw and taunted the young boy who confronted him.
David carried a stick, yet Goliath saw "several sticks", which may be
one of the indications of his impaired vision. Thus, Goliath suffered
from visual field restriction. Bitemporal hemianopsia occur in large
pituitary microadenoma because of optic chiasm compression in the
suprasellar region (1).
Goliath did not pass away after the stone hit his forehead:
"Therefore David ran, and stood upon the Philistine, and took his
sword, and drew it out of the sheath thereof, and slew him, and cut
off his head" (17:51). After the battle with the horrifying Goliath
"David took the head of the Philistine, and brought it to Jerusalem"
(17:54).
This was a thrilling battle, in which a cunning adolescent defeated
a frightening, clumsy giant from Gat. This victory showed that the
young David was very smart and skilful.
12
L. Ben-Nun King David
References
1. Berginer VM. Neurological aspects of the David-Goliath battle:
restriction in the giant's visual field. IMAJ.2000;2:725-7.
2. Prohets, Nevi'im, Samuel 1:17. In: The Jewish Bible, Tanakh, a new
translation of the Holy Scriptures into English. Jerusalem: Jewish Publication
Society; 1985, pp. 443-7.
3. Samuel 1:17. In: Prophets, Nevi'im (with translation into Russian),
Jerusalem: Mossad Harav Kook. 1978, 93-6.
4. The works of Flavius Josehus and the life of Josehus (written by
himself and accurately translated from the original Greek). Philadelphia:
Lippincott, Crambo and Co., 1854, Vol. 1, Chapter 9, pp. 106-8.
5. Lamberts SWJ. Acromegaly. In: Grossman A (ed.). Clinical
Endocrinology. Oxford Blackwell Scientific Publications, 1992, pp. 154-68.
KING SAUL. King Saul, the first King of Israel, ruled the country
about 3007 years ago. The son of Kish, he was a tall and handsome
child “... a choice young man, and a goodly: and there was not among
the children of Israel a goodlier person than he: from his shoulders
and upward he was higher than any of the people” (I Samuel 9:2).
When Saul grew up, he was chosen to be the King since “...he was
higher than any of the people from his shoulders and upward” and
“...there is none like him among all the people. And all the people
shouted, and said God save the King” (10:23,24). When Saul became
King, he participated in endless wars “So Saul took the kingdom over
Israel, and fought against all his enemies on every side...” (14:47).
However, later in his life signs of mental distress due to manic
depressive disorder appeared (1) “...an evil spirit from the Lord
troubled him” (16:14). Consequently, Saul’s servants summoned
David to play his harp, and “ ..he (the king) loved him greatly ; and he
became his armor-bearer” (16:21). On hearing the music, the
symptoms of Saul’s mental distress disappeared: “...David took a
harp ) )כינורand played with his hand: so Saul was refreshed, and was
well, and the evil spirit departed from him” (16:23).
When David killed Goliath, a terrifying giant from the area of Gat,
and subsequently defeated the Philistines, King Saul began to hate
David. The roots of this hatred were associated with the fact that the
13
L. Ben-Nun King David
people believed that "..Saul hath slain his thousands, and David his
ten thousands (Philistines)" (18:7).
David fought the Philistines and defeated them in another battle.
This victory had a negative impact on the King's mental state "And
the evil spirit from the Lord was upon Saul.. And Saul sought to smite
David even to the wall with his javelin…; but he slipped away out of
Saul's presence, and he smote the javelin into the wall: and David
fled, and escaped that night" (19:9,1). King Saul pursued David
throughout his life in order to kill him. In the end, David had an
opportunity to kill Saul, but he did not do it. Therefore, King Saul
appointed David to succeed him as King.
Thus, we are dealing with a patient, who has suffered from a
mental disorder. His mental status was severely disturbed. The
biblical text tells us that David played with a harp. The Complete
Hebrew-English Dictionary translates the Hebrew word כינורas violin,
psalterium, harp, lyra, and lyra Davidis (2). On what musical
instrument did King David play?
King Saul on hearing the beautiful sounds of music calmed down
and his distressing mental symptoms disappeared. Here, we see the
positive effect of music on the soul of an individual of the highest
socioeconomic stratum. The wonderful sounds of the music had a
positive effect on the King. David's simple, therapeutic intervention
bore fruit - King Saul relaxed, calmed down and his mental status
improved. This is an example of a therapeutic intervention provided
by the music (3).
References
1. Ben-Noun L. What was the Mental Disease that Afflicted King Saul ? Clin
Case Studies (CCS) USA. 2003;2:4-7.
15
L. Ben-Nun King David
DAVID'S FAMILY
DAVID, MERAB, AND MICHAL. King Saul decided to give his elder
daughter Merab in marriage to David. However, when “...Merab
Saul’s daughter should have been given to David,....she was given to
Adriel the Meholathite to wife” (I Samuel 18:19). Meanwhile, the
younger daughter Michal fell in love with David. Subsequently,
16
L. Ben-Nun King David
References
1. McDaniel S, Campbell TL, Seaburn DB. Family systems concepts. In:
McDaniel S, Campbell TL, Seaburn DB (eds.). Family-Oriented Primary
Care. A Manual for Medical providers. Springer-Verlag. New York, Berlin.
1990, pp.33-39.
2. McGoldrick M. The joining of families through marriage: the new
couple. In: Carter EA, Godrick M (eds.). The Family Life Cycle: A
Framework for Family Therapy Gardner Press, New York. 1980, pp. 93-
119.
3. Holland JA, de Valk HA. Ideal ages for family formation among
immigrants in Europe. Adv Life Course Res. 2013;18(4):257-69.
Reference
1. Terkelsen KG. Toward a theory of the family life cycle. In: Carter EA,
Goldrick M (eds.). The Family Life Cycle: A Framework for Family Therapy,
Gardner Press, New York. 1980, pp, 21-52.
2. Lopata, H. Z. Widowhood and husband sanctification. J Marriage
Family. 1981;43(2):439–50.
3. Bennett KM, Arnott L, Soulsby LK. "You're not getting married for the
moon and the stars": The uncertainties of older British widowers about the
idea of new romantic relationships. J Aging Stud. 2013;27(4):499-506.
4. Wu Z, Schimmele CM, Ouellet N. Repartnering after widowhood. . J
Gerontol B Psychol Sci Soc Sci. 2014 Jun 12. pii: gbu060. [Epub ahead of
print]
5. Schneider DS, Sledge PA, Shuchter SR, Zisook S. Dating and remarriage
over the first two years of widowhood. Ann Clin Psychiatry. 1996;8(2):51-7.
5. Gentry M, Shulman AD. Remarriage as a coping response for
widowhood. Psychol Aging. 1988;3(2):191-6.
7. Cleveland WP, Gianturco DT. Remarriage probability after
widowhood: a retrospective method. J Gerontol. 1976;31(1):99-103.
21
L. Ben-Nun King David
References
1."polygamy". Online Etymology Dictionary. Available 28 December 2014
at Polygamy - Wikipedia, the free encyclopedia. en.wikipedia.org/wiki/
Polygamy.
2. πολυγαμία. Henry George L, Robert S; A Greek–English Lexicon at the
Perseus Project. Available 28 December 2014 at Polygamy - Wikipedia, the
free encyclopedia. en.wikipedia.org/wiki/Polygamy.
3. Georgios B. s.v. πολυγαμία. Dictionary of Modern Greek (in Greek).
Lexicology Centre. 2002.
4. Koktvedgaard ZM. Polygamy: a cross-cultural analysis. Berg. 2008, p. 3.
ISBN 1-84520-220-1.
25
L. Ben-Nun King David
References
1. Ben-Nun L. The family life cycle of the Great King David. In: Ben–Nun L.
(ed.). Family medicine in Biblical Times. The Roots. B.N. Publication House.
Israel. 2005, pp. 165-84.
2. Ben-Nun L. The family life cycle and the medical record of King David
the Great. In Ben-Nun L. (ed.). The Kings of Israel. B.N. Publication House.
2009, pp. 31-7.
and HSV types 1 and 2 (28,29) are risk factors for subsequent or
concurrent HIV infection.
Approximately 10% of women will develop PID due to STDs during
their reproductive years, and a significant number will suffer
complications from the infections (7). PID presents a spectrum of
inflammatory disorders within the upper genital tract of women
including any combination of endometritis, salpingitis, pelvic
peritonitis, and tubo-ovarian abscess (30).
One of four women with PID experiences serious sequelae,
including tubal scarring, infertility, and ectopic pregnancy (31), or
chronic pelvic pain (32). In addition, genital papillomavirus infection
is associated with cervical dysplasia and may act as a cofactor in the
development of cervical cancer (33,34).
The STD and HIV epidemics are interdependent. Some behaviors,
such as frequent unprotected intercourse with different partners,
place people at high risk of both infections, and there is evidence that
conventional STDs increase the likelihood of HIV transmission. There
is biological evidence, too, that the presence of STDs increases
shedding of HIV, while treatment of these diseases reduces HIV
shedding. Therefore, control of the STIs has the potential to
contribute substantially to HIV prevention (35).
Among 2,982 individuals socializing at venues in seven
Madagascar towns, 78% of men and 74% of women reported new
sexual partnership or sex-trade for money, goods or services and 19%
of men and 18% of women reported symptoms suggestive STI in the
past four weeks. STI symptom levels were disproportionately high
among responders reporting either sex trade or new sexual
partnership in the past four weeks; 24% of men and 41% of women
reported condom use during the last sex act with a new partner (36).
This was an observational study of street-based sex workers
attending an inner-London genitourinary clinic between 2006 and
2007. The outreach team made contact with 120 street-based sex
workers in the borough, London. There were frequent reports of
recent recreational drug use, unprotected sex with clients and
unreliable contraception; seven were pregnant, six were HIV positive
and 12 had positive syphilis serology. A further 17 STDs were
identified. There were high frequency of HIV, syphilis, other bacterial
STDs, and unwanted pregnancies among sex workers attending this
clinic (37).
30
L. Ben-Nun King David
This study indicates that street-based sex workers are at risk for
contracting some STI.
AIDS is one of the most important diseases of our century that is
transmitted through sexual contacts. In order to deal more efficiently
with this disease we should understand its epidemiology,
characteristics, and the sexual behavior of a variety of populations.
In 2004, 71,755 new diagnoses of HIV were reported in the (WHO)
European region, which includes all European Union countries. The
number of newly diagnosed cases was lower than the peak observed
in 2001 (113,930), but was nearly twice the number in 1999 (39,602).
For different countries, reported rates reached more than 200 new
HIV diagnoses per million population in 2004; 568 in Estonia, 280 in
Portugal, and 212 in the Russian Federation (38).
Although the number of newly diagnosed cases in 2004 was lower
than in 2001, the rates of these infections are still high in European
countries.
In El Salvador, Guatemala, Honduras, Nicaragua, and Panama,
2,466 FSWs were evaluated. For FSWs, HIV seroprevalence ranged
from 0.2% in Nicaragua and Panama and 9.6% in Honduras, where
estimated HIV seroincidence was also the highest (3.2 per 100
person-years); 77% and 72% of FSWs reported using condoms
consistently with new and regular clients, respectively. The
prevalences of STDs were: 85.3% for HSV-2, 9.6% for syphilis, 20.1%
for C. trachomatis, 8.1% for N. gonorrhea, 11.0% for T. vaginalis, and
54.8% for bacterial vaginosis. HSV-2 infection was associated with
HIV infection (39).
African American women have high rates of most STIs, including
HIV. Black women (n=228) who used drugs completed a structured
questionnaire in a central Brooklyn, New-York-based research center
between 2003 and 2005. Thirty-eight (17%) women were HIV
seropositive; the prevalences of STIs included HSV-2 (79%),
trichomoniasis (37%), chlamydia (11%), and gonorrhea (2%). HIV-
infected women in comparison with uninfected women were
significantly more likely to have multiple positive screens and twice
more likely to report current sex work. Several STIs, including HIV,
seem to be endemic among black women who used drugs. Multiply
STIs infected individuals may unknowingly, but efficiently, contribute
to high STIs and HIV rates (40).
31
L. Ben-Nun King David
Women who work in sex work are at risk to be infected with STDs,
including HIV. Infected individuals may contribute unknowingly to the
high prevalence of STDs.
In Israel, despite the low sexual behavior of Israeli HIV patients,
they had a high prevalence of chronic STDs (e.g., HSV-2, HBV and
syphilis). The lower prevalence of chlamydia and gonorrhea among
HIV-immunosuppressed patients may be attributed to routine
antibiotic prophylaxis against opportunistic infections. Nevertheless,
as advocated by international health organizations, it appears
prudent to recommend the routine screening of these asymptomatic
HIV-positive patients for other STDs (41).
Syphilis, a STD, has afflicted humans since the dawn of history.
Throughout the centuries, its incidences and prevalences increased
and decreased, with recurrent epidemics spreading through the
continents. Now, we witness a recurrent upheaval of this STD
worldwide: in US (42), UK (43), France (44), Denmark (45), Germany
(46), Belgium (47), Finland (48), Russia (49), and China (50).
During 2001-2004, 7,083 cases of syphilis were diagnosed in Los
Angeles. Cases of confirmed or probable NS (n=109) occurring among
persons aged 19 to 65 years were identified during this period (1.5%).
Symptomatic NS was present in 1.2% of reported syphilis cases (86 of
7083). NS cases were inclusive of 71 (65%) men who have sex with
men. Forty-two (49%) of the symptomatic NS cases occurred during
secondary (n=28) or early latent (n=14) syphilis. Sixty-eight percent
(n=74) of the NS cases were HIV positive. The estimated incidence of
symptomatic NS among HIV-infected persons with early syphilis was
2.1% as compared with 0.6% among HIV-negative persons (51).
The aim of this research is to present syphilis among women
described as "indecent" according to the records of the Venereal
Diseases Hospital "Andreas Syggros", which is located in Athens,
during the period 1931-1935. In impoverished Greece of the Interwar
period, factors such as criminal ignorance, or lack of information on
STDs along with inadequate health controls of sex workers, resulted
in a dramatic spread of syphilis, whereas "Andreas Syggros" hospital
accommodated thousands of patients. The inflow of 1.300.000 Greek
refugees from Asia Minor, after the Greek defeat by the Turkish army
in the war of 1922, resulted in a notable change in the demographics
of the country, while the combination of miserable living conditions,
unemployment, economic crisis of the Interwar period, political
instability and dysfunction of the State led to an increased number of
32
L. Ben-Nun King David
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8. Sweet RL. Role of bacterial vaginosis in pelvic inflammatory disease.
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1992;19:93-101.
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11. Smith MA, Singer C. Sexually transmitted viruses other than HIV and
papillomavirus. Urol Clin North Am. 1992;19:47-61.
34
L. Ben-Nun King David
12. Soper DE, Brockwell NJ, Dalton HP, et al. Observations concerning the
microbial etiology of acute salpingitis. Am J Obstet Gynecol. 1994;170:1008-
17.
13. 1998 guidelines for treatment of sexually transmitted diseases.
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2007;83:351-6.
17. Summary of notifiable diseases, United States, 1997. Centers for
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19. Wright RA. Hepatitis B and other HBsAg carrier: an outbreak related
to sexual contact. JAMA. 1975; 232:717-21.
20. Koff RS, Slavin M, Connelly LJ, et al. Contagiousness of acute hepatitis
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21. Alter MJ, Ahtone J, Weisfuse I, et al. Hepatitis B virus transmission
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24. Saglio SD, Kurzman JT, Radner AB. HIV infection in women: an
escalating health concern. Am Fam Physician. 1996;54:1541-7.
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26. Plummer FA, Simonsen JN, Cameron DW, et al. Cofactors in male-
female transmission of HIV type. J Infect Dis.1991;163:233-9.
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28. Holmberg SD, Stewart JA, Gerber R, et al. Prior herpes simplex virus
type 2 infection as a risk factor for HIV infection. JAMA. 1988;259:1048-50.
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29. Allsworth JE, Lewis VA, Peiper JF. Viral sexually transmitted infections
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30. 1993 sexually transmitted diseases treatment guidelines. MMWR.
1993;42(RR-14):75.
31. Chow JM, Yonekura L, Richwald GA, et al. The association between
Chlamydia trachomatis and ectopic pregnancy. JAMA. 1990; 263: 3164-7.
32. Weström L. Effect of acute pelvic inflammatory disease on fertility.
Am J Obstet Gynecol. 1975;121:707.
33. Kassler WJ, Cates W Jr. The epidemiology and prevention of sexually
transmitted diseases. Urol Clin North Am. 1992;19:1-12.
34. Spitzer M, Krumholz BA. Human papillomavirus-related diseases in
the female patient. Urol Clin North Am. 1992;19:71-81.
35. Sangani P, Rutherford G, Wilkinson D. Population-based
interventions for reducing sexually transmitted infecftions, including HIV
infection. Cochrane Database Syst Rev. 2004;(2):CD001220.
36. Khan MR, Rasolofomanana JR, McClamroch KL, et al. High-risk sexual
behavior at social venues in Madagascar. Sex Trans Dis. 2008;35:738-45.
37. Creighton S, Tariq S, Perry G. Sexually transmitted infections among
UK street-based sex workers. Sex Transm Infect. 2008;84:32-3.
38. Nardone. Transmission of HIV/AIDS in Europe continuing. Euro
Surveillance. 2005;10: Issue 47.
39. Soto RJ, Ghee AE, Nunes CA, et al. Sentinel surveillance of sexually
transmitted infections/HIV and risk behaviors in vulnerable populations in 5
Central American countries. J Acquir Immun Defic Syndr. 2007;46:101-11.
40. Miller M, Liao Y, Wagner M, Korves C. HIV, the clustering of sexually
transmitted infections, and sex risk among African American women who
use drugs. Sex Trans Dis. 2008;35:696-702.
41. Joffe H, Bamberger E, Nurkin S, et al. Sexually transmitted diseases
among patients with human immunodeficiency virus in northern Israel.
IMAJ. 2006;8:333-6.
42. Taylor MM, Aynalem G, Olea LM, et al. A consequence of the syphilis
epidemics among men who have sex with men (MSM): neurosyphilis in Los
Angeles, 2001-2004. Sex Trans Dis. 2008;35:430-4.
43. Torjesen I. Disease: a warning from history. Health Serv L. 2008;
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44. Couturier E, Michel A, Janier M, et al. Syphilis surveillance in France,
2000-2003.Euro Surveill. 2004;9:8-10.
45. Cowan S. Syphilis in Denmark-Outbreak among MSM in Copenhagen,
2003-2004. Euro Surveill. 2004;9:25-7.
46. Marcus U, Bremer V, Hamouda O. Syphilis surveillance and trends of
the syphilis epidemic in Germany since the mid-90s. Euro Surveill. 2004;
9:11-4.
36
L. Ben-Nun King David
References
1. Oakley D, Bogue E-L. Quality of condom use as reported by female
clients of a family planning clinic. Am J Public Health. 1995;85:1526-30.
2. Murphy JC. The Condom Industry in the United States. Jefferson, NC:
McFarland & Co; 1990.
3. Cates W, Stone KM. Family planning, sexually transmitted diseases and
contraceptive choice: a literature update: Part I. Fam Plann Perspect. 1992;
24:75-84.
4. Jacobson JL. The other epidemic. World Watch. 1992;5:10-7.
5. Eaton DK, Kann L, Kinchen S, et al. Youth risk behavior surveillance –
United States, 2007. 2008;57:1-131.
6. Yan AF, Chiu YW, Stoesen CA, Wang MQ. STD-/HIV-related sexual risk
behaviors and substance use among U.S. rural adolescents. J Natl Med
Assoc. 2007;99:1386-94.
39
L. Ben-Nun King David
References
1. Becket JA. General system theory, psychiatry and psychotherapy. Int J
Group Psychotherapy. 1973;23:292-305.
2. Rothbaum F, Rosen K, Ujiie T, Uchida N. Family systems theory,
attachment theory, and culture. Fam Process. 2002;41(3):328-50.
In any case, when the days of mourning were over "When the
mourning was past, David sent and fetched her (Bathsheba) to his
house; and she became his wife, and bare him a son” (II Samuel
11:27). David’s family again expanded. Two additional members
entered David’s family life cycle – Bathsheba and the newborn son.
Holmes and Rahe developed a standard list of events, the
Schedule of Readjustment Rating Scale (1). Several hundred
responders rated the amount of adaptation or "life change units"
that each event was thought to entail. According to this Scale,
marriage has a mean "life change units" value of 50, ranked seventh
out of various life events while 'gain a new family member' has a
mean value of 39. Thus, marriages and subsequent births of children
exposed the King to stressful events.
Reference
1. Holmes TH, Rahe RH. The Social Readjustment Rating Scale. J
Psychosom Res. 1967;11:213.
References
1. Bittar Z. Rates of perinatal mortality and low birth weight among 3367
consecutive births in south of Beirut. J Med Liban. 1998;46:126-30.
2. Bang AT, Reddy HM, Bang RA, Deshmukh MD. Why do neonates die in
rural Gadchiroli, India (Part II): estimating population attributable risks and
contribution of multiple morbidities for identifying a strategy to prevent
deaths. J Perinatol. 2005;25 Suppl 1:S35-43.
3. Vaid A, Mammen A, Primrose B, Kang G. Infant mortality in an urban
slum. Ind J Pediatr. 2007;74:449–53.
4. McDermott J, Steketee R, Wirima J. Perinatal mortality in rural Malawi.
Bull World health Organ. 1996;74:165-71.
5. Jehan I, Harris H, Salat S, et al. Neonatal mortality, risk factors and
causes: a prospective population-based cohort study in urban Pakistan. Bull
World Health Org. 2009;87:130-8.
6. Chowdhury HR, Thompson S, Ali M, et al. Causes of neonatal deaths in a
rural subdistrict of Bangladesh: implications for intervention. J Health Popul
Nutr. 2010;28:375-82.
7. Boo NY, Nasri NM, Cheong SK, Sivamohan N. A 2-year study of neonatal
mortality in a large Malaysian hospital. Singapore Med J. 1991;32:142.
8. Onayade AA, Sule SS, Elusiyan JB. Determinants of neonatal mortality at
Wesley Guild Hospital, Ilesa, Nigeria. Niger J Med. 2006;15:271-6.
9. de Almeida MF, Alencar GP, Schoeps D, et al. Survival and risk factors for
neonatal mortality in a cohort of very low birth weight infants in the southern
region of São Paulo city, Brazil. Cad Saude Publica. 2011;27(6):1088-98.
10. Souza Rugolo LM, Bentlin MR, Mussi-Pinhata M, et al. Late-onset sepsis
in very low birth weight infants: a Brazilian Neonatal Research Network Study.
Trop Pediatr. J Trop Pediatr. 2014;60(6):415-21.
11. Turner C, Turner P, Hoogenboom G, et al. A three year descriptive study
of early onset neonatal sepsis in a refugee population on the Thailand
Myanmar border. BMC Infect Dis. 2013 21;13:601.
12. Hornik CP, Fort P, Clark RH, et al. Early and late onset sepsis in very-
low-birth-weight infants from a large group of neonatal intensive care units.
Early Hum Dev. 2012;88 Suppl 2:S69-74.
43
L. Ben-Nun King David
13. Manuck TA, Varner MW. Neonatal and early childhood outcomes
following early vs later preterm premature rupture of membranes. Am J
Obstet Gynecol. 2014 May 22. pii: S0002-9378(14)00498-0.
14. Gezer A, Parafit-Yalciner E, Guralp O, et al. Neonatal morbidity
mortality outcomes in pre-term premature rupture of membranes. J Obstet
Gynaecol. 2013;33(1):38-42.
15. Ben-Nun L. In: Ben-Nun L. (ed.). A Disease that Afflicted the Newborn
Son of King David. B.N. Publication House. Israel. 2011.
16. Ma Y, Guo S, Wang H, et al. Cause of death among Infants in rural
Western China: a community-based study using verbal autopsy. J Pediatr. 2014
Jun 11. pii: S0022-3476(14)00405-3.
BIRTH ASPHYXIA. Factors that place the newborn infant at high risk
for asphyxia include: 1] maternal conditions such as DM, preeclampsia,
hypertension, chronic renal disease, anemia (e.g., Hg <10 g/dl); blood
type or group alloimmunization; narcotic, barbiturate, tranquilizer, or
alcohol intoxication; history of previous perinatal loss; lupus, maternal
heart disease; maternal fever or other evidence of amnionitis; maternal
hypotension and hemorrhage, 2] labor and delivery conditions such as
forceps delivery other than low-elective or vacuum-extraction delivery;
breech or other abnormal presentation and delivery; cephalopelvic
disproportion: shoulder dystocia, prolonged second stage; Cesarian
section; prolapsed umbilical cord; cord compression, prolonged rupture
of membranes, abruption placentae, placenta previa, or other
antepartum hemorrhage, 3] fetal conditions such as premature
delivery; postmature delivery; acidosis determined by fetal scalp
capillary blood; abnormal heart rate pattern or dysrhythmia;
meconium-stained amniotic fluid; oligohydramnios; polyhydramnios;
decreased rate of growth: uterine size or fetal size determined by
ultrasonography; macrosomia; immaturity or pulmonary surfactant
system; fatal malformations determined by sonography; hydrops
fetalis; low biophysical profile; multiple births, in particular, discordant,
stuck, or monoamniotic, and abnormal umbilical artery (1).
Among the numerous fetal conditions associated with birth
asphyxia, LBW, Apgar scores, lower umbilical artery pH, and lower
neonatal Hg levels at birth, prematurity, fatal malformation, or a
combination of these conditions would be the most likely causes (2,3).
Asphyxiated infants have delayed onset of breathing, poor
movement and color, and an increased frequency of convulsions (4).
44
L. Ben-Nun King David
The biblical text does not mention any of these symptoms. However,
the lack of details does not prove the absence of birth asphyxia.
The biblical text does not tell us if Bathsheba suffered from some
maternal condition, or difficult labor, or some complication associated
with her labor. Although these details are lacking, it appears that
maternal and labor or delivery conditions were not responsible.
Were non-specific symptoms present? Did the newborn suffer from
birth asphyxia?
References
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McDonald MG (eds.). Fifth ed. Lippincott, Williams & Wilkins. Philadelphia,
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4. Ben-Nun L. A disease that afflicted the newborn son of King David. Ben-
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cardiac, nervous system and genetic involvement - a case report. Diagn Pathol.
2013 Sep 20;8:159.
12. Laux D, Bessières B, Houyel L, et al. Early neonatal death and congenital
left coronary abnormalities: ostial atresia, stenosis and anomalous aortic
origin. Arch Cardiovasc Dis. 2013;106(4):202-8.
13. Wren C, Irving CA, Griffiths JA, et al. Mortality in infants with
cardiovascular malformations. Eur J Pediatr. 2012;171(2):281-7.
14. Simon EM, Goldstein RB, Coakley FV, et al. Fast MR imaging of fetal CNS
anomalies in utero. A J N R Am J. Neuroradiol. 2000;21:1688-98.
15. Laifer-Narin S, Budorick NE, Simpson LL, Platt LD. Fetal magnetic
resonance imaging: a review. Curr Opin Obstet Gynecol. 2007;19:151-6.
16. Levine D, Barnes PD, Madsen JR, et al. Fetal central nervous system
anomalies: MR imaging augments sonographic diagnosis. Radiology. 1997;
204:635-42.
17. Ben-Nun L. Congenital anomalies. In: A Disease that Afflicted the
Newborn Son of King David. B. N. Publication House. Israel. 2011, pp. 62-72.
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References
1. Kaistha N, Mehta M, Singla N, et al. Neonatal septicemia isolates and
resistance patterns in a tertiary care hospital of North India. J Infect Dev Ctries.
2009;4:55-7.
2. Souza Rugolo LM, Bentlin MR, Mussi-Pinhata M, et al. Late-onset sepsis
in very low birth weight infants: a Brazilian neonatal research network study.
Trop Pediatr. J Trop Pediatr. 2014;60(6):415-21.
3. Stoll BJ, Hansen N. Infections in VLBW infants: studies from the NICHD
Neonatal Research Network. Semin Perinatol. 2003;27:293-301.
4. Mokuolu AO, Jiya N, Adesiyun OO. Neonatal septicaemia in Ilorin:
bacterial pathogens and antibiotic sensitivity pattern. Afr J Med Sci. 2002;
31:127-30.
5. Aurangzeb B, Hameed A. Neonatal sepsis in hospital-born babies:
bacterial isolates and antibiotic susceptibility patterns. J Coll Physician Surg
Pak. 2003;13:629-32.
6. Hornik CP, Fort P, Clark RH, et al. Early and late onset sepsis in very-low-
birth-weight infants from a large group of neonatal intensive care units. Early
Hum Dev. 2012;88 Suppl 2:S69-74.
7. Kayange N, Kamugisha E, Mwizamholya DL, et al. Predictors of positive
blood culture and deaths among neonates with suspected neonatal sepsis in a
tertiary hospital, Mwanza- Tanzania. BMC Pediatr. 2010;10:39.
8. Shitaye D, Asrat D, Woldeamanuel Y, Worku B. Risk factors and etiology
of neonatal sepsis in Tikur Anbessa University Hospital, Ethiopia. Ethip Med J.
2010;48:11-21.
9. Iijima S, Arai H, Ozawa Y, et al. Clinical patterns in extremely preterm (22
to 24 weeks of gestation) infants in relation to survival time and prognosis. Am
J Perinatol. 2009;26:399-406.
53
L. Ben-Nun King David
10. Rodríguez Cervilla J, Fraga JM, García Riestra C, et al. Neonatal sepsis:
epidemiologic indicators and relation to birth weight and length of
hospitalization time. An Esp Pediatr. 1998;48:401-8.
11. Tiskumara R, Fakharee SH, Liu CQ, et al, and Asia-Pacific Neonatal
Infections Study. Neonatal infections in Asia. Arch Dis Child Fetal Neonatal Ed.
2009;94:F144-8.
References
1. de Louvois J. Acute bacterial meningitis in the newborn. J Antimicrob
Chemoth. 1994;34 Suppl A:61-73.
2. Ríos-Reátegui E, Ruiz-González L, Murguía-de-Sierra T. Neonatal bacterial
meningitis in a tertiary treatment center. Rev Invest Clin. 1998;50:31-6.
3. Airede KI, Adeyemi O, Ibrahim T. Neonatal bacterial meningitis and
dexamethasone adjunctive usage in Nigeria. Niger J Clin Pract. 2008;11:235-45.
4. Grupo de Hospitales Castrillo. Neonatal meningitis. Epidemiological
study of the Grupo de Hospitales Castrillo. An Esp Pediatr. 2002;56:556-63.
5. Laving AM, Musoke RN, Wasunna AO, Revathi G. Neonatal bacterial
meningitis at the newborn unit of Kenyatta National Hospital. East Afr Med J.
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6. Airede AI. Neonatal bacterial meningitis in the middle belt of Nigeria.
Dev Med Chil Neurol. 1993;35:424-30.
7. Daoud AS, al-Sheyyab M, Abu-Ekteish F, et al. Neonatal meningitis in
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54
L. Ben-Nun King David
be small for their GA (p=0.003), have a CHD (p=0.007), and suffer from
hypoxic-ischemic encephalopathy (p=0.04). The presence of
hypotension, metabolic acidosis, thrombocytopenia, and
pneumoperitoneum was associated with a poor prognosis. Twelve of
the 13 (92%) NEC infants who died had a surgical intervention. In this
study, late preterm and term infants who developed NEC had other
underlying clinical diagnoses and had culture-proven sepsis. Mortality
rate was high in infants who required surgical intervention, indicating
that they were gravely ill from the onset. Thrombocytopenia,
hypotension and metabolic acidosis in late preterm and term infant
with NEC were associated with poor prognosis (3).
References
1. Niemarkt HJ, de Meij TG, van de Velde ME, et al. Necrotizing
Enterocolitis: A Clinical Review on Diagnostic Biomarkers and the Role of the
Intestinal Microbiota. Inflamm Bowel Dis. 2014 Sep 29. [Epub ahead of print].
2. Yu L, Sun B, Miao P, Feng X. Risk factors for prognosis of neonatal
necrotizing enterocolitis: an analysis of 82 cases. Zhongguo Dang Dai Er Ke Za
Zhi. 2013;15(12):1082-5.
3. Al Tawil K, Sumaily H, Ahmed IA, et al. Risk factors, characteristics and
outcomes of necrotizing enterocolitis in late preterm and term infants. J
Neonatal Perinatal Med. 2013;6(2):125-30.
DIARRHEA. Acute diarrhea afflicts many children less than one year
of age (1,2). Maternal risk factors include black ethnicity, youth, single
status, low educational level, and insufficient prenatal care (1). These
factors do not seem to apply in Bathsheba's case.
Complications of diarrhea that may lead to death include
prematurity, LBW, nausea/vomiting, electrolyte disorders, shock, and
cardiac arrest (2-5). Premature birth is the main factor that can be
linked to mortality before the age of one month. The biblical text gives
no description of diarrhea or any complication associated with diarrhea
56
L. Ben-Nun King David
in the newborn. For this reason, it seems unlikely that diarrhea was
responsible for his death.
References
1. Ho MS, Glass RI, Pinsky PF, et al. Diarrheal deaths in American children.
Are they preventable? JAMA. 1988;260:3281-5.
2. Kilgore PE, Holman RC, Clarke MJ, Glass RI. Trends of diarrheal disease--
associated mortality in US children, 1968 through 1991. JAMA. 1995;274:1143-
8.
3. Aye DT, Bact D, Sack DA, et al. Neonatal diarrhea at a maternity hospital
in Rangoon. Am J Public Health 1991;81:480-1.
4. Bendib A, Dekkar N, Lamdjadani N. Factors associated with neonatal,
infant and child mortality. Results of a national survey in Algeria. Arch Fr
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5. Mehal JM, Esposito DH, Holman RC, et al. Risk factors for diarrhea-
associated infant mortality in the United States, 2005-2007. Pediatr Infect Dis
J. 2012;31(7):717-21.
References
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tetanus. Cochrane database Syst Rev. 2005 Oct 19;(4):CD002959.
2. Finegold SM. Tetanus. In: Collier L, Balows A, Susman M, eds. Topley and
Wilaon's Microbiology and Microbial Infections. 9th ed. London; Arnold. 1998,
pp. 693-713.
3. Bhatia R, Prabhakar S, Grover VK. Tetanus. Neurol India. 2002;50:398-
407.
4. Department of Health Science. Ministry of Health and Population.
Annual Report 2006/2007. Kathmandu: Ministry of Health and Population.
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5. Poudel P, Budhathosi S, Manandhar S. Tetanus. Kathmandu University
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6. Lambo JA, Anokye EA. Prognostic factors for mortality in neonatal
tetanus: a systematic review and meta-analysis. Int J Infect Dis. 2013;17(12):
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7. Rai R, Singh DK. Neonatal tetanus: a continuing challenge. Indian J
Pediatr. 2012;79(12):1648-50.
8. Volpe JJ. Neurology of the Newborn. 3 rd ed. Philadelphia. WB Saunders.
1995, pp. 759-61.
9. Ben-Nun L. Neonatal tetanus. In: Ben-Nun L. (ed.). A Disease that
Afflicted the Newborn Son of King David. B.N. Publication House. Israel. 2011,
pp. 89-96.
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References
1. Yilgwan CS, Hyacinth HI, Oguche S. Factors associated with decreased
survival from neonatal malaria infection in Jos, North Central Nigeria. Niger J
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2. Snow RW, Marsh K. The consequences of reducing transmission of
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4. Singh J, Soni D, Mishra D, et al. Placental and neonatal outcome in
maternal malaria. Indian Pediatr. 2014;51(4):285-8.
5. Runsewe-Abiodun YT, Ogunfowora OB, Fetuga BM. Neonatal malaria in
Nigeria - a 2 year review. BMC Pediatr. 2006;6:19.
6. Liu X, Tao ZY, Fang Q, et al. A case of congenital plasmodium vivax
malaria from a temperate region in Central China. Malar J. 2012 Jun 6;11:182.
7. Le Hesran JY, Cot M, Personne P, et al. Maternal placental infection with
Plasmodium falciparum and malaria morbidity during the first 2 years of life.
Am J Epidemiol. 1997;146:826-31.
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1. Assaad F. Measles: summary of worldwide impact. Bull World Health
Org. 1983;5:452-9.
2. Hutchins S, Markowitz L, Atkinson W, et al. Measles outbreaks in the
United States, 1987 through 1990. Am J Infect Control. 1996;15:31-8.
3. Gunnarsdottir S, Briem H, Gottfredsson M. Extent and impact of the
measles epidemics of 1846 and 1882 in Iceland. Laeknabladid. 2014;100(4):
211-6.
4. Marinova L, Muscat M, Mihneva Z, Kojouharova M. An update on an
ongoing measles outbreak in Bulgaria, April-November 2009. Euro Surveill.
2009;14(50). pii: 19442.
5. Hennessey KA, Ion-Nedelcu N, Craciun MD, et al. Measles epidemic in
Romania, 1996-1998: assessment of vaccine effectiveness by case-control and
cohort studies. Am J Epidemiol. 1999;150:1250-7.
6. Grais RF, Dubray C, Gerstl S, et al. Unacceptably high mortality related to
measles epidemics in Niger, Nigeria, and Chad. PLoS Med. 2007;4:e24.
7. Ariyasriwatana C, Kalayanarooj S. Severity of measles: a study at the
Queen Sirikit National Institute of Child Health. J Med Assoc Thai. 2004;87:581-
8.
9. Ben-Nun L. Neonatal tetanus. In: Ben-Nun L. (ed.). A Disease that
Afflicted the Newborn Son of King David. B. N. Publication House. Israel. 2011,
pp. 101-7.
References
1. Myer L, Wilkinson D, Lombard C, et al. Impact of on-site testing for
maternal syphilis on treatment delays, treatment rates, and perinatal mortality
in rural South Africa: a randomised controlled trial. Sex Trans Infect. 2003;79:
208-13.
2. Chen XS, Yin YP. Syphilis: still a major cause of infant mortality. Lancet
Infect Dis. 2012;12(4):269-70; author reply 270-1.
3. Walker DG, Walker GJ. Syphilis: still a major cause of infant mortality.
Lancet Infect Dis. 2012;12(4):269; author reply 270-1.
4. Rutgers S. Syphilis in pregnancy: a medical audit in a rural district. Centr
Afr J Med. 1993;39:248-53.
5. Rosanna W. Peeling, Htun Ye. Diagnostic tools for preventing and
managing maternal and congenital syphilis: an overview. Bull World Health
Organ. 2004;82:439–46.
6. Tikhonova L, Salakhov E, Southwick K, et al. Congenital syphilis in the
Russian Federation: magnitude, determinants, and consequences. Sex Trans
Infect. 2003;79:106–10.
7. Kremenová S1, Zákoucká H, Kremen J. Issues of congenital syphilis in the
past twenty years. II. Clinical picture. Klin Mikrobiol Infekc Lek.2006;12(2):51-7.
8. Sangtawesin V, Lertsutthiwong W, Kanjanapattanakul W, et al. Outcome
of maternal syphilis at Rajavithi Hospital on offspring. J Med Assoc Thai.
2005;88:1519-25.
9. Southwick KL, Blanco S, Santander A, et al. Maternal and congenital
syphilis in Bolivia, 1996: prevalence and risk factors. Bull World Health Organ.
2001;79:33-42.
10. Ben-Nun L. Neonatal tetanus. In: Ben-Nun L. (ed.). A Disease that
Afflicted the Newborn Son of King David. B.N. Publication House. Israel. 2011,
pp. 107-13.
References
1. Chen A, Shi LP, Zheng JY, Du LZ. Clinical characteristics and outcomes of
respiratory distress syndrome in term and late-preterm neonates. Honghua Er
Ke Za Zhi. 2008;46:654-7.
2. Kamath BD, Macguire ER, McClure EM, et al. Neonatal mortality from
respiratory distress syndrome: lessons for low-resource countries. Pediatrics.
2011;127(6):1139-46.
3. Marraro GA, Chen C, Piga MA, et al. Acute respiratory distress syndrome
in the pediatric age: an update on advanced treatment. Zhongguo Dang Dai Er
Ke Za Zhi. 2014;16(5):437-47.
4. Kalter HD, Khazen RR, Barghouthi M, Odeh M. Prospective community-
based cluster census and case-control study of stillbirths and neonatal deaths
in the West Bank and Gaza Strip. Paediatr Perinat Epidemiol. 2008;22(4):321-
33.
5. Anderson MR. Update on pediatric acute respiratory distress syndrome.
Respir Care. 2003;48:261-76; discussion 276-8.
6. Gnanaratnem J, Finer NN. Neonatal acute respiratory failure. Curr Opin
Pediatr. 2000;12:227-32.
7. Hermansen CL, Lorah KN. Respiratory distress in the newborn. Am Fam
Physician. 2007;76:987-94.,
8. Wood BP. The newborn chest. Radiol Clin North Am. 1993;31:667-76.
64
L. Ben-Nun King David
between one month to one year, while the King's newborn son died on
the seventh day, 2] the term SIDS refers to a death that occurs
suddenly, while the condition of the newborn deteriorated gradually
during the first seven days of life, 3] the newborn came from a high
socioeconomic stratum, so there were enough servants to watch the
infant day and night, 4] there is no reason to suspect other risk factors
such as the sleeping position: prone or side, bed or room sharing with
parents, maternal or/and paternal smoking, thermal environment, face
cover, multiple births, a previous stillbirth or infant death, childcare
facility, or deprived social circumstances. Although LBW, prematurity,
and IUGT as risk factors for SIDS may be suspected in this case, the
biblical text gives no specific data to support this diagnosis (14).
References
1. Otto-Buczkowska E. Sudden infant death syndrome. Pol Merkur Lekarski.
2002;13:524-5.
2. Carl E. Hunt CE, Hauck FR. Sudden infant death syndrome. CMAJ.
2006;174:1861–9.
3. Kahn A, Groswasser J, Franco P, et al. Sudden infant deaths: stress,
arousal and SIDS. Early Hum Dev. 2003;75 Suppl:S147-66.
4. Caddell JL. Magnesium deficiency promotes muscle weakness,
contributing to the risk of sudden infant death (SIDS) in infants sleeping prone.
Mag Res. 2001;14(1-2):39-50.
5. Highet AR, Berry AM, Goldwater PN. Novel hypothesis for unexplained
sudden unexpected death in infancy (SUDI). Arch Dis Child. 2009;94:841-3.
6. Fleming PJ. Understanding and preventing sudden infant death
syndrome. Curr Opin Pediatr. 1994;6:158-62.
7. Moon RY, Patel KM, Shaefer SJ. Sudden infant death syndrome in child
care settings. Pediatrics. 2000;106(2 Pt 1):295-300.
8. Fleming PJ, Blair PS, Bacon C, et al. Environment of infants during sleep
and risk of the sudden infant death syndrome: results of 1993-5 case-control
study for confidential inquiry into stillbirths and deaths in infancy. Confidential
Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers.
BMJ. 1996;313(7051):191-5.
9. Leach CE, Blair PS, Fleming PJ, et al. Epidemiology of SIDS and explained
sudden infant deaths. CESDI SUDI Research Group. Pediatrics. 1999;
104(4):e43.
10. McGarvey C, McDonnell M, Hamilton K, et al. An 8-year study of risk
factors for SIDS: bed sharing versus non-bed-sharing. Arch Dis Child. 2006;
91:318-23.
11. Task Force on Sudden Infant Death Syndrome, Moon RY. SIDS and other
sleep-related infant deaths: expansion of recommendations for a safe infant
sleeping environment. Pediatrics. 2011;128(5):e1341-67.
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L. Ben-Nun King David
12. Mage DT, Donner EM. Is excess male infant mortality from sudden
infant death syndrome and other respiratory diseases X-linked? Acta Paediatr.
2014;103(2):188-93.
13. Pryce JW1, Paine SM, Weber MA, et al. Role of routine
neuropathological examination for determining cause of death in sudden
unexpected deaths in infancy (SUDI). J Clin Pathol. 2012;65(3):257-61.
14. Ben-Nun L. Sudden Infant Death Syndrome. In: Ben-Nun L. (ed.). A
Disease that Afflicted the Newborn Son of King David. B. N. Publication House.
Israel. 2011, pp. 120-33.
References
1. Murphy PA, Fullerton J. Outcomes of intended home births in nurse-
midwifery practice: a prospective descriptive study. Obstet Gynecol. 1998;92:
461-70.
2. Pang JW, Heffelfinger JD, Huang GJ, et al. Outcomes of planned home
births in Washington State: 1989-1996. Obstet Gynecol. 2002;100:253-9.
3. Anderson RE, Murphy PA. Outcomes of 11.788 planned home births
attended by certified nurse-midwives. A retrospective descriptive study. J Nurs
Midwifery. 1995;40:483-92.
4. Janssen PA, Saxell L, Page LA, et al. Outcomes of planned home birth
with registered midwife versus planned hospital birth with midwife or
physician. CMAJ. 2009;181:377-83.
5. Kennare RM, Keirse MJ, Tucker GR, Chan AC. Planned home and hospital
births in South Australia, 1991-2006: differences in outcomes. Med J Austr.
2010;192:76-80.
6. Ben-Nun L. Home-birth. In: Ben-Nun L. (ed.). A Disease that Afflicted the
Newborn Son of King David. B.N. Publication House. Israel. 2011, pp. 134-42.
References
1. Fenn B, Kirkwood BR, Popatia Z, Bradley DJ. Inequities in neonatal
survival interventions: evidence from national surveys. Arch Dis Child: Fetal &
Neonatal. 2007;92:F361–F366.
2. Hajizadeh M, Nandi A, Heymann J. Social inequality in infant mortality:
what explains variation across low and middle income countries? Soc Sci Med.
2014;101:36-46.
3. Dummer T, Parker L. Changing socioeconomic inequality in infant
mortality in Cumbria. Arch Dis Child. 2005;90:157–62.
4. Nattey C, Masanja H, Klipstein-Grobusch K. Relationship between
household socio-economic status and under-five mortality in Rufiji DSS,
Tanzania. Glob Health Action. 2013 Jan 24;6:19278.
5. Smith LK, Draper ES, Manktelow BN, Field DJ. Socioeconomic inequalities
in survival and provision of neonatal care: population based study of very
preterm infants. BMJ. 2009;339: b4702.
6. Calling S, Li X, Sundquist J, Sundquist K. Socioeconomic inequalities and
infant mortality of 46,470 preterm infants born in Sweden between 1992 and
2006. Paediatr Perinat Epidemiol. 2011;25(4):357-65.
7. Damghanian M, Shariati M, Mirzaiinajmabadi K, et al. Socioeconomic
inequality and its determinants regarding infant mortality in Iran. Iran Red
Crescent Med J. 2014;16(6):e17602.
is broader in scope than either QOL or quality of care both at the end
of life, although there is overlap among these constructs (4).
The death of the newborn baby was a traumatic exposure to a
negative stress. In King David's case, multidimensional parameters
such as physical, psychological, and social experiences and the
circumstances of the death all played a role in the negative
experiences and the great suffering caused by the sickness and death
of the newborn son.
Parents are attached to their unborn children, and loss around.
Parental grief is a normal response, and may last for many months.
Aspects of psychological management are associated with the time of
birth and is a serious trauma (5). Depression, anxiety disorder, PTSD
and somatoform disorder all have been linked to grief reactions in
response to perinatal loss (6).
In his reactions to this tragedy, King David showed a strong
character, one that was able to overcome various psychological
aspects of the grieving process. Both David and Bathsheba went
through the mourning process of the loss of their newborn son.
The purpose of this study was to understand mothers'
experiences and perspectives concerning neonatal death. Four
themes evolved: 1] Puzzlement on the brink of neonatal death:
neonatal death, as an unpredicted event, constitutes a puzzle for
mothers; they tend to seek the cause of the mishap, and in turn, fall
into a dilemma about whether to try to save the newborn. 2] Chaos
in the wake of the loss of babies: mothers' experience of physical,
mental, and behavioral changes might stymie their original positive
attitude toward the role of being the husband and wife. 3]
Adjustments in the wake of the loss: when mothers try to adjust
themselves, common approaches, such as good will with pep talk and
emotional utterance/sharing, are not ready helpful. Certain factors
also play a part, either positively or negatively, in the mental
adjustment process; they include responsibility for the household,
intentional mood-diversion, prohibiting the mother from
participating in funerals for the babies. 4] Professional guidance:
mothers expect to receive professional guidance to help them to face
the fact of death, especially in the movement of separation;
providing memorabilia and personalized follow-ups for mothers are
beneficial. In conclusion, mothers experiencing neonatal death
should be encouraged to express their grief through appropriate
emotional channels, and receive professional follow-up to rebuild
72
L. Ben-Nun King David
References
1. Holmes TH, Rahe RH. The Social Readjustment Rating Scale. J
Psychosom Res. 1967;11:213.
2. Cabodevilla I. Loss and mourning. An Sist Sanit Navar. 2007;30 Suppl
3:163-76.
3. Geerinck-Vercammen CR, Duijvestinj MJ. Coping with grief following
perinatal death: a multifaceted and natural process. Ned Tijdschr Geneeskd.
2004;148:1231-4.
4. Hales S, Zimmermann C, Rodin G. The quality of dying and death. Arch
Intern Med. 2008;168:912-8.
5. Hudges P, Riches S. Psychological aspects of perinatal loss. Curr Opin
Obstet Gynecol. 2003;15:107-11.
6. Scheidtr CE, Waller N, Wangler J, et al. Mourning after perinatal death-
prevalence symptoms and treatment – a review of literature. Psychother
Psychosom Med Psychol. 2007;57:4-11.
7. Chiang CC, Lee JT, Wang CH, Tang WR. Mothers' experiences and
perspectives of neonatal death: a qualitative retrospective inquiry. Hu Li Za
Ahi. 2007;54:48-55.
8. Aldwin CM. Life events. In: Aldwin CN (ed). Stress, Coping, and
Development. An Integrative Perspective. The Guilford Press. New York,
London. 1994, pp. 57-8.
73
L. Ben-Nun King David
FAMILY GROWTH
After David left Hebron “And David took him more concubines and
wives of Jerusalem.....And other children were born in Jerusalem:
Shammuah, Shobab, Nathan, Solomon, Ibhar, Elishua, Nepheg,
Japhia, Elishama, Eliada, and Eliphalet” (5:13-16). The King’s
polygamous family expanded significantly, and now included many
wives, concubines and 17 children.
Families are unique in permanence of membership and in the
primacy of affectional relationship over task performance. What are
the needs that are addressed uniquely in the family unit? There are
two fundamental orders of such needs:
1] Needs Pertinent to Survival. The family unit is uniquely
committed to the physical security of all members, hence to such
needs as food and shelter.
2] Needs to Development. Additionally, the family is committed
to the cognitive, emotional, and spiritual development of its
members, and hence is committed to creating and sustaining the
sense of being valued, the sense of being cared about, the sense of
being accepted "as it", and the sense of permanence of
affectionalties. The family unit, in this sense is a primary context for
need-attainment (1).
All these parameters can be attributable to King David who was
responsible for the survival of his polygamous family, and for the
development of his family members.
Reference
1. Terkelsen KG. Toward a theory of the family life cycle. In: Carter
EA, Goldrick M (eds.). The Family Life Cycle: A Framework for Family
Therapy, Gardner Press, New York. 1980, pp, 21-52.
74
L. Ben-Nun King David
THE WARRIOR
Throughout his life, David was involved in endless wars against the
Philistines. He was a real warrior and fought bravely with the enemy.
He won many wars, and many Philistines were taken prisoners. He
also conquered Moab, Hadadezer, the son of Rehob, the King of
Zobah, and the Syrians of Damascus (8:2,3,5). “And David reigned
over all Israel; and David executed judgment and justice to all his
people” (8:15).
his best friend was a positive stressful life event. In this way, King
David expressed great friendship towards his beloved Jonathan, and
another member joined the King’s family.
The pediatrician treating a child with a disability must focus not
only on the physical needs of the child but also on the emotional and
social issues associated with being disabled. This dual focus becomes
increasingly important as the child matures through adolescence and
transitions into adulthood. In addition, the pediatrician must
understand the complex interrelationships between the family and
their maturing, disabled child during the vital process of separation
from the family. This transition is particularly difficult for an
adolescent who is dependent on others for physical care and other
independent living skills. Many of transitional problems faced by
disabled adolescents and their parents have roots in early childhood.
With an awareness of the specific stressors on the parent caregivers
and an understanding of the influence of disability on the
developmental process, the pediatrician can play a major role in
easing the transition of a disabled adolescent into adulthood. By
guiding the parents of a young child through the important tasks of
childhood and adolescent, the pediatrician can set the stage for both
the parents and their disabled child to have independent, yet
supportive lives that are focused not on the disability but on mutual
respect and life satisfaction. It is recommended that disabled teens
and young adults be given help in independence skills; personal
counseling services should be available, and physicians should give
teen's age-appropriate information about disabilities. There are
needs for sex education, preparation for parenthood, and genetic
counseling. Other issues that should be addressed are early
vocational awareness, alternatives to work, and leisure time use. Just
because an adolescent is disabled, we cannot assume that he or she
will have self-esteem and self-concept difficulties. To adjust to being
devaluated by society, the disabled person must change societal
beliefs that strength, independence, and appearance are the
essential aspects of a QOL. The importance of being kind,
intelligence, and productive to one's capacity must become more
important (1).
The relationship between a pediatrician and a child with a
disability is important since the pediatrician accompanies such child
through childhood, and on to adolescence and adulthood. From the
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References
1. Hallum A. Disability and the transition to adulthood: issues for the
disabled child, the family, and the pediatrician. Curr Prob Pediatr.
1995;25:12-50.
2. Anan A, Yamaguchi M. Process of parental acceptance of a child's
disability: literature review. J UOEH. 2007;29:73085.
3. Taanila A, Järvelin MR, Kokkonen J. Cohesion and parents; social
relations in families with a chid with disability or chronic illness. Int J Rehabil
Res. 1999;22:101-9.
4. Taanila A, Syrjälä L, Kokkonen J. Järvelin MR. Coping of parents with
physically and/or intellectually disabled children. Child Care Health Dev.
2002;28:73-86.
5. Ben-Nun L. Coping with child's disability. In: Ben-Nun (ed.) Pediatrics
from Biblical to Contemporary Times. B.N. Publication House. Israel 2012,
pp. 179-83.
6. Kim SJ, Kang KA. Meaning of life for adolescents with a physical
disability in Korea. J Adv Nurs. 2003;43:145-55.
7. Platt C, Roper SO, Mandleco B, Freeborn D. Sibling cooperative and
externalizing behaviors in families raising children with disabilities. Nurs Res.
2014;63(4):235-42.
8. Whiting M. Support requirements of parents caring for a child with
disability and complex health needs. Nurs Child Young People. 2014;26(4):
24-7.
AMNON
References
1. Sigel E. Eating disorders. Adolesc Med State Art Rev. 2008;19(3): 547-72,
xi.
2. John F Morgan, Fiona Reid, Lacey JH. The SCOFF questionnaire:
assessment of a new screening tool for eating disorders. BMJ 1999;319:1467.
3. Trent SA, Moreira ME, Colwell CB, Mehler PS. ED management of
patients with eating disorders. Am J Emerg Med. 2013;31(5):859-65.
4. Soh N, Surgenor LJ, Touyz S, Walter G. Eating disorders across two
cultures: does the expression of psychological control vary? Aust N Z
Psychiatry. 2007;41:351-8.
5. Nicolas I. Long-term evolution and complications of eating disorders. Rev
Prat. 2008;58(2):151-5.
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ANOREXIA NERVOSA
Did Amnon suffer from AN? The essential features of AN are that
the individual refuses to maintain a minimally normal body weight for
his or her age and height (Criterion A), is intensely afraid of gaining
weight (Criterion B), and exhibits significant disturbance in the
perception of the shape or size of his or her body (Criterion C) (1). AN is
related to cultural, physical, and psychological pressures on vulnerable
adolescents or young adults (2). Of these criteria only one (Criterion A)
(1) can be attributed to Amnon. According to this definition, there are
insufficient criteria for a diagnosis of AN (3).
There are individuals, however, who do not strictly fulfill the DSM-IV
criteria (4). In 1995, The Society for Adolescent Medicine issued a
position paper on adolescent eating disorders, which identified a broad
spectrum of eating disorders among young people that could lead to
moderate or severe disturbance (5), while some believe that AN is
more of a dieting disorder than an eating disorder (6). Subsequently,
cases of eating disorders were classified as AN, bulimia, and partial
syndromes (3).
References
1. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,
Washington, DC, American Psychiatric Association, 1994.
2. Romeo F. Adolescent boys and anorexia nervosa. Adolescence.
1994;29:643-7.
3. Ben-Nun L. In: Ben-Nun L. (ed.). The Medical Record of Amnon the King
David's Son. Israel. 2014.
4. Morandé G, Celada J, Casas JJ. Prevalence of eating disorders in a Spanish
school-age population. J Adolesc Health. 1999;24:212-9.
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problem. All his all thoughts were concerned his half-sister Tamar, how
to invite her to his room, and how to sexually abuse her.
References
1. Chamay-Weber C, Narring F, Michaud PA. Partial eating disorders
among adolescents: a review. J Adolesc Health. 2005;37(5):417-27.
2. Allen KL, Byrne SM, Forbes D, Oddy WH. Risk factors for full- and partial-
syndrome early adolescent eating disorders: a population-based pregnancy
cohort study. J Am Acad Child Adolesc Psychiatry. 2009;48(8):800-9.
3. Striegel-Moore RH, Seeley JR, Lewinsohn PM. Psychosocial adjustment
in young adulthood of women who experienced an eating disorder during
adolescence. J Am Acad Child Adolesc Psychiatry. 2003;42(5):587-93.
References
1. Higgins JF, Gooddyer IM, Birch J. Anorexia nervosa and food avoidance
emotional disorder. Arch Dis Childhood. 1989;64:346-51.
2. Goëb JL, Azcona B, Troussier F, et al. Food avoidance emotional disorder
in 3 to 10-year-old children: a clinical reality. Arch Pediatr. 2005;12(9):1419-23.
3. Equit M, Pälmke M, Becker N, et al. Eating problems in young children -a
population-based study. Acta Paediatr. 2013;102(2):149-55.
diagnostic criteria for MDD had a significantly lower body weight than
those without a current episode of MDD. In turn, patients with high
weight loss had higher mean depression scores (The Hamilton Rating
scale for Depression, HAMD, SDS) than patients with less weight deficit.
With increase of body weight, a highly significant decrease of
depressive symptoms was found. The DSM III criteria for MDD may not
specifically distinguish between starvation-related psychopathology in
AN and primary affective disorder (2).
Obesity has been linked to both MDD and BED in clinical and
epidemiological studies. The present study compared weight loss
among patients with and without MDD and BED who participated in a
hospital-based weight loss program modeled after the Diabetes
Prevention Program. Of 131 obese patients who enrolled in treatment,
17% were diagnosed with MDD only, 13% were diagnosed with BED
only, 17% were diagnosed with both MDD and BED, and 53% lacked
either diagnosis in a pretreatment clinical interview. After treatment,
patients with MDD only attained 63% of the weight loss that non-
depressed patients attained. Patients with BED only attained 55% of
the weight loss that non-binge eaters attained. The effect of MDD on
weight loss was not accounted for by the presence of BED or vice versa.
Only 27% of patients with both MDD and BED achieved clinically
significant weight loss compared with 67% of patients who had neither
disorder. Results were insignificantly altered when gender, age, and
diabetes status were adjusted. In conclusion, both MDD and BED were
prevalent among this obese clinical population, and each disorder was
independently associated with worse outcomes (3).
References
1. Fosson A, Knibbs J, Bryant-Waugh, Lask B. Early onset anorexia nervosa.
Arch Dis Childhood. 1987;62:114-8.
2. Herpertz-Dahlmann B, Remschmidt H. Anorexia nervosa and depression.
On the relation of body weight and depressive symptoms. Nervenarzt.
1989;60(8):490-5.
3. Pagoto S, Bodenlos JS, Kantor L, et al. Association of major depression
and binge eating disorder with weight loss in a clinical setting. Obesity (Silver
Spring). 2007;15(11):2557-9.
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References
1. Behar A R. Eating disorders not otherwise specified, partial syndromes
and subclinical disorders: a warning in primary care. Rev Med Chil. 2008;
136(12):1589-98.
2. Voderholzer U, Cuntz U, Schlegl S. Eating disorders: state of the art
research and future challenges. Nervenarzt. 2012;83(11):1458-67.
3. Rockert W, Kaplan AS, Olmsted MP. Eating disorder not otherwise
specified: the view from a tertiary care treatment center. Int J Eat Disord.
2007;40 Suppl:S99-S103.
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References
1. Sommerfeldt B, Skårderud F. What is self-harm? Tidsskr Nor Laegeforen.
2009;129(8):754-8.
2. Skårderud F, Sommerfeldt B. Self-harm and eating disorders. Tidsskr Nor
Laegeforen. 2009;129(9):877-81.
3. Peebles R, Wilson JL, Lock JD, M.D. Self-Injury in Adolescents With Eating
Disorders: Correlates and Provider Bias. J Adolesc Health. 2011;48(3):310-3.
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grabbing, oral sex, anal sex, sexual penetration with an object, and/or
sexual intercourse.
The words: Amnon “...being stronger than she, forced her, and lay
with her (Tamar)” II Samuel 13:14) indicate that sexual relations were
performed against Tamar's will. These sexual relations can be defined
as rape with Tamar as a victim (6).
References
1. DeVore HK, Sachs CJ. Sexual assault. Emerg Med Clin North Am. 2011;
29(3):605-20
2. Mollen CJ, Goyal MK, Frioux SM. Acute sexual assault: a review.
Pediatr Emerg Care. 2012;28(6):584-90; quiz 591-3.
3. Snyder HN. Sexual assault of young children as reported to law
enforcement: victim, incident and offender characteristics. U.S. Department
of Justice. Office of Justice Programs. 2000; NCJ 182990.
4. Reynolds MW, Peipert JF, Collins B. Epidemiologic issues of sexually
transmitted diseases in sexual assault victims. Obstet Gynecol Surv. 2000;
55:51-7.
5. Glasser JB, Hammerschlag MR, McCormack WM. Epidemiology of
sexually transmitted diseases in rape victims. Rev Infect Dis. 1989;11:246-54.
6. Ben-Nun L. Psychological consequences of sexual abuse. In: Ben-Nun
L. (ed.). Psychiatry in Biblical Times. B.N. Publication House. 2007, pp. 121-8.
public streets (48%), the main location of assaults was at home (20%).
Female compared with male victims were significantly more likely to be
assaulted at home (OR 6.13, 95% CI 4.41-8.54) and by a known assailant
(family member, friend, partner/ex-partner; OR 8.20, 95% CI 5.85-
11.48). In conclusion, the results highlight the notable contribution of
domestic violence to assaults presenting to hospital emergency
department. Such findings can be used to plan interventions such as
screening hospital patients for domestic violence. Emergency
department data have the potential to inform hospital-based initiatives
to address issues such as assaults in the local population (9).
The objective of this study was to analyze demographic and event
characteristics of patients presenting to the emergency department for
evaluation after sexual assault, using a Sexual Assault Nurse Examiner
standardized database. Data were collected on 1,172 patients; 92%
were women, with a mean age of 27 years. The sample was 59.1%
black, 38.6% white, and 2.3% "other". Survivors of sexual assault were
overwhelmingly female, relatively young, who often knew the
perpetrator of the event, and were likely to be threatened and showed
signs of physical trauma (10).
Sexual behavior was examined in 17-year-old girls, Sweden. Data
were collected by anonymous self-administered 2,583 questionnaires.
Response rates from students were 92%, and for school non-attenders
44%. STDs and pregnancy were reported by 15% of early starters and
pregnancy by 14%, p<0.001 and 0.002, respectively, when compared
with later starters. Sexual abuse was reported by 20% of the early and
11% of later starters, p=0.002. A majority of 83% of the girls had
experienced voluntary intercourse, and 49% were early starters. Five
girls were mothers. STD was reported by 19% and induced abortion by
14% (11).
This study examined the prevalence of sexual aggression and
victimization in a large convenience sample (n = 2,149) of first-year
college students from different universities in Germany. Participants
were asked about both victimization by, and perpetration of, sexual
aggression since the age of 14. Both same-sex and heterosexual victim-
perpetrator constellations were examined. Prevalence rates were
established for different victim-perpetrator relationships (partners,
acquaintances, and strangers) and for incidents involving alcohol
consumption by one or both partners. The overall perpetration rate
was 13.2%, for men and 7.6% for women. The overall victimization rate
was 35.9% for women and 19.4% for men. A disparity between
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victimization and perpetration reports was found for both men and
women. Perpetration and victimization rates were highest among
participants who had sexual contacts with both opposite-sex and same-
sex partners. Sexual aggression and victimization rates were higher
between current or former partners and acquaintances than between
strangers. Alcohol consumption by one or both partners was involved in
almost 75% of all victimization and almost 70% of all perpetration
incidents. The findings portray a comprehensive picture of the scale of
sexual aggression and victimization in college students with different
sexual lifestyles (12).
This study covers information from 890 cases submitted to the
forensic science laboratory, the Republic of Ireland, in the time
between January 2004 to December 2005. The most common age
category of victims was 16-30 years, the most likely time of occurrence
was Saturday or night/Sunday morning during the summer months of
June, July or August. The victim most likely knew the assailant even if
only recently met. Loss of memory, mainly associated with the
consumption of alcohol, was a significant factor in many cases (13).
A retrospective study of emergency department visits for adult
female sexual assault in all Rhode Island emergency department, 1995-
2001, was conducted. Of the 780 patients, 78.2% sustained
anal/vaginal penetration, 5.0% genital touching only, and 3.7% oral sex
only, and 13.1% did not know what happened to them. Of those
women who were assaulted anal/vaginally, 83.8% were offered
chlamydia/gonorrhea testing, 69.4% syphilis testing, 82.9% pregnancy
testing, 77.0% chlamydia/gonorrhea prophylaxis, 47.6% emergency
contraception, and 19.2% HIV prophylaxis (14).
The main objective of this study was to carry out the
epidemiological and clinical characteristics of supposed victims of
sexual abuse and to evaluate case management. A prospective study
was conducted about cases of presumed sexual abuse received at the
gynecological and obstetrical clinic department of Aristide-le-Dantec
hospital, Sénégal from January 2003 to May 2005. Of 55 cases reported,
0.4% represented admissions in the clinic during the period of study.
Twenty percent of them (20%) were referred on judicial requisition. The
mean time between sexual abuse and consultation was 15 days.
Victims were 14 years old in average, nullipare in 96.5% of cases and
living in the suburban area of Dakar. The presumed "violenter" was a
man of 32 years, belonging to the environment of the victim in 70% of
cases (spiritual guide, joint-tenant, or friend of the family). The type of
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majority (76.1%) of the survivors, but rape kit examinations were not
performed as the kits were not available. Although appropriate medical
management was routinely commenced, only 12.7% of survivors
returned for follow-up. In conclusion, seasonal and diurnal patterns
exist in the prevalence of sexual assault in Ile-Ife and most survivors
reported in the hospital presented early. Rape kit examinations were,
however, not executed, due to non-availability. Personnel training,
protocol development, provision of rape kits and free treatment of
sexual assault survivors are, therefore, recommended. Public
enlightenment on preventive strategies based on the observed
periodicity and age patterns is also suggested (19).
An anonymous survey with questions on gender-based violence,
demographic and socioeconomic characteristics and childhood
experiences with violence was administered to students at a major
public university in Santiago. Ninety percent of subjects reported that
the most severe form of undesired sexual contact they had experienced
since 14 years was rape; 6% indicated attempted rape and 16% another
form of sexual victimization; 17% of subjects reported having
experienced some form of undesired sexual contacts in the past 12
months alone. Factors associated with increased odds of victimization
included low parental education, childhood sexual abuse, and the
association between witnessing domestic violence and victimization. A
substantial proportion of young women experienced rape, attempted
rape or other forms of forced sexual contact, indicating a need for
further attention to this public health problem in Chile (20).
The assault records and forensic examination findings of 153
consecutive women who attended a sexual assault service in
Newcastle, Australia, between 1997 and 1999, were reviewed. All the
women were examined within 72 hours of the assault. Of the women,
111 (73.4%) were aged under 30 years and only 4% were over 50 years.
Penile-vaginal penetration was the most common type of sexual assault
(86%). Non-genital injuries were found in 46% of the women (mostly
minor) and genital injury in 22%. Genital injuries in the absence of non-
genital injury were rare (3%). Independent risk factors for the
detection of non-genital injury were reported threats of violence. Risk
factors for genital injury were the presence of non-genital injury,
threats of violence and being over the age of 40 years. If the woman
knew the alleged assailant, this was protective for both non-genital and
genital injury (21).
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References
1. Elliott DM, Mok DS, Briere J. Adult sexual assault: prevalence,
symptomatology, and sex difference in the general population. J Trauma
Stress. 2004;17:203-11.
2. Zinzow HM, Grubaugh AL, Frueh BC, Magruder KM. Sexual assault,
mental health, and service use among male and female veterans seen in
Veterans Affairs primary care clinics: a multi-site study. Psychiatry Res.
2008;159(1-2):226-36.
3. Ellis L, Widmayer A, Palmer CT. Perpetrators of sexual assault continuing
to have sex with their victims following the initial assault: evidence for evolved
reproductive strategies. Int J Offender Ther Comp Criminol. 2008 Apr 2.
4. Olshen E, McVeigh KH, Wunch-Hitzig RA, Ricket VI. Dating violence,
sexual assault, and suicide attempts among urban teenagers. Arch Pediatr
Adolesc Med. 2007;161:539-45.
5. Cichowski SB, Dunivan GC, Komesu YM, Rogers RG. Sexual abuse history
and pelvic floor disorders in women. South Med J. 2013;106(12): 675-8.
6. Sam Soto S, Gayón Vera E, Garcia Pioa CA. Gynecological clinical study in
girls and adolescent victims of sexual abuse. Ginecol Obstet Mex. 2008;76:404-
16.
7. Elwood LS, Smith DW, Resnick HS, et al. Predictors of rape: findings from
the National Survey of Adolescents. J Trauma Stress. 2011;24(2):166-73.
8. Wolitzky-Taylor KB, Ruggiero KJ, Danielson CK, et al. Prevalence and
correlates of dating violence in a national sample of adolescents. J Am Acad
Child Adolesc Psychiatry. 2008;47:755-62.
9. Ramsay SE, Bartley A, Rodger AJ. Determinants of assault-related
violence in the community: potential for public health interventions in
hospitals. Emerg Med J. 2013 Aug 16.
10. Avegno J, Mills TJ, Mills LD. Sexual assault victims in the emergency
department: analysis by demographic and event characteristics. J Emerg Med.
J Emerg Med. 2009;37(3):328-34.
11. Edgardh K. Sexual behaviour and early coitarche in a national sample of
17 year old Swedish girls. Sex Trans Infect. 2000;76:98-102.
12. Krahé B, Berger A. Men and women as perpetrators and victims of
sexual aggression in heterosexual and same-sex encounters: a study of first-
year college students in Germany. Aggress Behav. 2013;39(5):391-404.
13. McDermott SD, McBride BM, Lee-Gorman M. Sexual assault statistics
from the Republic of Ireland for 2004-2005. Med Sci Law. 2008; 48:142-50.
108
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14. Merchant RC, Phillips BZ, Delong AK, et al. Disparities in the provision of
sexually transmitted disease and pregnancy testing and prophylaxis for
sexually assaulted women in Rhode Island emergency departments. J Womens
Health (Larchmt). 2008;17:619-29.
15. Faye Dieme ME, Traore AL, Gueye SM, et al. Sexual abuse:
epidemiological, clinical aspects and management at gynaecological and
obstetrical department of Dakar University Hospital. J Gynecol Obstet Biol
Reprod (Paris). 2008;37(4):358-64.
16. Adama-Hondégla AB, Aboubakari AS, Fiagnon K, et al. Epidemiological
and clinical aspects of the management of sexual aggression among female
victims in Lomé. Afr J Reprod Health. 2013;17(1):67-72.
17. Krishnakumar P, Satheesan K, Geeta MG, Sureshkumar K. Prevalence
and Spectrum of Sexual Abuse Among Adolescents in Kerala, South India.
Indian J Pediatr. 2013 Oct 25.
18. Cerdas L, Arroyo C, Gómez A, et al. Epidemiology of rapes in Costa
Rica: Characterization of victims, perpetrators and circumstances surrounding
forced intercourse. Forensic Sci Int. 2014;242C:204-209.
19. Badejoko OO, Anyabolu HC, Badejoko BO, et al. Sexual assault in Ile-Ife,
Nigeria. Niger Med J. 2014;55(3):254-9.
20. Lehrer JA, Lehrer VL, Lehrer EL, Oyarzún PB. Prevalence of and risk
factors for sexual victimization in college women in Chile. Int Fam Plan
Perspect. 2007;33:168-75.
21. Palmer CM, Mcnulty AM, D'Este C, Dnovan B. Genital injuries in women
reporting sexual assault. Sex Health. 2004;1:55-9.
22. Feehan M, Nada-Raja S, Martin JA, Langley JD. The prevalence and
correlates of psychological distress following physical and sexual assault in a
young adult cohort. Violence Vict. 2001;16:49-61.
towards this particular group of people. This study is based upon data
obtained from a cross-sectional survey of students in a tertiary
institution in South Western Nigeria. Participants voluntarily and
anonymously completed a baseline semistructured questionnaire which
elicited information on demographic information, sexual behaviors' and
substance use among others. Of the 368 respondents, the majority 225
(60.9%) was in the age group of 20-24 years. A total of 152 participants
(41.3%) were either currently or had previously indulged in heavy
drinking of alcohol and a significant association was between the use of
alcohol and having multiple sexual partners and use of commercial sex
workers (p<0.05). Ninety-four (25.5%) and 52 (14.1%) were currently
smokers or smoked cigarette and marijuana before; while 56 (15.2%)
were currently using or have before used narcotic drugs. The
relationship between hard drug use and non-use of condom was
significant (p<0.05). Ninety-two (25.0%) have more than one sexual
partners at the same given period; the male respondents indulged
more in having multiple partners than the female (p<0.05). As many as
155 (47.8%) of the sexually active respondents had never used condom
during sexual intercourse. Of this group of the respondents, 88 (27.1%)
have had sexual relationship with commercial sex workers at one time
or the other. Condom use was low among the sexually active
respondents. Only 29.3% of the respondents always use condom when
having any sexual relationship. This study indicates that students
indulge in health risk behaviors such as "unsafe sexual practices",
alcohol, cigarette smoking and other substance use. The males are
more involved in having multiplicity of sexual partners than their
female counterpart. A significant association is found between the use
of alcohol and having multiple sexual partners. Comprehensive health
education and intervention programs are needed to influence positive
behavioral change among this group of students working in partnership
with schools authorities and other local community groups (5).
STIs remain a public health problem of major significance in most of
the world. Adolescents make up about 20% of the world population, of
whom 85% live in developing countries. They are at a greater risk of
STIs because they frequently have unprotected intercourse, biologically
may be more susceptible to infection, often are engaged in multiple
monogamous relationships of limited duration, and face multiple
obstacles in accessing confidential health care services. Young people
who begin to have sexual intercourse in early or middle adolescence
are more likely to develop a STI than those who postpone intercourse
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L. Ben-Nun King David
References
1. Bartlett R, Holditch-Davis D, Belyea M. Problem behaviors in adolescents.
Pediatr Nurs. 2007;33(1):13-8.
2. Goldenberg D, Telzer EH, Lieberman MD, et al. Neural mechanisms of
impulse control in sexually risky adolescents. Dev Cogn Neurosci. 2013;6:23-9.
3. Lotrean LM, Laza V, Ionut C, de Vries H. Assessment of health risk
behaviours and their interrelationships among young people from two
counties of Romania. Z Gesundh Wiss. 2010;18(4):403-11.
4. Smith SJ. Risky sexual behavior among young adult Latinas: are
acculturation and religiosity protective? J Sex Res. J Sex Res. 2015;52(1):43-54.
5. Bamidele JO, Asekun-Olarinmoye EO, Odu OO, et al. Afr J Med Med Sci.
2007;36(2):129-36.
6. Ljubojevid S, Lipozenčid J. Sexually transmitted infections and
adolescence. Acta Dermatovenerol Croat. 2010;18(4):305-10.
7. Letamo G, Mokgatlhe LL. Predictors of risky sexual behaviour among
young people in the era of HIV/AIDS: evidence from the 2008 Botswana AIDS
Impact Survey III. Afr J Reprod Health. 2013;17(3):169-81.
8. Marchand E, Smolkowski K. Forced Intercourse, Individual and Family
Context, and Risky Sexual Behavior among Adolescent Girls. J Adolesc Health.
2013;52(1):89-95.
9. Hembling J, Andrinopoulos K. Evidence of increased STI/HIV-related risk
behavior among male perpetrators of intimate partner violence in Guatemala:
results from a national survey. AIDS Care. 2014;26(11):1411-8.
10. Samek DR, Iacono WG, Keyes MA, et al. The developmental progression
of age 14 behavioral disinhibition, early age of sexual initiation, and
subsequent sexual risk-taking behavior. J Child Psychol Psychiatry. 2014;
55(7):784-92.
and psychological violence in PMWI. When all categories for each other
by linear regression analysis were adjusted, sexual IPV was significantly
associated with hair pulling, arm-twisting, spanking or biting,
dominance and isolation abuse and violence directed at the pregnant
woman's abdomen. In conclusion, sexual assaults are more likely to co-
occur with some types of physical and psychological violence than with
others. This knowledge is important for improving our understanding of
sexual violence in intimate partner relationships and in the efforts to
detect IPV. Bruises, loss of hair and bite marks suggest that sexual acts
were committed against the victim's will (6).
This study explores the cumulative effect of sexual assault and
physical abuse by a current or former intimate partner on help seeking.
Using a dataset of 1,072 IPV victims from eight states, women who had
experienced sexual assault in addition to physical abuse (44%) used
more help, but were more likely to say that they did not seek help
when they needed it. Among those who were aware of services, fear
was the greatest obstacle to reaching out for help. Implications include
the need for information on best practices in addressing the sequelae
of both physical and sexual assault in victim service agencies (7).
IPV against women is a serious problem throughout the world. Each
year a substantial number of women experience psychological,
physical, and sexual aggression from an intimate partner, with many
women experiencing serious mental and physical health outcomes
because of their victimization. A number of services are available to
women who sustain IPV (e.g., shelters, advocacy, and legal protection),
and the combination of these services has been termed a CCR to IPV.
The purpose of this manuscript is to review the individual components
of CCRs for IPV victims, examine the extant literature on a number of
the individual CCR components, and suggest directions for future
research on CCRs for IPV victims. There is a significant lack of research
on various CCR components, that research on the integration of CCR
services is limited, and theoretical guidance for CCR programs is almost
non-existent (8).
The aim of this study was to evaluate if disclosure of abuse among
female university students and among women at an emergency
department varied based on three different types of data collection
method used; and to explore women's development of symptoms of
PTSD and the outcome on health. Cross-sectional research design was
used (n=306 women). The women who experienced IPV in their current
relationship, and had symptoms of PTSD, reported significantly lower
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References
1. Toohey JS. Domestic violence and rape. Med Clin North Am.
2008;92(5): 1239-52, xii.
2. Edin K, Nilsson B. Between desire and rape - narratives about being
intimate partners and becoming pregnant in a violent relationship. Glob
Health Action. 2013;6:20984.
3. Marshall LL. Development of the severity of violence against women
scales. J Fam Violence. 1992;7:103-121.
4. Tolman RM. The development of a measure of psychological
maltreatment of women by their male partners. Violence Vict. 1989;
4(3):159-177.
5. Tolman RM. The validation of the psychological maltreatment of
women inventory. Violence Vict. 1999;14(1): 25-35.
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oral health care environment; and was attrition from their employment
associated with sexual harassment. A questionnaire, Sexual Harassment
in the Dental Hygiene Profession, designed by the author, was used. A
list of currently licensed and registered dental hygienists was obtained
from the Virginia Board of Dental Examiners and the questionnaire was
sent to 540 randomly selected registered Virginia dental hygienists.
Two weeks after the initial mailing, a second questionnaire was sent to
non-respondents. The survey elicited data on experience, management,
and personal opinions relative to sexual harassment, as well as
demographic information. Of returned and useable 285 surveys (53%),
54% of dental hygienists experienced sexual harassment. The
perpetrators of the harassment were either male dentists (73%) or
male clients (45%). Less than 10% reported being harassed by women.
While 70% of the sexually harassed respondents indicated that filing
formal complaints was an effective strategy for managing sexual
harassment, less than 1% actually did so. Of all dental hygienists
(harassed or not), 90% did not receive training in their dental education
to manage sexual harassment, and 85% would like the American Dental
Hygienists' Association to develop model guidelines and policies.
Demographic characteristics were typical of practicing dental hygienists
in Virginia; 99% female, 96% Caucasian, and 86% married with a mean
age of 40 years. In conclusion, information about managing sexual
harassment needs to be incorporated into the dental hygiene curricula.
This curriculum addition should include information on identifying
sexual harassment incidents, strategies for controlling unacceptable
behavior, the legal rights of employees, and the process of filing a
formal complaint. Dental hygienists need to identify sexual harassment
behaviors and receive prevention training though continuing education
courses (2).
Nurses sexually harassed at work face frustration and emotional and
economic consequences. Historically before the 1970s, nurses had little
legal recourse and tolerated sexual harassment as a necessary "evil"
associated with working. The Civil Rights Act of 1964 created the option
for legal remedies for sexual harassment/discrimination cases.
Successful court cases established the legal criteria for sexual
harassment. Prevention requires coordinated activities of employers,
individual employees, and the healthcare profession. Sexual
harassment at work increases anxiety and undermines the nurse's
ability to focus on the delivery of safe and competent care (3).
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References
1. Garrett LH. Sexual assault in the workplace. AAOHN J. 2011; 59(1):15-
22.
2. Pennington A, Darby M, Bauman D, et al. Sexual harassment in
dentistry: experiences of Virginia dental hygienists. J Dent Hyg. 2000;4(4):
288-95.
3. Valente SM, Bullough V. Sexual harassment of nurses in the
workplace. Nurses who are J Nurs Care Qual. 2004;19(3):234-41.
4. Celik Y, Celik SS. Sexual harassment against nurses in Turkey. J Nurs
Scholarsh. 2007;39(2):200-6.
5. Fitzgerald LF, Shullman SL, Nancy Bailey, et al. The incidence and
dimensions of sexual harassment in academia and the workplace. J Vocat
Behav 1988;32(2): 152-175.
6. Fineran S, Gruber JE. Youth at work: adolescent employment and
sexual harassment. Child Abuse Negl. 2009;33(8):550-9.
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screening positive for PTSD for both sexual orientation groups. Results
revealed a number of other predictors of mental health status for
women veterans, some of which differed by sexual orientation.
Findings indicate a significant burden of interpersonal trauma for both
heterosexual and lesbian/bisexual women veterans and provide
information on the distinct association of various traumas with current
PTSD and depression by sexual orientation (10).
References
1. O'Brien BS, Sher L. Military sexual trauma as a determinant in the
development of mental and physical illness in male and female veterans. Int J
Adolesc Med Health. 2013;25(3):269-74.
2. Williams I, Bernstein K. Military sexual trauma among U.S. female
veterans. Arch Psychiatr Nurs. 2011;25(2):138-47.
3. Harned MS, Ormerod AJ, Palmieri PA, et al. Sexual assault and other
types of sexual harassment by workplace personnel: a comparison of
antecedents and consequences. J Occup Health Psychol. 2002;7(2):174-88.
4. Burgess AW, Slattery DM, Herlihy PA. Military sexual trauma: a silent
syndrome. J Psychosoc Nurs Ment Health Serv. 2013;51(2):20-6.
5. Sadler AG, Booth BM, Cook BL, Doebbeling BN. Factors associated with
women's risk of rape in the military environment. Am J Ind Med. 2003;43(3):
262-73. Erratum in: Am J Ind Med. 2003;44(1):110.
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6. Kang H, Dalager N, Mahan C, Ishii E. The role of sexual assault on the risk
of PTSD among Gulf War veterans. Ann Epidemiol. 2005;15(3):191-5.
7. Luterek JA, Bittinger JN, Simpson TL. Posttraumatic sequelae associated
with military sexual trauma in female veterans enrolled in VA outpatient
mental health clinics. J Trauma Dissociation. 2011;12(3):261-74.
8. Cobb Scott J, Pietrzak RH, Southwick SM, et al. Military sexual trauma
interacts with combat exposure to increase risk for posttraumatic stress
symptomatology in female Iraq and Afghanistan veterans. J Clin Psychiatry.
2014;75(6):637-43.
9. Rossiter AG, Smith S. The invisible wounds of war: caring for women
veterans who have experienced military sexual trauma. J Am Assoc Nurse
Pract. 2014;26(7):364-9
10. Lehavot K, Simpson TL. Trauma, posttraumatic stress disorder, and
depression among sexual minority and heterosexual women veterans. J Couns
Psychol. 2014;61(3):392-403.
the second group. The type of sexual assault was penetration in the
majority of the cases for the two groups. Vaginal, oral and anal
penetration was respectively involved in 55%, 23% and 13% of the
cases in the first group. General body trauma was found in 39.1% of the
cases and in 6.3% of the cases of the second group. Genital trauma
occurred in 35.7% of the cases in the first group and in 19.5% of the
cases in the second group. Hymenal, vulvo-vaginal and anal lesions
were in 11%, 20% and 7%, respectively, of the cases examined.
Toxicological analysis was performed in 14.3% of the cases examined. In
47% of the tested cases, drug was detected. Cytology was performed in
61.5% of the cases. Detection of spermatozoa was in 30.3% of these
cases. This study has shown that sexual assault victims had different
characteristics according to the time between the sexual assault and
the examination. Public health campaigns against sexual abuse and
rape as well as medical management of the sexually assaulted victims
should adapt to the needs and the characteristics of these two different
populations of victims (1).
The main aim of this study was to describe the medico-legal findings
in a population of sexual assault cases assessed in an urban French
referral centre, to analyze the subsequent legal dispositions in each
case and to determine whether the characteristics of the assault and
the medico-legal findings were associated with conviction of the
assailant. A retrospective study of medicolegal reports in all the sexual
assault cases was reported in Tours (France) during a seven-year
period. Two groups of victims were defined: children under 15 years old
and victims aged 15 years or more. Legal outcomes were obtained from
courtroom proceedings. A total of 756 cases during the study period
were enrolled. The mean age of the study population was 16.5 years
and 68.3% of the cases involved children less than 15 years old. In 57%
of these cases, the assailant was a family member; 31.7% of all the
victims were aged 15 years or more. The assailant was an acquaintance
of the victim in 62.2% of the cases. Drug-facilitated assault was
suspected in 2.9% of the cases. In 46.2% of the cases, formal criminal
charges were not filed due to insufficient evidence; 36.3% of the
assailants were convicted. Examination at the request of the police
authorities and previous acquaintance of the assailant by the victim
were associated with conviction. Allegations of penetration, the
presence of general body trauma and the presence of genital trauma
were not necessarily associated with conviction. Medical examiners
need to be circumspect when they record non-medical variables.
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References
1. Grossin C, Sibille I, Lorin de la Grandmaison G, et al. Analysis of 418 cases
of sexual assault. Forensic Sci Int. 2003;131(2-3):125-30.
2. Saint-Martin P, Bouyssy M, O'Byrne P. Analysis of 756 cases of sexual
assault in Tours (France): medico-legal findings and judicial outcomes. Med Sci
Law. 2007;47(4):315-24.
3. Riggs N, Houry D, Long G, et al. Analysis of 1,076 cases of sexual assault.
Ann Emerg Med. 2000;35(4):358-62.
4. Negriff S, Schneiderman JU, Smith C, et al. Characterizing the sexual
abuse experiences of young adolescents. Child Abuse Negl. 2013 Oct 3. pii:
S0145-2134(13)00252-4.
5. Livingston JA, Hequembourg A, Testa M, Vanzile-Temsa C. Unique
aspects of adolescent sexual victimization experiences. Psychol Women Q.
2007;31:331-43.
6. Möller AS, Bäckström T, Söndergaard HP, Helström L. Patterns of injury
and reported violence depending on relationship to assailant in female
Swedish sexual assault victims. J Interpers Violence. 2012; 27(16):3131-48.
7. Germerott T, Bode-Jänisch S, Thali MJ. Physical and gynecological
examinations in female victims of sexual violence with special emphasis on
crime-reporting behaviour. Arch Kriminol. 2012;230(3-4):88-98.
8. Santos-Iglesias P, Sierra JC. Sexual victimization among Spanish college
women and risk factors for sexual revictimization. J Interpers Violence. 2012;
27(17):3468-85.
9. Bartels SA, Scott JA, Mukwege D, et al. Patterns of sexual violence in
Eastern Democratic Republic of Congo: reports from survivors presenting to
Panzi Hospital in 2006. Confl Health. 2010;4:9.
10. Hassan Q, Bashir MZ, Mujahid M, et al. Medico-legal assessment of
sexual assault victims in Lahore. J Pak Med Assoc. 2007;57(11):539-42.
11. Amenu D, Hiko D. Sexual assault: pattern and related complications
among cases managed in Jimma University Specialized Hospital. Ethiop J
Health Sci. 2014;24(1):3-14.
result from attempts to restrain the victim, whereas others (e.g. bite
marks) may have a sexual motive or be part of a sado-masochistic
ritual. A standard nomenclature for injuries (i.e. using the terms
'bruises', 'abrasions', 'lacerations', 'incisions and 'stab wounds') should
avoid ambiguity between medical examiners (1).
The objective of this study was to establish inter-rater reliability for
genital injury detection among experienced forensic sexual assault
examiners. Cross-sectional observational study testing inter-rater
agreement of injury assessment among eight experienced sexual
assault examiners who each viewed two-four digital images from 50
cases. Each case was rated by four examiners and included images
before and after toluidine blue dye application. Overall agreement and
kappa (κ) were calculated. Examiners had perfect agreement in 60
cases; in 24 cases three examiners agreed; in five cases two agreed and
one was unsure; and in nine cases there were two "yes" and two "no"
ratings or one "yes," one "no," and two "unsure" ratings. Overall
agreement was 82% (κ, 0.57) when yes/unsure and no/unsure
combinations equaled disagreement and 86% (κ, 0.66) when only
yes/no dyads equaled disagreement. Neither the number of images nor
any single examiner fundamentally influenced results. Highly
experienced examiners tended to agree with each other (86%) slightly
more often than moderate examiners agreed with each other (75%). In
conclusion, the set of experienced forensic examiners achieved
moderate inter-rater agreement in assessment of the presence of
female genital injury on selected digital images obtained during sexual
assault examination (2).
All females who were 15 years or older, presenting after sexual
assault to an urban emergency department Seattle, US, underwent
standardized evaluation. Of 8,199 women, 52% had general body
injury, 20% had genital-anal trauma, and 41% were without injury.
General body trauma was associated with being hit or kicked,
attempted strangulation, and stranger assault. Genital-anal injury was
more frequent in victims younger than 20 and older than 49 years,
virgins and those examined within 24 hours and after anal assault.
General body injury was primarily associated with situational factors,
whereas genital-anal injury was less frequent and was related to victim
age, virginal status, and the time of examination (3).
A retrospective chart review of new urogynecological patients seen
at the University of New Mexico Hospital was conducted. All women
underwent a standardized history and physical examination and
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References
1. Crane J. Interpretation of non-genital injuries in sexual assault. Best
Pract Res Clin Obstet Gynaecol. 2013;27(1):103-11.
2. Sachs CJ, Benson A, Schriger DL, Wheeler M. Reliability of female genital
injury detection after sexual assault. J Forensic Nurs. 2011;7(4):190-4.
3. Sugar NF, Fine DN, Eckert LO. Physical injury after sexual assault: findings
of a large case series. Am J Obstet Gynecol. 2004;190:71-6.
4. Cichowski SB, Dunivan GC, Komesu YM, Rogers RG. Sexual abuse history
and pelvic floor disorders in women. South Med J. 2013;106(12): 675-8.
5. Postma R, Bicanic I, van der Vaart H, Laan E. Pelvic floor muscle
problems mediate sexual problems in young adult rape victims. J Sex Med.
2013;10(8):1978-87.
6. Jones JG, Worthington T. Genital and anal injuries requiring surgical
repair in females less than 21 years of age. J Pediatr Adolesc Gynecol. 2008;
21:207-11.
7. Keller P, Lechner M. Injuries to the cervix in sexual assault victims. J
Forensic Nurs. 2010;6(4):196-202.
8. Anderson SL, Parker BJ, Bourguignon CM. Predictors of genital injury
after nonconsensual intercourse. Adv Emerg Nurs J. 2009;31(3):236-47.
References
1. Gomez AM. Sexual violence as a predictor of unintended pregnancy,
contraceptive use, and unmet need among female youth in Colombia. J
Womens Health (Larchmt). 2011;20(9):1349-56.
2. Speizer IS, Pettifor A, Cummings S, et al. Sexual violence and
reproductive health outcomes among South African female youths: a
contextual analysis. Am J Public Health. 2009;99 Suppl 2:S425-31.
3. Kalonda JC. Sexual violence in Congo-Kinshasa: necessity of
decriminalizing abortion. Rev Med Brux. 2012;33(5):482-6.
4. Teklehaimanot KI, Smith CH. Rape as a legal indication for abortion:
implications and consequences of the medical examination requirement. Med
Law. 2004;23(1):91-102.
5. Ludermir AB, Valongueiro S, Araújo TV. Common mental disorders and
intimate partner violence in pregnancy. Rev Saude Publica. 2014;48(1):29-35.
6. Salazar M, San Sebastian M. Violence against women and unintended
pregnancies in Nicaragua: a population-based multilevel study. BMC Womens
Health. 2014 Feb 12;14:26.
References
1. Da Ros CT, Schmitt Cda S. Global epidemiology of sexually transmitted
diseases. Asian J Androl. 2008 Jan;10(1):110-4.
2. Draughon JE. Sexual assault injuries and increased risk of HIV
transmission. Adv Emerg Nurs J. 2012;34(1):82-7.
3. Hagemann CT, Nordbø SA, Myhre AK, et al. Sexually transmitted
infections among women attending a Norwegian Sexual Assault Centre. Sex
Transm Infect. 2014;90(4):283-9.
4. Argo A, Zerbo S, Triolo V, et al. Legal aspects of sexually transmitted
diseases: abuse, partner notification and prosecution. G Ital Dermatol
Venereol. 2012;147(4):357-71.
5. Kalichman SC, Simbayi LC. Sexual assault history and risks for sexually
transmitted infections among women in an African township in Cape Town,
South Africa. AIDS Care. 2004;16(6):681-9.
6. Adefolalu AO. Prevalence of HIV infection among survivors of sexual
assault at presentation in hospital. Trop Doct. 2013;43(3):106-7.
7. Banani S, Schlaeffer F, Leibenson L, et al. Prevalence of sexually
transmitted diseases (STD) in HIV positive women in southern Israel].
Harefuah. 2013;152(4):204-6, 248.
perpetrator rapes, stranger rapes and those with weapons would result
in more psychological trauma and thus more enduring symptoms. The
findings point to the importance of understanding the socio-cultural
dimensions, including dynamics of blame and stigma of rape on mental
health sequelae (12).
This study investigated the relationship between changes in PTSD,
depression, and anxiety symptoms in the first 12 weeks following
sexual assault. Participants were 126 women who had been sexually
assaulted in the previous four weeks. Lower level mediation analyses
revealed that changes in PTSD symptoms had a greater impact on
changes in depression and anxiety than vice versa. In conclusion, the
finding highlights the role of PTSD symptoms in influencing subsequent
change in other psychological symptoms (13).
References
1. Campbell L, Keegan A, Cybulska B, Forster G. Prevalence of mental
health problems and deliberate self-harm in complainants of sexual violence. J
Forensic Led Med. 2007;14:75-8.
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abuse were significantly more dissociative than those who did not
report such a history (6).
References
1. Machado CL, de Azevedo RC, Facuri CO, et al. Posttraumatic stress
disorder, depression, and hopelessness in women who are victims of sexual
violence. Int J Gynaecol Obstet. 2011;113(1):58-62.
2. Nickerson A, Steenkamp M, Aerka IM, et al. Prospective investigation of
mental health following sexual assault. Depress Anxiety. 2013;30(5):444-50.
3. Foa EB, McLean CP, Capaldi S, Rosenfield D. Prolonged exposure vs.
supportive counseling for sexual abuse-related PTSD in adolescent girls: a
randomized clinical trial. JAMA. 2013;310(24):2650-7.
4. Dancu CV, Riggs DS, Hearst-Ikeda D, et al. Dissociative experiences and
posttraumatic stress disorder among female victims of criminal assault and
rape. J Trauma Stress. 1996;9(2):253-67.
5. Elklit A, Christiansen DM. Risk factors for posttraumatic stress disorder in
female help-seeking victims of sexual assault. Violence Vict. 2013;28(3): 552-
68.
References
1. Bicanic I, Snetselaar H, De Jongh A, Van de Putte E. Victims' use of
professional services in a Dutch sexual assault centre. Eur J Psychotraumatol.
2014 Jun 18;5.
2. Nesvold H, Friis S, Ormstad K. Sexual assault centers: attendance rates,
and differences between early and late presenting cases. Acta Obstet Gynecol
Scand. 2008;87(7):707-15.
3. Golan A, Dishi-Galitzky M, Barda J, Lurie S. The care of sexual assault
victims: the first regional center in Israel - 10 years experience. Isr Med Assoc J.
2012;14(11):658-61.
FAMILY FUNCTIONING
Fleck (1) suggested five parameters of family functioning. These are:
1. Leadership: this is a result of the parents' personalities, the
characteristics of the marital coalition, the complementary of the
parental roles, and the parents' use of power – that is, their methods of
discipline.
2. Family boundaries: this covers ego boundaries, generation
boundaries, and family-community boundaries.
3. Affectivity: important in this parameter is interpersonal intimacy,
the equivalence of family triads, family members' tolerance of each
other's feelings, and unit emotionality.
4. Communication: relevant here are responsiveness of family
members to each other, the extent to which verbal and no-verbal
communications are consistent, the ways in which family members
express themselves, the clarity of the syntax of their talk, and the
nature of members' abstract and metaphorical thinking.
5. Task/goal performance: this covers the nurturance given to
members by the family, the ways in which the children master the
process of separation from the family, behavior control and guidance,
the nature of family members' peer relationships and the guidance they
are given in the leisure activities, how the family copes with crises, and
the adjustment of members after they leave the family of origin.
Leadership in David's family was concentrated in the King's hands,
and only he could give permission to Tamar to visit her "sick" brother,
Amnon. The visit was well organized and carried out within the family
boundary. At this time, Amnon, Tamar, Absalom and the King were
strongly connected emotionally with each other. The communication
pattern was positive, and their relationships were based on trust. The
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References
1. Fleck S. Family functioning and family pathology. Psychiatric Ann.
1980;10:46-54.
2. Ben-Nun L. Tamar and Amnon. In: Ben-Nun L. (ed.). The Family Life Cycle
and the Medical Record of King David the Great. Research in Biblical Times
from the Viewpoint of Contemporary Medicine. B.N. Publishing House. Israel.
2009, pp. 56-77.
REVENGE. Absalom did not forget that Amnon had defiled their
sister, and he was eager for revenge. There was no way to achieve a
peaceful reconciliation between the two brothers. The painful
triangle - Tamar, Absalom, and Amnon - could never achieve a
peaceful coexistence. Resources were not used to solve this family
crisis. Even the King did not intervene or make any efforts to
reconcile this triangle.
After two years, at the first opportunity, Absalom commanded his
men to kill Amnon and the mission was performed "..Smite Amnon;
then kill him, fear nor.. be courageous, and be valiant.." (II Samuel
13:28). With the aid of external forces, Amnon paid with his life for
his disgusting behavior. Amnon's death affected profoundly David's
family: "..the king's sons came, and lifted their voices and wept: and
the king also and all his servants wept very sore" (13:36). Later,
"Absalom fled, and went to Talmai, the son of Ammihud, king of
Geshur. And David mourned for his son every day" (13:37).
Eventually Amnon was assassinated for his disgraceful behavior.
Here we are dealing with a violent death (1).
In healthy families, the ambience is nurturing, and the
relationships are filled with love, caring, affection, and loyalty. In
dysfunctional families, the relationships take on qualities like hate,
guilt and retribution; the ambience is disjunctive. However, in both
healthy and dysfunctional families, the attachments are intense and
their vicissitudes pervade the whole life of the family. Secondly,
these interactions continue over whole lifetimes. Thirdly, the
outcome of these interactions is physical survival and personal
development for all members. The purpose of the family is to evoke
between members sequences of affectional interactions sustained
over lifetimes, thereby producing survival and development for all
family members (2).
Family change is the interpersonal process by which the family
adapts, alters, or becomes different. The family is more than the
sum of its parts. Interpersonal structures and processes that enable it
to be both stable and adaptable over time organize the family (3).
Amnon's reckless behavior led the King's family into a severe
crisis. The attachment between Absalom, Amnon and Tamar was
broken, and the stable family homeostasis was disrupted. The
relationships between the siblings reached such a level of hatred that
only the death of Amnon could calm the situation. Absalom never
accepted and never forgave Amnon for defiling his beautiful sister.
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References
1. Ben-Nun L. In: Ben-Nun L. (ed.). The Medical Record of Amnon the
King David's Son. Israel. 2014.
2. Terkelsen KG. Toward a theory of the family life cycle. In: Carter EA,
Goldrick M (eds.). The Family Life Cycle: A Framework for Family Therapy,
Gardner Press, New York. 1980, pp, 21-52.
3. McDaniel S, Campbell TL, Seaburn DB. Family system concepts. Tools
for assessing the family in primary care. In: McDaniel S, Campbell TL,
Seaburn DB (eds.). Family-Oriented Primary Care. A Manual for Medical
Providers. Springe-Verlag. New York, Berlin. 1990, pp. 33-39.
humane reaction of the father, the King who suffered a great deal
after losing his son forever.
References
1. Smilkstein G. The Family Apgar: a proposal for a family function test
and its use by physicians. J Fam Pract. 1978;6:1231-9.
2. Pilkington FB. Grieving a loss: the lived experience for elders residing
in an institution. Nurs Sci Q. 2005;18:233-42.
3. Flórez. Grief. An Sist Sanit Navar. 2002;25 Suppl 3:77-85.
4. Kalish RA. Death and survivorship: the final transition. Ann Am Acad
Pol Soc Sci. 1982;464:163-73.
5. Hazzard A, Weston J, Gutterres C. After a child's death: factors related
to parental bereavement. J Dev Behav Pediatr. 1992;13:24-30.
6. Neimeyer RA, Klass D, Dennis MR. A social constructionist account of
grief: loss and the narration of meaning. Death Stud. 2014;38(8):485-98.
7. Holmes TH, Rahe RH. The social readjustment rating scale. J
Psychosom Res. 1967;11:213.
ABSALOM
Two years after Amnon's assassination, Absalom fled. Here, Joab
"..went to Geshur, and brought Absalom to Jerusalem. So Absalom
dwelt two full years in Jerusalem, and saw not the King's face" (II
Samuel 14:23,28). After Absalom's servants set fire to Joab's field
(14:30), he (Absalom) came to the king, and prostrated himself before
the king; and the king kissed Absalom" (14:33). After this meeting with
his father, the King, "… Absalom prepared him chariots, and horses, and
fifty men to run before him" (15:1). So Absalom decided that " ..every
man came nigh to him to do him obeisance , he put forth his hand, and
took him, and kissed him" (15:5). Here Absalom behaved like a king,
thus ignoring his father.
Absalom prepared to fight with King David's army. In spite of this "So
the king commanded Joab and Abishai and Ittai, saying, Deal gently for
my sake with the young man, even with Absalom. Beware that none
touch the young man Absalom" (18:5,12). Meanwhile "And Absalom
rode on a mule, and the mule went under the thick boughs of a great
oak, and his head caught fast in the oak…. And the mule that was under
him went away" (18:9). So "..Absalom hanged in an oak" (18:10).
Subsequently "And he (Joab) took three spears in his hand, and thrust
them through the heart of Absalom, who was still alive in the midst of
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the oak. And then ten young men that bore Joab's armour came round
in a circle and smote Absalom, and slew him " (18:14,15). Absalom was
buried like a traitor "And they took Absalom, and cast him into a great
pit in the wood, and laid a very great heap of stones upon him (18:17).
So "…it is called unto this day, Absalom's place" (18:18).
Reference
1. Collins Cobuild. Essential English Dictionary. Collins. London,
Glasgow. 1988.
References
1. Velinovid M, Vranes M, Obrenovid-Kirdanski B, et al. Penetrating wound
of the heart manifested with peripheral embolism - case report. Vojnosanit
Pregl. 2012;69(9):803-5.
2. Olsovsky MR, Wechsler AS, Topaz O. Cardiac trauma. Diagnosis,
management, and current therapy. Angiology. 1997;48(5):423-32.
3. Miyoshi Y, Ohara K. Traumatic cardiac injury. Kyobu Geka. 2004;57(8
Suppl):742-50.
case of Absalom, three sharp spears were thrust into his heart
causing life-threatening complications (1).
In large series, gunshot wounds are the predominant cause of
cardiac penetrating trauma (2-5). Penetrating cardiac injury carries
high mortality rates. It has been commonly associated with stabbing,
but increased urban violence has led to growing numbers of gunshot
heart wounds. The latter has higher mortality rates among
penetrating cardiac injuries and may affect multiple heart chambers,
with mortality rates even higher (6).
Penetrating war injuries of heart and great vessels are among the
most serious injuries in war. The mortality rate is 58% (7).
The cause of injury is shrapnel, bullets, cluster bomb particles,
and others (blast etc). The most frequent localization of the injuries is
the right and left ventricles, left atrium, superior caval vein, inferior
caval vein, and isolated pericardial injury. Immediately after injury,
patients suffer from shock, pericardial tamponade, and bleeding (8).
Although bullets penetrating the heart are fatal, retained cardiac
bullets can sometimes have a silent course without causing any C-V
complication (9).
Penetrating cardiac injuries are a dramatic and lethal form of
trauma. Most of these patients reach the hospital already dead or in
severe shock. The prognosis is determined by early diagnosis and
operation (10).
Life-threatening sequelae (hemorrhage and cardiac tamponade)
result from the external injury rather than the intracardiac
component. Intracardiac damage is manifested as the delayed
recognition of a cardiac murmur and some degree of CHF, and when
these appear one must suspect intracardiac trauma (11).
It is obvious that in Absalom's case, the penetrating heart injury
was not treated and his injury was fatal (1).
References
1. Ben-Nun L. Predictors of survival. In Ben-Nun L. (ed.) How did Absalom
the Son of King David Die? B.N. Publication House. Israel. 2014, pp. 73-86.
2. Asensio JA, Berne JD, Demetriades D, et al. One hundred five
penetrating cardiac injuries: a 2-year prospective evaluation. J Trauma.
1998;44:1073-82.
3. Molina EJ, Gaughan JP, Kulp H, et al. Outcomes after emergency
department thoracotomy for penetrating cardiac injuries: a new
perspective. Interact Cardiovasc Thorac Surg. 2008;845-8.
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References
1. McCullough ME, Kurzban R, Tabak BA. Cognitive systems for revenge
and forgiveness. Behav Brain Sci. 2013;36(1):1-15.
2. Aureli F, Schaffner CM. Why so complex? Emotional mediation of
revenge, forgiveness, and reconciliation. Behav Brain Sci. 2013;36(1):15-6.
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References
1. Olson, DH, Sprenkle DH, Russel C. Circumflex model of marital and
family systems: I. Cohesion and adaptability dimensions, family types and
clinical applications. Family Process. 1979;18:3-28.
2. Olson DH, Russel C, Sprenkle DH. Circumflex model of marital and
family systems: VI. Theoretical update. Family Process. 1983;22:69-83.
Absalom. And the victory that day turned into mourning for all the
people...” (II Samuel 19:1-3).
These biblical verses indicate the great suffering of a human being
who has lost his son forever. In spite of Absalom's rebellion, the King
was attached to his beloved son. The grief was so painful that the
King wished to die instead of his beloved son.
Mourning characterized the grief of a person who has lost a loved
one forever. Mourning is not a disease; it is one of the most painful
facts of life. In fact, the more we are attached to someone, the more
we will suffer his or her losses. This is unavoidable. The grief
expressing our attachment is accompanied by immediate and intense
regression with repeated need for consolation. For some people, it
can be the means of coming to terms with their own mortality (1).
There are several stages of mourning: the living person's
ambivalence toward the deceased, the recollection corresponding to
the progressive acceptance of the loss, which represents the first
phase of the mourning process. During the healing phase, the
mourner is gradually capable of recalling the good times during the
life of the deceased and then progressively of evacuating the
souvenirs and starts living and opening to others again (1).
The biblical text gives no details about the stages of mourning that
King David and his family went through although it is likely that the
whole family passed through all these stages.
Stress is an environmental event, a process, and an outcome. One
approach defines stress in terms of life events, that is, as "stimulus".
Circumstances or events that require the person to adapt produce
feelings of tension. These "stressors" may be major catastrophic
events (a flood or earthquake), major life events (the death of a loved
one), or chronic hassles (managing a chronic medical condition) (2).
The death of beloved son acted as a severe negative stressor,
leading subsequently to a negative outcome. This negative stressor
caused the King negative feelings of despair, anxiety, and depressive
reaction.
The purpose of this study was to describe fathers' grief and the
changes the death of a child has brought to fathers' lives.
Participants included eight fathers who lost their child. The grief of
the father manifested itself individually and dynamically in various
anticipatory feelings and in physical, social, and behavioral reactions.
The death of the child brought both positive and negative changes to
the father's life (3).
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We see that the death of a beloved son led to physical, social and
behavioral reactions in the King. Did the death of his beloved son
bring changes to the King's life?
The human being needs ties to grow and develop. When some of
these ties are broken, a period of great intensity arises that we call
mourning. If the loss is radical and definitive, as in the case of death,
all of the person's dimensions are affected (the physical, emotional,
cognitive, behavioral, social, and spiritual) to such an extent that the
person can feel unable to overcome that and/or develops a
pathological mourning that requires intervention for recovery. Many
factors intervene in the type of mourning such as circumstances of
the death, relation to the deceased, personality, previous experience
and the socio-family context. For there to be complete recovery
following a loss, the person affected passes through a series of stages
or phases and must carry out basic tasks: 1]. Accept the reality of
loss. 2]. Express emotions and pain. 3]. Adapt to a setting from which
the loved one is absent. 4]. Emotionally resituate the deceased and
continue living (4).
All these parameters can be ascribed to King David who lost his
beloved son, Absalom, forever.
Absalom's sudden death was an unpleasant experience that the
King went through. Parents of boys or children who died suddenly
experienced despair, anger, guilt, and depersonalization (5). The
sudden, unexpected death of Absalom caused his father despair,
anger, guilt, and probably depersonalization. From a contemporary
view, David required professional psychiatric intervention.
Major stressful life events, particularly those that have chronic
hardships, create a crisis for families that often leads to disruption
the family's style of functioning (6). The death of two young
unmarried sons, Amnon and subsequently Absalom were stressful
negative life events causing the King's family severe hardships and
affecting the family functioning.
TO SUM UP: King David was exposed three times to the mourning
process. First, when his newborn son died, secondly, when Amnon,
his son was killed and the third time when his rebellious son,
Absalom, was killed. In the case of the newborn child, the King
mourned for the child who suffered from an incurable disease, but
recovered quickly after the child died. In the case of his two sons -
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Amnon, who paid with his life for a disgraceful affair with his half-
sister Tamar, and of Absalom, a rebellious son who decided to fight
against his father, similar grief reactions were observed.
References
1. Barbier D. Mourning. Presse Med. 2001;30:1668-71.
2. Ahmed SA, Lemkau JP. Psychosocial influences on health. In: Rakel RE
(ed.). Textbook of Family Practice. Sixth ed. Saunders, Philadelphia, London.
2002, pp. 43-51.
3. Aho AL, Tarkka MT, Astedt-Kurki P, Kaunonen M. Fathers' grief after
the death of a child. Issues Ment Health Nurs. 2006;27:647-63.
4. Carbodevilla I. Loss and mourning. An Sist Sanit Navar. 2007;30 Suppl
3:163-76.
5. Hazzard A, Weston J, Gutterres C. After a child's death: factors related
to parental bereavement. J Dev Behav Pediatr. 1992;13:24-30.
6. Patterson JM, Garwick W. Levels of meaning in family stress theory.
Family Process. 1994;33:287-394.
References
1. Berman EM. Adult Developmental stages and marital interaction.
Audio-Digest (Psychiatry). 1978;7:5.
2. Baker P. Some Basic theoretical concepts. In: Philip Barker Basic
Family Therapy. Second ed. Blackwell Scientific Publications. Oxford
London Edinburg. 1981, pp. 33-54.
3. Medalie JH, Kitson GC, Zyzanski SJ. A family epidemiological
model: a practice and research concept for family medicine. J Fam
Practice. 1981;12:78-87.
THE GIBEONITES
A subsequent story indicates a source of stress. There was a
famine in the days of David. King Saul was blamed for this famine
because he killed the Gibeonites, so King David asked the Gibeonites
to end this famine. The Gibeonites demanded that the King hand
over seven men to be hanged as vengeance for their killed people.
Because of his oath and friendship with Jonathan, King David spared
Jonathan’s son Mephibosheth. The King’s decision fell on two sons of
Saul’s concubine Rizpah, Armoni and Mephibosheth, and five sons of
Saul’s daughter Michal, the wife of Adriel, and son of Barzillai the
Meholathite. These seven men were taken to the Gibeonites and
were hanged (II Samuel 21:7-9).
Model of stress includes three conceptual domains: sources of
stress, mediators of stress, and outcomes of stress (1). The sources of
stress are conceptualized as physical or psychological demands on a
system (e.g., the body), which upset its normal steady state of
functioning. The mediators are primarily resources (physical,
psychological, or social) and coping behaviors that influence whether
or not stress is experienced, how it is managed; how long it lasts, and
whether or not it prevents or reduces the outcome. The outcomes
focus on changes in functioning of some level of the system, from the
organ to the family (2,3).
According to this model the famine following King Saul’s murder
of the Gibeonites, was the source of stress. The famine had a
negative impact on the people, making their physical and
psychological demands on them. The mediators included physical,
psychological, and social resources used by King David to end the
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References
1. Patterson J. Families experiencing stress. I The Family adjustment
and adaptation response model. II Applying the FAAR Model to health-
related issues for intervention and research. Fam Systems Med.
1988;6:202-35.
2. Seley H. The stress of life. New York: McGraw-Hill, 1956.
3. Hill R. Generic features of families under stress. Social Casework.
1958;49:139-50.
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References
1. Smilkstein G. The family in crisis. In: Taylor R (ed.). Family
Medicine-Principles and Practices. Springer Verlag. New York. 1978, pp.
235-324.
2. Holmes TH, Rahe RH. The social readjustment rating scale. J
Psychosom Res. 1967;11:213.
After Saul’s death, David and his two wives dwelt in Hebron.
David’s family entered a new phase of its life cycle when David was
anointed as King over Judah and subsequently over Israel. At this
time, David became King, and his family started a new cycle of life.
The King also had ten concubines, locked in his house in
Jerusalem, until they died. The concubines lived in an isolated
environment, depending entirely on the King. It was the King, the
ruler, the decision-making authority, who was responsible for their
fate. There was no right of dispute, disagreement or contradiction to
the King’s decision or other arrangements for these women.
Throughout his life, David was involved in endless wars against the
Philistines. He was a real warrior and fought bravely with the enemy.
He won many wars, and many Philistines were taken prisoners. He
also conquered Moab, Hadadezer, the son of Rehob, the King of
Zobah, and the Syrians of Damascus. King David’s family was
consolidated and the sons helped their father to rule the country.
David’s polygamous family, consisting of many wives and children,
changed constantly. Feelings of tension, admiration, love and hatred
characterized the internal family system. A special friendship
developed between David and Jonathan, the son of King Saul. When
Saul and his three sons, among them Jonathan, were killed, King
David found Mefivoshet, Jonathan’s son, and treated him as his own
son.
David behaved disgracefully in his sexual relations with Bathsheba
that led to her pregnancy. In order to hide his reckless action, King
David prepared a plan to destroy Uriah, Bathsheba's husband. Uriah,
a brave soldier, was sent to a fierce battle where he was killed. Uriah
was assassinated in order to hide the King’s disgraceful behavior.
When Bathsheba heard that Uriah was dead, she mourned for her
husband. In this story, we also see Bathsheba's infidelity. King David
and Bathsheba behaved immorally and both were at risk of
contracting some STD.
When the days of mourning were over King David married
beautiful Bathsheba. David’s family again expanded. Two additional
members entered David’s family life cycle: Bathsheba and a newborn
son. Unfortunately, an incurable disease afflicted the newborn son.
The King was severely distressed; he did not sleep and did not eat.
On the seventh day, his newborn son died. After hearing this sad
news, the King washed, changed his clothes, and ate. The King
believed that if his son died, he the great King could not change the
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rules of this world, he could not bring his child to life, so he had lost
his child forever.
In other story, right at the beginning, it is written that Amnon,
King David’s son, became “..so lean, from day to day” An extensive
evaluation of the medical situation that caused Amnon to be lean
showed that there are insufficient data for a diagnosis of anorexia
nervosa. It most likely that Amnon suffered from a partial eating
disorder syndrome.
Later, Amnon sexually abused his sister Tamar. Tamar suffered
from PTSD, and/or low self-esteem, and/or anxiety, fear, depression
and anger. Because of Amnon’s disgusting behavior, hatred
developed between two brothers - Amnon and Absalom, and the
family atmosphere was poisoned. No compromise could be found in
the triangle: Amnon - Absalom - Tamar.
Absalom, Amnon’s brother, did not forgive his brother for this sin.
At the first opportunity, Absalom commanded his men to kill Amnon
and the mission was performed. The King mourned for his son
Amnon.
Absalom rebelled against his father, King David. By this behavior,
Absalom showed his extreme hatred towards his father. Fighting
broke out between the camps of Absalom and King David, and
Absalom was killed. Absalom death affected the King profoundly and
he mourned for his son.
There was a famine in the days of David. King Saul was blamed for
this famine because he killed the Gibeonites, so King David asked the
Gibeonites to end this famine. The Gibeonites demanded that the
King hand over seven men to be hanged as vengeance for their killed
people. The King’s decision fell on two sons of Saul’s concubine
Rizpah, Armoni and Mephibosheth, and five sons of Saul’s daughter
Michal, the wife of Adriel, and son of Barzillai the Meholathite. These
seven men were taken to the Gibeonites, and were hanged.
The famine following King Saul’s murder of the Gibeonites was the
source of stress. The famine had a negative impact on the people,
making their physical and psychological demands on them. The
mediators included physical, psychological, and social resources used
by King David to end the famine. In order to resolve this stress, seven
members of King Saul’s family had to be sacrificed. David respected
King Saul all his life in spite of Saul’s wish to destroy him. Now was
the decisive moment, the moment for revenge. His vengeance
overtook the dead King Saul even in the grave. The act of revenge
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References
1. Ben-Noun L. In: Ben-Noun L. (ed.). The Diseases and Psychosocial
Problems that Affected King David. (In Hebrew). Israel. 2003.
2. Ben-Nun L. In: Ben-Nun L (ed.). The Family Life Cycle and the Medical
Record of King David the Great. B.N. Publication House. Israel. 2009.
EYE DISEASES
The impact of visual loss has profound implications for the person
affected and society as a whole (1) with self-reported VI as an
independent factor associated with mortality (2).
The majority of blind people live in developing countries, and
generally, their blindness could have been avoided or cured. Given
the current predictions that the number of blind people worldwide
will roughly double by the year 2020, there is no room for
complacency. As the world's population increases and a greater
proportion survives into late adulthood, the number of people with
visual loss will inexorably rise. As the longevity of the world's
population increases, the visual requirements at the workplace are
also changing. People with low vision may be at a disadvantage in
many common activities, and may face unemployment – particularly
in technological societies (1).
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References
1. West S, Sommer A. Prevention of blindness and priorities for the
future. Bull World Health Organ. 2001;79:244-8.
2. Berdaux G, Brézin AP, Fagnani F, et al. Self-reported visual impairment
and mortality: a French nationwide perspective. Ophthalmic Epidemiol.
2007;14:80-7.
3. Rosenberg EA, Sperazza LC. The visually impaired patient. Am Fam
Physician. 2008;77:1431-6.
4. Sommer A, Taylor HR, Ravilla TD, et al. Challenges of ophthalmic care
in the developing world. JAMA Ophthalmol. 2014;132(5):640-4.
5. Rohrschneider K, Greim S. Epidemiology of blindness in Baden,
Germany. Klin Monatsbl Augenheilkd. 2004;221:116-21.
6. Hiratsuka Y, Ono K, Kanai A. The present state of blindness in the
world. Nippon Ganka Zasshi. 2001;105:369-73.
7. Evans JR, Fletcher AE, Wormald RPL. Causes of visual impairment in
people aged 75 years and older in Britain: an add-on study to the MRC trial
of assessment and management of older people in the community. Br J
Ophthalmology. 2004;88:365-11.
8. Quillen DA. Common causes of vision loss in elderly patients. Am Fam
Physician. 1999;60:99-108.
9. Causes and prevalence of visual impairment among adults in the
United States. The eye diseases prevalence research group. Arch
Ophtalmol. 2004;122:477-85.
10. Ben-Noun L. What was the disease of the legs that afflicted King Asa?
Gerontology. 2001;47:96-9.
Reference
1. Fotouhi A, Hashemi H, Mohammad K, Jalali KH; Tehran Eye Study. The
prevalence and causes of visual impairment in Tehran: the Tehran eye study.
Brit J Ophthalmology. 2004;88:740-5.
EPIDEMIOLOGY OF BLINDNESS
There are over 300 million people living in the world today who
are visually impaired and a further 45 million who are blind. The large
majority (90%) of these people lives in developing countries, and up
to 75% of blindness are avoidable. With cataracts being the major
cause of blindness and VI, many ophthalmic aid programs are aimed
at alleviating the enormous burden caused by this readily treatable
disease. Having said that, caution should be exercised that short
surgical visits to remote rural areas that are not coordinated with
local national eye care managers should be discouraged because they
do little for the development of sustainable eye care programs. With
this in view, it has become imperative to design blindness prevention
and ophthalmic support programs that are workable, comprehensive,
economical and sustainable (1).
Of the 38 million people who are blind worldwide, 22 million are
over the age of 60 years (WHO Estimate) (2). Poor vision and
blindness increase significantly with age for all races and ethnicities
(3-5). These data, combined with life expectancy that is on the
increase (6), indicate that it is essential to provide effective
ophthalmologic care for the elderly.
From the most recent data, the magnitude of VI and its causes in
2010 have been estimated, globally and by WHO region. The
definitions of VI are the current definitions of presenting vision in the
ICD version 10. A systematic review was conducted of published and
unpublished surveys from 2000 to the present. For countries without
data on VI, estimates were based on newly developed imputation
methods that took into account country economic status as proxy.
Surveys from 39 countries satisfied the inclusion criteria for this
study. Globally, the number of people of all ages visually impaired is
estimated at 285 million, of whom 39 million are blind, with
uncertainties of 10-20%. People 50 years and older represent 65%
and 82% of visually impaired and blind, respectively. The major
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relative increase in older adults, the blind population has been stable
and the population with MSVI may have increased (8).
Cataract remains the major cause of blindness, especially in the
less developed countries, while AMD in developed countries.
Substantial improvements have been achieved in the control of
blinding diseases, mainly in respect of onchocerciasis and
xerophthalmia. The WHO alliance for the eradicating of trachoma by
the year 2020 has been set up (9). The age-related eye diseases will
rapidly become the most common causes of blindness and visual loss
and, with the exception of cataract, are the more difficult to identify,
diagnose, and treat (10).
The objective of this study was to estimate the economic burden
of vision loss and eye disorders in the US population younger than 40
years in 2012. Participants included the US population younger than
40 years in 2012. Costs based on consensus guidelines were
categorized. Medical costs attributable to diagnosed eye-related
disorders, undiagnosed vision loss, and medical vision aids using
Medical Expenditure Panel Survey and MarketScan data were
estimated. The prevalence of VI and blindness were estimated using
National Health and Nutrition Examination Survey data. Costs from
lost productivity using Survey of Income and Program Participation
were estimated. Costs of informal care, low vision aids, special
education, school screening, government spending, and transfer
payments based on published estimates and federal budgets were
estimated. QALYs lost based on published utility values were
estimated. Man outcome measures included costs and QALYs lost in
2012. The economic burden of vision loss and eye disorders among
the US population younger than 40 years was $27.5 billion in 2012
(95% CI $21.5-$37.2 billion), including $5.9 billion for children and
$21.6 billion for adults 18 to 39 years of age. Direct costs were $14.5
billion, including $7.3 billion in medical costs for diagnosed disorders,
$4.9 billion in refraction correction, $0.5 billion in medical costs for
undiagnosed vision loss, and $1.8 billion in other direct costs. Indirect
costs were $13 billion, primarily because of $12.2 billion in
productivity losses. In addition, vision loss cost society 215,000
QALYs. In conclusion, a substantial burden resulted from vision loss
and eye disorders in the US population younger than 40 years, a
population excluded from previous studies. Monetizing QOL losses at
$50,000 per QALY would add $10.8 billion in additional costs,
indicating a total economic burden of $38.2 billion. Relative to
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diabetic retinopathy were fourth and fifth most common causes for
blindness for all regions at both times. URE, followed by cataract,
macular degeneration, glaucoma and diabetic retinopathy were the
most common cause for MSVI in 1990 and 2010. In conclusion, in
highly developed countries, prevalence of blindness and MSVI has
been reduced by 50% and 38%, respectively, and the number of blind
people and people with MSVI decreased by 17.4% and 12.6%,
respectively, even with the increasing number of older people in the
population. In high-income countries, macular degeneration has
become the most important cause of blindness, but UREs continue to
be the leading cause of MSVI (14).
The main aim of this study was to determine the prevalence,
causes, and risk factors for blindness and VI in the elderly population
of Lebanese nursing homes, to encourage the development of an
effective campaign against blindness. Transversal study was
conducted in all nursing homes in two Lebanese regions (298
residents). All respondents (89.6%) underwent a complete ocular
examination. Personal and medical data were gathered for each
participant. The prevalence of blindness (VA ≤20/200 in both eyes)
was 22.4% (20.3% in residents aged between 80 and 89 years old,
42.9% in patients 90 years or older). The prevalence of VI (VA ≤20/40
and>20/200 in the best eye) was 36%. The rate of blindness in
underprivileged residents was found to be double than that of the
well-off residents (27% and 15%, respectively). Cataract was the
leading cause of blindness, followed by AMD and OAG. At least 55%
of the causes of blindness and 58% of the causes of VI were
potentially curable or avoidable. In conclusion, blindness and VI were
high among Lebanese nursing home residents. This is an observation
given that the leading ocular diseases are treatable and that good
vision is essential to these residents' QOL (15).
The main aim of this study was to estimate the magnitude,
temporal trends and subregional variation in the prevalence of
blindness, and MSVI in sub-Saharan Africa. A systematic review was
conducted of published and unpublished population-based surveys as
part of the Global Burden of Disease, Risk Factors and Injuries Study
2010. The prevalence of blindness and VI by country and subregion
was estimated. In sub-Saharan Africa, 52 studies satisfied the
inclusion criteria. The estimated age-standardized prevalence of
blindness decreased by 32% from 1.9% (95% CI 1.5%-2.2%) in 1990 to
1.3% (95% CI 1.1%-1.5%) in 2010 and MSVI by 25% from 5.3% (95% CI
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References
1. Muecke J, Sia DI, Newland H, Casson RJ, Selva D. Perspective on
ophthalmic support in countries of the developing world. Clin Experiment
Ophthalmol. 2013;41(3):263-71.
2. Thylefors B, Negrel AD, Parajasegaram R, Dadzie KY. Global data on
blindness. Bull World Health Organ. 1995; 73:115-21.
3. Rysculova A, Turczyn K, Makuc DM, et al. Self-reported age-related
eye diseases and visual impairment in the United States: results of the 2002
national health interview survey. Am J Public Health. 2008;98:454-61.
4. Foster A. Patterns of blindness. In: Tasman W, Jaeger EA (eds.).
Duane's Clinical Ophtalmology. Philadelphia, Lippincott. 1991, Vol. 5, Chapt.
53.
5. Kollarits CR. The aging eye. In: Calkins E, Davis PJ, Ford AB (eds.). The
Practice of Geriatics. Philadelphia, Saunders. 1986, pp. 248-58.
6. Manton KG, Stallard E. Cross-sectional estimates of active life
expectancy for the U.S. elderly and oldest-old populations. J Gerontol. 1991;
46:S170-82.
7. Pascolini D Mariotti SP. Global estimates of visual impairment: 2010.
Br J Ophthalmol. 2012;96(5):614-8.
8. Stevens GA, White RA, Flaxman SR, et al. Global prevalence of vision
impairment and blindness: magnitude and temporal trends, 1990-2010.
Ophthalmology. 2013;120(12):2377-84.
9. Thylefors B, Resnikoff S. Progress in the control of world blindness
and future perspectives. Sante. 1998;8:140-3.
10. West SK. Looking forward to 20/20: a focus on the epidemiology of
eye diseases. Epidemiol Rev. 2000;22:64-70.
11. Wittenborn JS, Zhang X, Feagan CW, et al. The economic burden of
vision loss and eye disorders among the United States population younger
than 40 years. Ophthalmology. 2013;120(9):1728-35.
12. Jin YP, Wong DT. Self-reported visual impairment in elderly
Canadians and its impact on healthy living. Can J Ophthalmol. 2008;43:407-
13.
13. Looker HC, Nyangoma SO, Cromie DT, et al. Rates of referable eye
disease in the Scottish National Diabetic Retinopathy Screening Programme.
Br J Ophthalmol. 2014;98(6):790-5.
14. Bourne RR, Jonas JB, Flaxman SR, et al. Prevalence and causes of
vision loss in high-income countries and in Eastern and Central Europe:
1990-2010. Br J Ophthalmol. 2014;98(5):629-38.
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References
1. Harvey P. Common eye diseases of elderly people: identifying and
treating causes of vision loss. Gerontology. 2003;49:1-11.
2. Gohdes DM, Balanurugan A, Larsen BA, Mayalahn C. Age-related
diseases: an emerging challenge for public health professionals. Prev
Chronic Dis. 2005;2(3):A17.
3. Mitchell J, Bradley C. Quality of life in age-related macular
degeneration: a review of the literature. Health Qual. Life Outcomes. 2006;
Dec 21;4:97.
4. Bressler NM, Bressler SB, Fine SL. Age-related macular degeneration.
Surv Ophtalmol. 1988;32:3375-413.
5. Pauleikhoff D, Scheider A, Wiedmann P, et al. Neovascular age-related
macular degeneration in Germany: Encroachment on the quality of life and
the functional implications. Ophthalmologe. 2009;106:242-51.
6. Ratnapriya R, Chew EY. Age-related macular degeneration-clinical
review and genetics update. Clin Genet. 2013;84(2):160-6.
7. Zampatti S, Ricci F, Cusumano A, et al. Review of nutrient actions on
age-related macular degeneration. Nutr Res. 2014;34(2):95-105.
8. Sharma K, Sharma NK, Anand A. Why AMD is a disease of ageing and
not of development: mechanisms and insights. Front Aging Neurosci. 2014
Jul 10;6:151.
9. Schramm EC, Clark SJ, Triebwasser MP et al. Genetic variants in the
complement system predisposing to age-related macular degeneration: A
review. Mol Immunol. 2014 Jul 15. pii: S0161-5890(14)00163-1.
References
1. Harvey P. Common eye diseases of elderly people: and treating causes
of vision loss. Gerontology elderly people: identifying. 2003;49:1-11.
2. Hyman L. Epidemiology of AMD. In: Hampton GR, Nelsen PT (eds.).
Age Related Macular Degeneration: Principles and Practice. New York:
Raven Press. 1992, pp.1-35.
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References
1. Wong WL, Su X, Li X, et al. Global prevalence of age-related macular
degeneration and disease burden projection for 2020 and 2040: a
systematic review and meta-analysis. Lancet Glob Health. 2014;2(2):e106-
16.
2. Friedman DS, O'Colmain BJ, Muñoz B, et al. Prevalence of age-related
macular degeneration in the United States. Arch Ophthalmol.
2004;122(4):564-72. Erratum in Arch Ophthalmol. 2011;129(9):1188.
3. Rudnicka AR, Jarrar Z, Wormald R, et al. Age and gender variations in
age-related macular degeneration prevalence in populations of European
ancestry: a meta-analysis. Ophthalmology. 2012;119(3):571-80.
4. Owen CG, Jarrar Z, Wormald R, et al. The estimated prevalence and
incidence of late stage age related macular degeneration in the UK. Br J
Ophthalmol. 2012;96(5):752-6.
5. Erke MG, Bertelsen G, Peto T, et al. Prevalence of age-related macular
degeneration in elderly Caucasians: the Tromsø Eye Study. Ophthalmology.
2012;119(9):1737-43.
6. Kawasaki R, Yasuda M, Song SJ, et al. The prevalence of age-related
macular degeneration in Asians: a systematic review and meta-analysis.
Ophthalmology. 2010;117(5):921-7.
7. Joachim N, Mitchell P, Younan C, et al. Ethnic variation in early age-
related macular degeneration lesions between white Australians and
Singaporean Asians. Invest Ophthalmol Vis Sci. 2014;55(7):4421-9.
8. Helgadóttir G, Jónasson F, Sigurdsson H, et al. Age related macular
degeneration. Laeknabladid. 2006;92:685-96.
9. Rohrshneider K, Greim S. Epidemiology of blindness in Baden,
Germany. Klin Monatsbl Augesheilkd. 2004;221:116-21.
10. Adeoti CO. Prevalence and causes of blindness in a tropical African
population. West Afr J Med. 2004;23:249-52.
6. Kawasaki R, Wang JJ, Aung T, et al. Prevalence of age-related macular
degeneration in a Malay population: the Singapore Malay Eye Study.
Ophthalmology. 2008;115(10):1735-41.
12. Xu L, Wang Y, Li Y, et al. Causes of blindness and visual impairment
in urban and rural areas in Beijing: the Beijing Eye Study. Ophthalmology.
2006;113:1134.e1-11.
13. Hatef E, Fotoufi A, Hashemi H, et al. Prevalence of retinal diseases
and their pattern in Tehran: The Tehran Eye Study. Retina. 2008;28:755-762.
14. Avisar R, Friling R, Cnir M, et al. Estimation of prevalence and
incidence rates and causes of blindness in Israel, 1998-2003. Isr Med Assoc J.
2006;8:880-1.
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References
1. Soubrane G, Haddad WM, Coscas G. Age-related macular
degeneration. Presse Med. 2002;31:1282-7.
2. Nowak JZ. Age-related macular degeneration (AMD): pathogenesis
and therapy. Pharmacol Rep. 2006;58:353-63.
3. Klein R, Peto T, Bird A, Vannewkirk MR. The epidemiology of age-
related degeneration. Am J Ophtalmol. 2004;137:486-95.
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References
1. Harvey P. Common eye diseases of elderly people: identifying and
treating causes of vision loss. Gerontology. 2003;49:1-11.
2. Soubrane G, Hadda WM, Coscas G. Age-related macular degeneration.
Prese Med. 2002;31:1282-7.
CATARACT
Cataract is the leading cause of blindness, accounting for 50% of
blindness worldwide. Although significant progress has been made
toward identifying risk factors for cataract, there is no proven
primary prevention or medical treatment (1). Age-related cataracts
are by far the most common type of cataracts (2). Most cataracts are
bilateral (2) although cataract may occur in only one eye and may
mature more rapidly in one eye than in the other (2,3).
Cataract, namely subscapular, in elderly subjects is associated
with an increased mortality risk (4). Cataract, which is a lens opacity
that interferes with visual function, is the leading cause of blindness
in the world today (5), and accounts for approximately 16 million
cases of blindness (VA <20/400, Snelen equivalent) worldwide (WHO
1997 estimate) (6).
The objective of this study was to determine the prevalence of
cataract and pseudophakia/aphakia in the US and to project the
expected change in these prevalence figures by 2020. Summary
prevalence estimates of cataract and of pseudophakia/aphakia were
prepared separately for black, white, and Hispanic persons (for whom
only cataract surgery data were available) in five-year age intervals
starting at 40 years for women and men. The estimates were based
on a standardized definition of various types of cataract: cortical,
greater than 25% of the lens involved; posterior subcapsular, present
according to the grading system used in each study; and nuclear,
greater than or equal to the penultimate grade in the system used.
Data were collected from major population-based studies in the US,
and, where appropriate, Australia, Barbados, and Western Europe.
The age-, gender-, and race/ethnicity-specific rates were applied to
2000 US Census data, and projected population figures for 2020, to
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these risk indicators should be carried out using fresh data to confirm
the validity of the risk model. Once validated this model should
provide an equitable approach for peer-to-peer comparisons in the
context of revalidation (12).
The purpose of this study was to assess the prevalence and causes
of avoidable blindness in Atsinanana Region, Madagascar, with the
RAAB survey. The hospital records to supplement the findings for
public health care planning were analyzed. Only villages within a
two-hour walk from a road, about half of the population of
Atsinanana, were included. Seventy-two villages were selected by
population-proportional-to-size sampling. In each village, compact
segment sampling was used to select 50 people over age 50 for eye
examination using standard RAAB methods. Records at the two
hospitals providing cataract surgery in the region were analyzed for
information on patients who underwent cataract surgery in 2010.
Cataract incidence rate and target cataract surgery rate was modeled
from age-specific prevalence of cataract. The participation rate was
87% and the sample prevalence of blindness was 1.96%. Cataract was
responsible for 64% and 85.7% of blindness and severe VI,
respectively. VI was due to cataract (69.4%) and RE (14.1%). There
was a strong positive correlation between cataract surgical rate by
district and the proportion of people living within two hours of a
road. There were marked differences in the profiles of the cataract
patients at the two facilities. The estimated incidence of cataract at
the 6/18 level was 2.4 eyes per 100 people over age 50 per year. In
conclusion, although the survey included only people with
reasonable access, the main cause of VI was still cataract. The
incidence of cataract is such that it ought to be possible to eliminate
it as a cause of VI, but changes in service delivery at hospitals and
strategies to improve access will be necessary for this change (13).
The purpose of this cross-sectional population-based survey was
to determine the extent and causes of blindness and VI in the
Varamin district, Iran, in 2009. A total of 3,000 noninstitutional
inhabitants aged ≥50 years were involved in this study from February
to August 2009. A standard protocol was used according to the RAAB
method after an initial four-day workshop. The clusters were selected
through probability-proportionate-to-size sampling. In each cluster,
people were selected by a "cluster compact sampling" method. VA
was measured using a standard tumbling "E" chart without and with
pinhole. Ophthalmologists examined participants with VA <6/18 in
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borderline visual outcome (PVA <6/18 but ≥6/60). Eyes that received
surgery in charitable organizations had a higher rate of intraocular
lens implantation and good visual outcome (VA ≥6/18) compared
with eyes that were operated on elsewhere. In conclusion, the
prevalence of blindness, SVI, and VI was high among rural residents in
Hainan. Cataract remained the leading cause of avoidable blindness.
Outcomes of cataract surgery performed in public hospitals were
suboptimal. Quality-control initiatives should be introduced to
improve cataract surgery outcomes (15).
References
1. Javitt JC, Wang F, West SK. Blindness due to cataract: epidemiology
and prevention. Annu Rev Public Health. 1996;17:159-77.
2. Sperbuto RD, Seigel D. Senile lens and senile macular changes in a
population-based sample. Am J Ophthalmology. 1980;90:86-91.
3. Newell FW. The lens. Acquired cataracts. In: Newell FW (ed.).
Ophthalmology. Principles and Concepts, ed. 6. St Louis , Moshby. 1986, pp.
364-77.
4. Xu L, Cui TT, Wang YX, Jonas JB. Cataract and mortality. The Beijing
eye study. Graefes Arch Clin Exp Ophthalmol. 2008;246:615-7.
5. Thylefors B, Negrel AD, Parajasegaram R, Dadzie KY. Global data on
blindness. Bull World Health Organ. 1995; 73:115-21.
6. Harvey P. Common eye diseases of elderly people: and treating causes
of vision loss. Gerontology elderly people: identifying. 2003;49:1-11.
7. Congdon N, Vingerling JR, Klein BE, et al. Prevalence of cataract and
pseudophakia/aphakia among adults in the United States. Arch Ophthalmol.
2004;122(4):487-94.
8. Varma R, Richter GM, Torres M, et al. Four-year incidence and
progression of lens opacities: the Los Angeles Latino Eye Study. Am J
Ophthalmol. 2010;149(5):728-34.e1-2.
9. Klein BE, Klein R, Lee KE, Gangnon RE. Incidence of age-related
cataract over a 15-year interval the Beaver Dam Eye Study. Ophthalmology.
2008;115:477-82.
10. Bilioska E, Moll A, Kowalszyk G, Omulecki W. Epidemiology of
cataract in clinical material of Department of Ophthalmology, Medical
University of Lódź. Klin Oczna. 2004;106(3 Supl):450-2.
11. Shah SP, Dineen B, Jadoon Z, et al. Lens opacities in adults in
Pakistan: prevalence and risk factors. Ophtalmic Epidemiol. 2007;14:381-9.
12. Sparrow JM, Taylor H, Qureshi K, et al. The cataract national data set
electronic multi-centre audit of 55,567 operations: case-mix adjusted
surgeon's outcomes for posterior capsule rupture. Eye (Lond).
2011;25(8):1010-5.
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13. Randrianaivo JB, Anholt RM, Tendrisoa DL, et al. Blindness and
cataract surgical services in Atsinanana region, Madagascar. Middle East Afr
J Ophthalmol. 2014;21(2):153-7.
14. Rajavi Z, Katibeh M, Ziaei H, et al. Rapid assessment of avoidable
blindness in Iran. Ophthalmology. 2011;118(9):1812-8.
15. Li EY, Liu Y, Zhan X, et al. Prevalence of blindness and outcomes of
cataract surgery in Hainan Province in South China. Ophthalmology. 2013;
120(11):2176-83.
References
1. Abraham AG, Condon NG, West Gower E. The new epidemiology of
cataract. Ophthalmol Clin North Am. 2006;19(4):415-25.
2. Cohen DL, Neil HA, Sparrow J, et al. Lens opacity and mortality in
diabetes. Diab Med. 1990;7:615-7.
3. Jacques PF, Chylack LT, McGandy RB, at el. Antioxidant status in
persons with and without senile cataract. Arch Ophtalmol. 1988;106:337-
340.
4. Richter GM, Torres M, Choudhury F, et al. Risk factors for cortical,
nuclear, posterior subcapsular, and mixed lens opacities: the Los Angeles
Latino Eye Study Ophthalmology. 2012;119(3):547-54.
5. Rim TH, Kim MH, Kim WC, et al. Cataract subtype risk factors identified
from the Korea National Health and Nutrition Examination survey 2008-
2010. BMC Ophthalmol. 2014 Jan 10;14:4.
6. Ben-Noun L. The disease that caused weight loss in King David the
great. J Gerontol Med Sci. 2003;59A:M143-5.
SYMPTOMATOLOGY
The chief symptom of acquired cataract is a gradual decrease of
vision that is not associated with pain or inflammation of the eye.
Double vision in one eye (monocular diplopia) is caused by the lens
opacity splitting light bundles, but this disappears with further
decrease in vision. In the early stages, lights may be surrounded by a
collar halo (1).
Dilatation of the pupil that occurs in dim illumination improves
vision. Glare and constriction of the pupil in bright illumination
reduce vision, particularly in patients with PSC that obstruct the
visual axis. Patients may complain of spots in the visual field that,
unlike those caused by vitreous floaters remain fixed. In nuclear
cataracts, there is often an increase in the refractive power of the
lens so that patients are able to read without glasses (1).
Paradoxically, in the incipient stage of cataract distant vision is
blurred, but near vision may improve slightly, so the patient will read
better without glasses ("second sight"). This artificial myopia is due to
the greater refractive index of the lens in the incipient stage. The
gradual decrease of vision is not associated with pain or
inflammation of the eye (2). Opacity of the lens can vary from a small
local opacity to a diffuse general loss of transparency (3).
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References
1. Newell FW. The Lens. In: Klein EA (ed.). Newell FW Ophthalmology.
Principles and Concepts. Mosby. Sixth ed. St Louis, Toronto. 1986, pp. 364-
377.
2. Shock JP, Harper RA. Lens. Age related cataract (senile cataract). In:
Vaughan D, Asbury T, Riordan-Eva (eds.). A Lange Medical Book. General
Ophthalmology, ed. 14. Norwalk, Appleton-Lange. 1995, pp. 165-7.
3. Harvey P. Common eye diseases of elderly people: and treating causes
of vision loss. Gerontology elderly people: identifying. 2003;49:1-11.
4. Newell FW. The lens. Acquired cataracts. In: Newell FW (ed).
Ophthalmology. Principles and Concepts, ed. 6. St Louis , Moshby. 1986, pp.
364-77.
GLAUCOMA
Glaucoma is a worldwide leading cause of irreversible vision loss.
Because it may be asymptomatic until a relatively late stage,
diagnosis is frequently delayed (1). The glaucomas are a range of
disorders with a characteristic type of optic nerve damage. These
diseases are the second commonest cause of blindness in the world,
and the commonest cause of irreversible blindness (2). The
glaucomas are associated with an increased rate of mortality,
particularly CAG, in elderly subjects (3).
A general understanding of the disease pathophysiology,
diagnosis, and treatment may assist primary care physicians in
referring high-risk patients for comprehensive ophthalmologic
examination and in more actively participating in the care of patients
affected by this condition. The objective of this study was to describe
current evidence regarding the pathophysiology and treatment of
OAG and CAG. A literature search was conducted using MEDLINE, the
Cochrane Library, and manuscript references for studies published in
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Reference
1. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and
treatment of glaucoma: a review. JAMA. 2014;311(18):1901-11.
2. Khaw PT, Shah, Elkigton AR. Glaucoma – 1: Diagnosis. BMJ.
2004;328:97-99.
3. Xu L, Wang YX, Jonas JB. Glaucoma and mortality in the Beijing Eye
Study. Eye. 2008;22:434-8.
TYPES. There are two main types of glaucoma: OAG and CAG. If
the cause is evident, glaucoma is designated as secondary, but if the
cause is unknown, as primary (1).
Reference
1. Newell FW. The Glaucomas. In: Newell FW Ophthalmology. Principles
and Concepts. Klein EA ed. Mosby. Sixth ed. St Louis, Toronto. 1986, pp. 378-
98.
prevalence of POAG in urban was higher than that in rural. PCAG was
more common in women than in men (12).
In Israel, more than 10% of the screened population had ocular
hypertension, pre-perimetric glaucoma, or glaucoma (13).
References
1. Harvey P. Common eye diseases of elderly people: identifying and
treating causes of vision loss. Gerontology. 2003;49:1-11.
2. Pizzarello LD. The dimensions of the problem of the eye disease
among the elderly. Ophtalmology. 1987;94:1191-5.
3. Rysculova A, Turczyn K, Makuc DM, et al. Self-reported age-related
eye diseases and visual impairment in the United States: results of the 2002
national health interview survey. Am J Public Health. 2008;98:454-61.
4. Varma R, Ying-Lai M, Francis BA, et al. Prevalence of open-angle
glaucoma and ocular hypertension in Latinos: the Los Angeles Latino Eye
Study. Ophthalmology. 2004;111:1439-048.
5. Congdon N, Wang F, Tielsch JM. Issues in the epidemiology and
population-based screening of primary angle-closure glaucoma. Surv
Ophthalmol. 1992;36:411-23.
6. Bonomi L, Marchini G, Marraffa M, et al. Epidemiology of angle-
closure glaucoma: prevalence, clinical types, and association with peripheral
anterior chamber depth in the egna-Neumarket Glaucoma Study.
Ophthalmology. 2001;107:998-1003.
7. Vijaya L, George R, Arvind H, et al. Prevalence of primary-closure
disease in an urban south Indian population and comparison with a rural
population. The Chennai Glaucoma Study. Ophthalmology. 2008;115: 655-
60.
8. Yamamoto T, Iwase A, Araie M, et al. The Tajimi Study report 2:
prevalence of primary angle closure and secondary glaucoma in a Japanese
population. Ophthalmology. 2005;112:1661-9.
9. Foster PJ. The epidemiology of primary closure and associated
glaucomatous optic neuropathy. Semin Ophthalmol. 2002;17:50-8.
10. Moore DB, Walton C, Moeller KL, et al. Prevalence of self-reported
early glaucoma eye drop bottle exhaustion and associated risk factors: a
patient survey. BMC Ophthalmol. 2014 Jun 13;14:79.
11. Cheng JW, Zong Y, Zeng YY, Wei RL. The prevalence of primary angle
closure glaucoma in adult Asians: a systematic review and meta-analysis.
PLoS One. 2014 24;9(7):e103222.
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12. Cheng JW, Cheng SW, Ma XY, et al. The prevalence of primary
glaucoma in mainland China: a systematic review and meta-analysis. J
Glaucoma. 2013;22(4):301-6.
13. Nesher R, on behalf of the Israel Glaucoma Screening Group.
Prevalence of increased intraocular pressure and optic disk cupping:
multicenter glaucoma screening in Israel during the 2009 and 1010 World
glaucoma weeks. IMAJ. 2014;16:483-6.
References
1. Khan HA, Leibowitz HM, Ganley JP, et al. The Framingham eye study.
Outline and major prevalence study. Am J Epidemiol. 1977;106:17-32.
2. Epstein D, Pavan-Langston D. Glaucoma. In: Pavan–Langston D (ed.).
Manual of Ocular Diagnosis and Therapy. Little, Brown and Company. 1982,
pp. 195-222.
3. Newell FW. The Glaucomas. In: Newell FW Ophthalmology. Principles
and Concepts. Klein EA ed. Mosby. Sixth ed. St Louis, Toronto. 1986, pp. 378-
98.
4. Forsman E, Kivelä T, Vesti E. Lifetime visual disability in open-angle
glaucoma and ocular hypertension. J Glaucoma. 2007;16:313-9.
5. Cross JM, Girkin CA, Owsley C, McGwin G Jr. The association between
thyroid problems and glaucoma. Br J Ophthalmol. 2008;92: 1503-5.
References
1. Khaw PT, Shah, Elkigton AR. Glaucoma – 1: Diagnosis. BMJ.
2004;328:97-99.
2. Epstein D, Pavan-Langston D. Glaucoma. In: Pavan–Langston D (ed).
Manual of Ocular Diagnosis and Therapy. Little, Brown and Company. 1982,
pp. 195-222.
3. Newell FW. The Glaucomas. In: Newell FW Ophthalmology. Principles
and Concepts. Klein EA ed. Mosby. Sixth ed. St Louis, Toronto. 1986, pp. 378-
398.
References
1. Kerrigan-Baumrind LA, Quigley HA, Pease ME, et al. Number of
ganglion cells in glaucoma eyes compared with threshold visual fields tests
in the same persons. Invest Ophtalmol Vis Sci. 2000;41:741-8.
2. Gaton D. Screening fo glaucoma. IMAJ. 2014;16:509-10.
3. Sehi M, Iverson SM. Glaucoma Diagnosis and Monitoring Using
Advanced Imaging Technologies. US Ophthalmic Rev. 2013;6(1):15-25.
4. Kotowski J, Wollstein G, Ishikawa H, Schuman JS. Imaging of the optic
nerve and retinal nerve fiber layer: an essential part of glaucoma diagnosis
and monitoring. Surv Ophthalmol. 2014;59(4):458-67.
5. Greenfield DS, Weinreb RN. Role of optic nerve imaging in glaucoma
clinical practice and clinical trials. Am J Ophthalmol. 2008;145(4):598-603.
6. Badalà F, Nouri-Mahdavi K, Raoof DA, et al. Optic disk and nerve fiber
layer imaging to detect glaucoma. Am J Ophthalmol. 2007;144(5):724-32.
7. Vessani RM, Moritz R, Batis L, et al. Comparison of quantitative
imaging devices and subjective optic nerve head assessment by general
ophthalmologists to differentiate normal from glaucomatous eyes. J
Glaucoma. 2009;18(3):253-61.
OPTIC NEUROPATHY
AION is the most common cause of acute optic neuropathy after
age 50, but may also occur in younger patients. The diagnosis is
clinical and includes painless visual loss associated with a relative
afferent pupillary defect and disc edema. In almost all cases, there is
an underlying crowded optic nerve with a small cup-to-disc ratio. The
visual prognosis is usually poor, although up to 43% of patients may
improve over time. The fellow eye is involved in up to 15% of patients
within five years, but the risk of recurrence in the same eye is less
than 5%. There is no treatment for acute NAION but it is essential to
evaluate these patients for underlying treatable atheromatous
vascular risk factors. A coagulation workup should also be considered
in younger patients. It is essential to rule out giant cell arteritis in all
patients over the age of 50 with IONs. Posterior ischemic neuropathy
(in which the optic nerve is normal acutely) is rare and should be
considered a diagnosis of exclusion (1).
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References
1. Luneau K, Newman NJ, Biousse V. Ischemic optic neuropathies.
Neurologist. 2008;14(6):341-54.
2. Kollaritis CR. The aging eye. In: Calkin E, Davis PJ. Ford AB (eds.). The
Practice of Geriatrics. Philadelphia, Saunders. 1986, pp. 248-58.
3. Cohen MM, Lessel S. The neuro-opthalmology of aging. In: Albert M
(ed). Clinical Neurology of Aging. New York, Oxford University Press. 1984,
pp. 313-44.
4. Ho SF, Dhar-Munshi S. Nonarteritic anterior ischaemic optic
neuropathy. Curr Opin Ophthalmol. 2008;19(6):461-7.
5. Miller NR, Arnold AC. Current concepts in the diagnosis, pathogenesis
and management of nonarteritic anterior ischaemic optic neuropathy. Eye
(Lond). 2014 Jul 4. doi: 10.1038/eye.2014.144. [Epub ahead of print]
6. Özkiriş M, Akin I, Özkiriş A, et al. Ischemic optic neuropathy after
carotid body tumor resection. J Craniofac Surg. 2014;25(1):e58-61.
OPTIC ATROPHY
The optic nerve is a bundle of nerve fibers that carry images from
retina to the brain. Each fiber carries a part of the visual information
to the brain. If these nerve fibers become damaged, the brain does
not receive all of this vision information and sight becomes blurred.
Optic atrophy means the loss of some or most of the nerve fibers in
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the optic nerve. The effects range from visual change to severe visual
loss (1).
Optic atrophy is the result of diseases or injuries to RGC or their
axons that produces degeneration of axons anterior to the lateral
geniculate body. The chief symptom of optic atrophy is loss of central
and peripheral vision. Etiological classification of optic atrophy
includes glaucoma, DM, brain tumor, RGC or nerve fiber disease
(pigmentary degeneration of retina, chorioretinal degeneration,
inflammation, and atrophy), inflammation (demyelinating disease,
meningitis, encephalitis, and abscess), tabes dorsalis, metastatic
septicemia, optic neuropathy, papiledema, toxicity (arsenic, lead,
methanol, ethanol, quinine, cigarette smoking, tobacco, chloroquine,
ethambutol, and chlorphenicol), vitamin B deficiency (beriberi,
pellagra, and pernicious anemia), sarcoidosis, glioma, hereditary and
trauma (2-5).
DOA is a neuro-ophthalmic condition characterized by a bilateral
degeneration of the optic nerves, causing insidious visual loss,
typically starting during the first decade of life. The disease affects
primary the RGC and their axons forming the optic nerve, which
transfer the visual information from the photoreceptors to the lateral
geniculus in the brain. The prevalence of the disease varies from
1/10000 in Denmark due to a founder effect to 1/30000 in the rest of
the world. DOA patients usually suffer of moderate visual loss,
associated with central or paracentral visual field deficits and color
vision defects. The severity of the disease is highly variable, the VA
ranging from normal to legal blindness. The ophthalmic examination
discloses on fundoscopy isolated optic disc pallor or atrophy, related
to the RGC death. About 20% of DOA patients harbour extraocular
multi-systemic features, including neurosensory hearing loss, or less
commonly chronic progressive external ophthalmoplegia, myopathy,
peripheral neuropathy, multiple sclerosis-like illness, spastic
paraplegia or cataracts. Two genes (OPA1, OPA3) encoding inner
mitochondrial membrane proteins and three loci (OPA4, OPA5,
OPA8) are currently known for DOA. Additional loci and genes (OPA2,
OPA6 and OPA7) are responsible for X-linked or recessive optic
atrophy. All OPA genes yet identified encode mitochondrial proteins
embedded in the inner membrane and ubiquitously expressed, as are
the proteins mutated in the LHON. OPA1 mutations affect
mitochondrial fusion, energy metabolism, control of apoptosis,
calcium clearance and maintenance of mitochondrial genome
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integrity. OPA3 mutations only affect the energy metabolism and the
control of apoptosis. Patients are usually diagnosed during their early
childhood, because of bilateral, mild, otherwise unexplained visual
loss related to optic discs pallor or atrophy, and typically occurring in
the context of a family history of DOA. OCT further discloses non-
specific thinning of RNFL, but a normal morphology of the
photoreceptors layers. Abnormal visual evoked potentials and the
pattern ERG may also reflect the dysfunction of the RGCs and their
axons. Molecular diagnosis is provided by the identification of a
mutation in the OPA1 gene (75% of DOA patients) or in the OPA3
gene (1% of patients). Visual loss in DOA may progress during
puberty until adulthood, with very slow subsequent chronic
progression in most of the cases. In DOA patients with associated
extra-ocular features, the visual loss may be more severe over time.
To date, there is no preventative or curative treatment in DOA;
severely visually impaired patients may benefit from low vision aids.
Genetic counseling is commonly offered and patients are advised to
avoid alcohol and tobacco consumption, as well as the use of
medications that may interfere with mitochondrial metabolism. Gene
and pharmacological therapies for DOA are currently under
investigation (6).
Autosomal DOA is a major cause of VI in young adults that is
characterized by selective RGC loss. To define the prevalence and
natural history of this optic nerve disorder, a population-based
epidemiologic and molecular study of presumed DOA cases in the
north of England was performed. This case series included 76
affected probands with a clinical diagnosis of DOA identified from the
neuro-ophthalmology and neurogenetics database. OPA1 genetic
testing was performed using a PCR-based sequencing strategy. OPA1-
negative cases were then screened for large-scale OPA1
rearrangements and OPA3 mutations. Additional affected family
members identified through contact tracing were examined, and
longitudinal visual data were analyzed. The prevalence and
molecular characteristics of DOA in the north of England and visual
function and disease progression among patients with OPA1-positive
mutations were evaluated. The detection rate of OPA1 mutations
was 57.6% among probands with a positive family history of optic
atrophy (19/33) and 14.0% among singleton cases (6/43).
Approximately two thirds of families with DOA harbored OPA1
mutations (14/22, 63.6%), and five novel OPA1 mutations were
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References
1. Brodie SE. Aging and disorders of the eye. In: Brocklehurst JC, Tallis RC,
Fillit HM (eds.). Textbook of Geriatric Medicine and Gerontology ed. 4.
Churchill Livingstone. 1992, pp. 472-9.
2. Lindsey B. De Lott. What is Optic Atrophy? Available 10 December
2014 www.kellogg.umich.edu › Patient Care›.
3. Epstein DL, Pavan-Langston D. Glaucoma. In: Pavan-Langston D (ed.).
Manual of Ocular Diagnosis and Treatment. Boston, Little, Brown. 1982, pp.
195-222.
4. Newell FW. The optic nerve. Optic atrophy. In: Newell FW (ed.).
Ophthalmology. Principles and Concepts, ed. 6. St Louis, Mosby. 1986, pp.
361-2.
5. Spoor TCC. Optic atrophy. In: Spoor TCC (ed.). Atlas of Optic Nerve
Disorders. New York, Raven Press. 1992, pp. 57-67.
6. Lenaers G, Hamel C, Delettre C, et al. Dominant optic atrophy.
Orphanet J Rare Dis. 2012 Jul 9;7:46.
7. Yu-Wai-Man P, Griffiths PG, Burke A, et al. The prevalence and natural
history of dominant optic atrophy due to OPA1 mutations. Ophthalmology.
2010;117(8):1538-46, 1546.e1.
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REFRACTIVE ERROR
RE is prevalent among the causes of VI among the elderly (1). It is
defined as a state in which the optical system of the non-
accommodating eye fails to bring parallel rays of light into focus
anterior or posterior to the fovea, respectively, resulting in blurred
vision (1).
The objective of this population-based cohort study was to study the
frequency and causes of VI in relation to RE. A total of 6,597
participants from Rotterdam Study I (baseline and four follow-up
examinations) and 2,579 participants from Rotterdam Study II (baseline
and two follow-up examinations), all 55 years or older, were included.
Participants underwent an extensive ophthalmic examination, including
BCVA and objective refraction, fundus photography, visual field
perimetry, and OCT imaging of macula and optic disc. Cumulative risks
and ORs of VI for various RE categories were calculated and were
determined causes by using all screening information as well as medical
records. Main outcome measures included unilateral and bilateral low
vision (WHO criteria, VA <0.3 and VA ≥0.05; US criteria, VA <0.5 and VA
≥0.1) and blindness (WHO criteria, VA <0.05; US criteria, VA<0.1).
Cumulative risks of VI ranged from virtually 0 in all RE categories at 55
years of age to 9.5% standard error, 0.01) for emmetropia and 15.3%
(SE, 0.06) for high hyperopia to 33.7% (standard error, 0.08) for high
myopia at 85 years of age. The major causes of VI in highly hyperopic
persons were AMD, cataract, and combined causes (each 25%); in
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those in Malays, but lower than those in Chinese. Risk factors for
myopia were similar across the three ethnic groups in Singapore (8).
The purpose of this cross-sectional survey of all adults aged 40
and over within a desert and coastal community study was to assess
the contribution of trachoma, cataract and RE to visual morbidity
among Indigenous adults living in two remote communities of the
Northern Territory, Australia. Main outcome measures included VA,
clinical signs of trachoma using the simplified WHO grading system
and assessment of cataract through a non-dilated pupil. Two
hundred and sixty individuals over the age of 40 years participated in
the study. The prevalence of VI (<6/12) was 17%. The prevalence of
blindness (<3/60) was 2%, 40-fold higher than seen in an urban
Australian population when adjusted for age. In total, 78% of adults
who grew up in a desert community had trachomatous scarring
compared with 26% of those who grew up in a coastal community
(p≤0.001). In the desert community, the prevalence of trachomatous
trichiasis was 10% and corneal opacity reached 6%. No trachomatous
trichiasis or corneal opacity was seen in the coastal community. In
conclusion, trachoma, cataract and URE remain significant
contributors to visual morbidity in at least two remote indigenous
communities (9).
References
1. The prevalence of refractive errors among adults in the United States,
Western Europe, and Australia. The eye diseases prevalence research
group. Arch Ophtalmol. 2004; 122:495-505.
2. Verhoeven VJ, Wong KT, Buitendijk GH, et al. Visual Consequences of
Refractive Errors in the General Population. Ophthalmology. 2014 Sep 7. pii:
S0161-6420(14)00641-1.
3. Sherwin JC, Khawaja AP, Broadway D, et al. Uncorrected refractive
error in older British adults: the EPIC-Norfolk Eye Study. Br J Ophthalmol.
2012;96(7):991-6.
4. Sherwin JC, Lewallen S, Courtright P. Blindness and visual impairment
due to uncorrected refractive error in sub-Saharan Africa: review of recent
population-based studies. Br J Ophthalmol. 2012;96(7):927-30.
245
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the iris mass. Histopathologically, the iris mass was consistent with
metastatic RCC. Further evaluation disclosed a mass of the left
kidney. The patient underwent a left nephrectomy and was found to
have RCC, with focal penetration into the renal capsule. One month
after the nephrectomy, he developed a highly vascular nodule of the
left bulbar conjunctiva. An excisional biopsy was performed, and
histopathology disclosed an additional focus of RCC. In conclusion,
iris and conjunctival involvement may be a clinical manifestation of
RCC. RCC should be considered in the differential diagnosis of a
fleshy, vascular iris and a conjunctival nodule (24).
Three cases of RCC metastatic to the eye and orbit are reported.
The case reports of a 67-year-old man, a 58-year-old man, and a 23-
year-old woman with metastatic RCC are described. The iris mass
occurred in a 67-year-old man, a known case of RCC. Whereas the
orbital metastasis in the 58-year-old man was the initial presenting
sign in a hitherto undiagnosed patient, the orbital metastasis in the
23-year-old female patient was detected following nephrectomy for
RCC. RCC metastasizing to the eye and orbit are very rare, with only
68 cases reported previously. In patients presenting with atypical
orbital or ocular masses, the possibility of RCC metastasis should be
considered, especially if there is a history of previous renal disorder.
Incisional biopsy with histopathological evaluation is important to
diagnose this condition and facilitate appropriate therapy (25).
A 60-year-old woman presented with proptosis of the left eye.
Imaging showed a well-circumscribed tumor in the region of the
medial rectus muscle. Excision biopsy revealed a diagnosis of
metastatic RCC that was confirmed on abdominal imaging. RCC can
rarely present as a well-circumscribed orbital mass and should be
included in the differential diagnosis of such lesions (26).
A case of lung cancer in which symptoms due to orbital metastasis
were recognized. A 55-year-old man presented with a chief complaint
of double vision. Orbital MRI demonstrated a right intraorbital mass
with bone destruction, which resulted in oculomotor nerve palsy and
optic nerve disturbance. Chest CT scan showed a four cm mass in the
right S6, which was diagnosed on biopsy as a poorly differentiated
adenocarcinoma. A whole-body scintigram revealed multiple bone
metastases: the right orbital wall, the lower cervical spine, the left knee
joint, and so on. Based on the clinical findings, the orbital tumor was a
metastasis from the lung. Systemic chemotherapy and irradiation of the
right orbital tumor and the left knee joint were performed. Though a
252
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References
1. Solomon SD, Smith JH, O'Brien J. Ocular manifestations of systemic
malignancies. Curr Opin Opthalmol. 1999;10:447-51.
2. De Potter P, Disneur D, Levecq L, Snyers B. Ocular manifestations of
cancer. J Fr Optalmol. 2002;25:194-202.
3. Matus G, Dicato M, Focan C. Cancer associated retinopathy (CAR). Two
clinical cases and review of the literature. Rev Med Liege. 2007;62:166-9.
4. Kubicka-Trzaska A, Romanowska-Dixon B. Malignant uveitis masquerade
syndromes. Klin Oczna. 2008;110:199-202.
5. Salah S, Khader J, Yousef Y, et al. Choroidal metastasis as the sole initial
presentation of metastatic lung cancer. Hematol Oncol Stem Cell Ther.
2012;5(1):60-5.
6. Singh N, Kulkarni P, Aggarwal AN, et al. Choroidal metastasis as a
presenting manifestation of lung cancer: a report of 3 cases and systematic
review of the literature. Medicine (Baltimore). 2012;91(4):179-94.
7. Jiang K, Brownstein S, Sekhon HS, et al. Ocular metastasis of lung
adenocarcinoma with ELM4-ALK translocation: A case report with a review of
the literature. Saudi J Ophthalmol. 2013;27(3):187-92.
8. Albadainah F, Khader J, Salah S, Salem A. Choroidal metastasis secondary
to prostatic adenocarcinoma: Case report and review of literature. Hematol
Oncol Stem Cell Ther. 2013 Sep 5. pii: S1658-3876(13) 00068-X.
9. Antosz ZS, Walocha J, Poręba R, et al. Sudden loss of vision due to breast
cancer metastasis to the eyeball. Neuro Endocrinol Lett. 2014;35(4):249-51.
10. Tamai H, Ishida K, Murakami K, et al. Compression neuropathy caused by
cancer metastasis to the optic nerve canal. BMC Res Notes. 2013 Dec 20;6:546.
11. Benhaddou R, Sayouti A, Khoumiri R, et al. Iris metastasis from lung
cancer. J F Ophtalmol. 2008;31:427-9.
12. Furuichi S, Omori C, Nakayama T, et al. Relapse of small cell carcinoma of
the lung with metastases to iris. Nihon Kokyuk Gakkai Zasshi. 2000;38:417-20.
13. Arat YO, Boniuk M. Red lesions of the iris, choroid, and skin secondary to
metastatic carcinoma of the thyroid: a review. Surv Ophtalmol. 2007;52:523-8.
14. Lee WB, Sy HM, Filip DJ, Grossniklaus HE. Metastatic esophageal
adenocarcinoma presenting in the iris. Am J Ophthalmol. 2007;144:477-9.
15. Ferry AP, Font RL. Carcinoma metastatic to the eye and orbit II. A
clinicopathological study of 26 patients with carcinoma metastatic to the
anterior segment of the eye. Arch Ophtalmol. 1975;93:472-82.
16. Lachostergios PJ, Voutsadakis IA, Papandreou CN. Orbital metastasis of
breast carcinoma. Breast Cancer (Auckl). 2009 Dec 2;3:91-7.
17. Font RL, Maturi RK, Small RG, Garcia-Rojas M. Hepatocellular carcinoma
metastatic to the orbit. Arch Ophthalmol. 1998;116(7):942-5.
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18. Fonseca Júnior NL, Frizon L, Paves L, et al. An unusual orbital metastatic
lesion: the only finding in a case of hepatocellular carcinoma: case report. Arq
Bras Oftalmol. 2008;71(6):865-7.
19. Gupta R, Honavar SG, Vemuganti GK. Orbital metastasis from
hepatocellular carcinoma. Surv Ophthalmol. 2005;50(5):485-9.
20. Jiang H, Wang Z, Xian J, Ai L. Bilateral multiple extraocular muscle
metastasis from hepatocellular carcinoma. Acta Radiol Short Rep. 2012 Jan
12;1(1).
21. Kurli M, Finger PT. The kidney, cancer, and the eye: current concepts.
Surv Ophtalmol. 2005;50:507-18.
22. Alsuhaibani AH, Carter KD, Nerad JA, Lee AG. Prostate carcinoma
metastasis to extraocular muscles. Ophtal Plast Reconstr Surg. 2008;24:233-5.
23. Scott IU, Tanenbaum M, Kay MD, Gould E. Extraocular muscle metastasis
16 years following primary prostate carcinoma. Ophtalmic Surg Lasers.
2001;32:479-80.
24. Ware GT, Haik BG, Morris WR. Renal cell carcinoma with involvement of
iris and conjunctiva. Am J Ophthalmol. 1999;127(4):460-1.
25. Shome D, Honavar SG, Gupta P, et al. Metastasis to the eye and orbit
from renal cell carcinoma - a report of three cases and review of literature. Surv
Ophthalmol. 2007;52(2):213-23.
26. Mudiyanselage SY, Prabhakaran VC, Davis GJ, Selva D. Metastatic renal
cell carcinoma presenting as a circumscribed orbital mass. Eur J Ophthalmol.
2008;18(3):483-5.
27. Mori H, Maekawa N, Satoda N, et al. A case of primary lung cancer with
initial symptoms due to orbital metastases. Nihon Kokyuki Gakkai Zasshi.
2003;41(1):19-24.
28. Henning M, Hu Q, Siegelmann-Danieli N. Orbital metastasis as the
presenting symptom of extensive stage small cell lung cancer. Eur J Intern Med.
2008;19(1):65-6.
29. Kikawada M, Shimizu S, Uno M, et al. An elderly case of lung cancer
presenting with symptoms of orbital metastasis. Nihon Ronen Igakkai Zasshi.
2001;38(4):560-3.
30. Burkat CN, Van Buren JJ, Lucarelli MJ. Characteristics of orbital multiple
myeloma: a case report and literature review. Surv Ophthalmol. 2009;54(6):697-
704.
31. Fung S, Selva D, Leibovitch I, et al. Ophthalmic manifestations of multiple
myeloma. Opthalmologica. 2006;219:43-8.
32. Omoti AE, Omoti CE. Ophthalmic manifestations of multiple myeloma.
West Afr J Med. 2007;26:265-8.
33. Chin KJ, Kempin S, Milman T, Finger PT. Ocular manifestations of multiple
myeloma: three cases and a review of the literature. Optometry.
2011;82(4):224-30.
34. Hassan M, Alirhayim Z, Sroujieh L, Hassan S. Multiple myeloma of the
orbit. Case Rep Ophthalmol Med. 2012;2012:252310.
35. Sharma A, Kaushal M, Chaturvedi NK, Yadav R. Cytodiagnosis of multiple
myeloma presenting as orbital involvement: a case report. Cytojournal. 2006
Aug 10;3:19.
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36. Hsu VJ, Agarwal MR, Chen CS, Rossi C. IgA orbital plasmacytoma in
multiple myeloma. Ophthal Plast Reconstr Surg. 2010;26(2):126-7.
37. Adkins JW, Shields JA, Shields CL, et al. Plasmacytoma of the eye and
orbit. Int Ophthalmol. 1996-1997;20(6):339-43.
38. Romero IL, Campos FA, Damasceno RW, et al. Plasmacytoma of the orbit
involving lacrimal gland with secondary transformation into multiple myeloma:
case report. Arq Bras Oftalmol. 2009;72(2):236-8.
39. Ben-Noun L. The disease that caused weight loss in King David the Great.
J Gerontol Med Sci. 2003;59A:M143-5.
40. Ben-Noun L. What was the disease of the bones that affected King
David? J Gerontol Med Sci. 2002;57:M152-4.
41. Ben-Noun L. In: Ben-Noun L. (ed.). The Family Life Cycle and the Medical
Record of King David the Great. B.N. Publication House. 2009. Israel.
OTHER CAUSES
Other causes of vision loss include trachoma, leprosy,
onchocerciasis, xerophthalmia, HSV keratitis, retinal detachment, and
inherited retinal degenerative disorders (1).
Trachoma is the commonest infectious cause of blindness
worldwide. Recurrent infection of the ocular surface by C.
trachomatis, the causative agent, leads to inturning of the eyelashes
(trichiasis) and blinding corneal opacification. Trachoma is endemic in
more than 50 countries. It is currently estimated that there are about
1.3 million people blind from the disease and a further 8.2 million
have trichiasis. Several estimates for the burden of disease from
trachoma have been made, giving quite variable results. The variation
is partly because different prevalence data have been used and partly
because different sequelae have been included. The most recent
estimate from the WHO placed it at around 1.3 million DALYs. A key
issue in producing a reliable estimate of the global burden of
trachoma is the limited amount of reliable survey data from endemic
regions (2,3).
Trachoma is correlated with poverty, limited access to healthcare
services and water. In 2003, the WHO estimated that 84 million
people were suffering from active trachoma, and 7.6 million were
severely visually impaired or blind because of trachoma: this study
provides an updated estimate of the global prevalence of trachoma
based on the most recent information available. A literature search
of recent published and unpublished surveys in the 57 endemic
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countries was carried out: the result of surveys that used the WHO
trachoma grading system and additional information from regional
and country experts served as a basis to determine the prevalence of
trachoma in each country. Population-based surveys provided recent
information for 42 out of 57 endemic countries with 40.6 million
people estimated to be suffering from active trachoma, and 8.2
million are estimated to have trichiasis. In conclusion, the current
estimate of prevalence of trachoma is lower than the previous WHO
estimates: this can be explained by the success in implementing
control strategy, by more accurate data, as well as by socio-economic
development in endemic countries (3).
Leprosy control programs are highly successful. As a result,
leprosy control will be more and more integrated into the general
health services. The existing vertical, specialized control programs
will be dismantled. Eye complications in leprosy have decreased. This
is a result of earlier diagnosis and highly effective MDT of leprosy,
combined with timely treatment of secondary nerve damage by
steroids. Most ocular morbidity is now found among elderly and
disabled leprosy patients who were diagnosed before effective MDT
treatment became available. Many of these patients live in leprosy
settlements. Age-related cataract has become the leading cause of
blindness in leprosy. The second cause of blindness is corneal
opacification, mainly as a result of neglected exposure keratitis and
corneal anaesthesia. The miotic pupils in late multibacillary leprosy,
in combination with small central lens opacities, may lead to
blindness. The Vision 2020 Initiative prioritizes cataract surgery.
Leprosy patients should be actively included. Disabled leprosy
patients can benefit from screening programs for REs and the
provision of spectacles and low vision aids. Determining the most
feasible surgical methods for lagophthalmos surgery remains a
challenge. For all health and eye care staff, training in leprosy and its
eye complications is needed, as well as a change in attitude towards
leprosy patients. Staff must be prepared to welcome them in the
general health services (4).
Of 742 outpatients screened for ocular disease, 177 (24%) had eye
lesions due to leprosy. These were more in the lepromatous
spectrum of the disease and showed increasing trend with age of
patient and duration of the disease. Madarosis was the commonest
lesion (76%). The serious and sight threatening lesions like
lagophthalmos, corneal anaesthesia, corneal opacities and ulcers,
260
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References
1. Whicher JP. Blindness. In: Vaughan D, Asbury T, Riordan-Eva P (eds.). a
Lange medical book. General Ophthalmology, ed. 14. Appleton-Lange, Norwalk.
1995; pp. 396-400.
2. Burton MJ, Mabey DC. The global burden of trachoma: a review. PLoS
Negl Trop Dis. 2009;3(10):e460.
3. Mariotti SP, Pascolini D, Rose-Nussbaumer J. Trachoma: global magnitude
of a preventable cause of blindness. Br J Ophthalmol. 2009; 93(5):563-8.
4. Hogeweg M, Keunen JE. Prevention of blindness in leprosy and the role of
the Vision 2020 Programme. Eye (Lond). 2005;19(10):1099-105.
5. Soshamma G, Suryawanshi N. Eye lesions in leprosy. Lepr Rev. 1989;
60(1):33-8.
6. Ebeigbe JA, Kio F. Ocular leprosy in institutionalized Nigerian patients.
Ghana Med J. 2011;45(2):50-3.
7. Enk CD. Onchocerciasis - river blindness. Clin Dermatol. 2006;24(3): 176-
80.
8. Babalola OE. Onchocerciasis as a risk factor for night blindness.
Ophthalmic Epidemiol. 2012;19(4):204-10.
9. López-Rodríguez N, Faus F, Sierra J, et al. Night blindness and
xerophthalmia after surgery for morbid obesity. Arch Soc Esp Oftalmol.
2008;83(2):133-5.
10. Sommer A. Xerophthalmia, keratomalacia and nutritional blindness. Int
Ophthalmol. 1990;14(3):195-9.
11. Menon K, Vijayaraghavan K. Sequelae of severe xerophthalmia - a
follow-up study. Am J Clin Nutr. 1980;33(2):218-20.
12. Farooq AV, Shukla D. Herpes simplex epithelial and stromal keratitis: an
epidemiologic update. Surv Ophthalmol. 2012;57(5):448-62.
13. Souza PM, Holland EJ, Huang AJ. Bilateral herpetic keratoconjunctivitis.
Ophthalmology. 2003;110(3):493-6.
14. Feltgen N, Walter P. Rhegmatogenous retinal detachment - an
ophthalmologic emergency. Dtsch Arztebl Int. 2014;111(1-2):12-21.
15. Rozet JM, Gerber S, Ducroq D, et al. Hereditary macular dystrophies. J Fr
Ophtalmol. 2005;28(1):113-24.
16. Hamel CP. Cone rod dystrophies. Orphanet J Rare Dis. 2007 Feb 1;2:7.
17. Hamel C. Retinitis pigmentosa. Orphanet J Rare Dis. 2006 Oct 11;1:40.
OSTEOPOROSIS
What does the phrase “...my bones wasted away... ” mean? The
1990 Consensus Development Panel defined osteoporosis as a
“disease characterized by low bone mass and micro architectural
deterioration of bone tissue, leading to enhanced bone fragility and a
consequent increase in fracture risk” (1). In recent years,
osteoporosis is defined as a skeletal disorder characterized by
compromised bone strength predisposing to an increased risk of
fracture. Bone strength reflects integration of bone density and bone
quality (2).
Osteoporosis is the most common skeletal disorder in the elderly,
being characterized by impaired bone strength and increased risk of
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References
1. Consensus Development Conference. Prophylaxis and treatment of
osteoporosis. Am J Med. 1991;90:107-11.
2. Kishimoto H. Change in the definition of osteoporosis especially on
bone quality. Clin Calcium. 2005;15:736-40.
3. Nuti R, Brandi ML, Isaia G, et al. New perspectives on the definition
and the management of severe osteoporosis: the patient with two or more
fragility fractures. J Endocrinol Invest. 2009;32(9):783-8.
4. Czrewioski E, Badurski JE, Marcinowska-Suchowierska E, Osieleniec J.
Current understanding of osteoporosis according to the position of the
World Health Organization (WHO) and International Osteoporosis
Foundation. Ortop Traumatol Rehabil. 2007;9:337-56.
5. Liu H, Page NM, Goldzweig CL, et al. Screening for osteoporosis in
men: a systematic review for an American College of Physicians guideline.
Ann Intern Med. 2008;148:685-701.
6. Semionov K, Lieberman IH. Vertebral augmentation in osteoporosis
and bone metastasis. Curr Opin Support Palliat Care. 2007;1:323-7.
7. Stazi AV. Micronutrient deficiencies in osteoporosis. Minerva Med.
2013;104(4):455-70.
8. Wade SW, Strader C, Fitzpatrick LA, et al. Estimating prevalence of
osteoporosis: examples from industrialized countries. Arch Osteoporos.
2014;9(1):182.
9. Rosenblum AL. Connective tissue disorder in diabetes. In: Alberti
K.G.M.M, Zimmet P, DeFronzo R.A, Keen H (eds.). International Textbook
of Diabetes. Vol. 2. 2nd ed. New York, NT: John Wiley & Sons. 1997, pp.
1517-29.
10. Blake GM, Fogelman I. The role of DXA bone density scans in the
diagnosis and treatment of osteoporosis. Postgrad Med. 2007;83:509-17.
11. Trevisan C. New proposals for the definition of severe osteoporosis.
Aging Clin Exp Res. 2007;19(4 Suppl):3-6.
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TYPES. Bone loss occurs during the normal aging process. The
term "primary" osteoporosis refers to osteoporosis that results from
the involutional losses associated with aging and, in women,
additional losses related to natural menopause. Osteoporosis caused
or exacerbated by other disorders or medication exposures is
referred to as "secondary" osteoporosis (1).
Involutional or age-dependent senile osteoporosis occurs in men
aged 70 or older and is characterized by trabecular and cortical bone
loss leading to hip, vertebral, proximal humerus, proximal tibia, and
pelvis fractures (2).
Secondary osteoporosis is a common cause of osteoporosis, and
there are many medical conditions associated with osteoporosis.
Many of these present well before osteoporosis develops, and
knowledge of these pre-existing conditions may influence the
decision about whether to test and/or treat for osteoporosis. Men
and premenopausal women with unexplained osteoporosis or a
history of fragility fracture should undergo investigation for
secondary osteoporosis. Postmenopausal women with risk factors for
secondary osteoporosis should be carefully evaluated. Beyond the
well-recognized association with glucocorticoids, an increasing list of
drugs has been implicated in causing bone loss and fractures. With
appropriate consideration of secondary causes and relevant
investigations, many of these conditions are preventable with newer
therapies (3).
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References
1. Stein E, Shane E. Secondary osteoporosis. Endocrinol Metab Clin North
Am. 2003;32(1):115-34, vii.
2. Riggs BL, Melton LJ. Medical progress. Involutional osteoporosis. N
Engl J Med. 1986;314:1676-86.
3. Kok C, Sambrook PN. Secondary osteoporosis in patients with an
osteoporotic fracture. Best Pract Res Clin Rheumatol. 2009;23(6):769-79.
4. Boling EP. Secondary osteoporosis: underlying disease and the risk for
glucocorticoid-induced osteoporosis. Clin Ther. 2004;26(1):1-14.
5. De Nijs RN. Glucocorticoid-induced osteoporosis: a review on
pathophysiology and treatment options. Minerva Med. 2008;99(1):23-43.
References
1. Herrera A, Lobo-Escolar A, Mateo J, et al. Male osteoporosis: A review.
World J Orthop. 2012;3(12):223-34.
2. Laurent M, Gielen E, Claessens F, et al. Osteoporosis in older men:
recent advances in pathophysiology and treatment. Best Pract Res Clin
Endocrinol Metab. 2013;27(4):527-39.
References
1. Baker C, McFarland KF. Endocrinology. In: Rakel RE (ed.). Textbook of
Family Practice. 3rd ed. St Louis, Mo: W.B. Saunders. 1984, pp. 949-97.
2. Han JY, Lee J, Kim GE, et al. A case of Cushing syndrome diagnosed by
recurrent pathologic fractures in a young woman. J Bone Metab. 2012;
19(2):153-8.
3. Yoshihara A, Okubo Y, Tanabe A, et al. A juvenile case of Cushing's
disease incidentally discovered with multiple bone fractures. Intern Med.
2007;46(9):583-7.
References
1. Wojcicka A, Bassett JH, Williams GR. Mechanisms of action of thyroid
hormones in the skeleton. Biochim Biophys Acta. 2013;1830(7):3979-86.
2. Sun L, Davies TF, Blair HC, et al. TSH and bone loss. An N Y Acad Sci.
2006;1068:309-18.
3. Galliford TM, Murphy E, Williams AJ, et al. Effects of thyroid status on
bone metabolism: a primary role for thyroid stimulating hormone or thyroid
hormone? Minerva Endocrinol.2005;30:237-46.
4. Seeman E, Wahner HW, Offord KP, et al. Differential effects of endocrine
dysfunction and the appendicular skeleton. J Clin Invest. 1982; 69:1302.
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Acromegaly
References
1. Gregerman RI. Selected endocrine problems: disorders of pituitary,
adrenal, and parathyroid glands; pharmacologic use of steroids;
hypocalcemia and hypercalcemia; water metabolism; hypoglycemia; and
hormone use of unproven value. In: Barker LR, Burton JR, Zieve PD, Finucane
TE (eds.). Principles of Ambulatory Medicine. 5th ed. Baltimore, MD:
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2. Mazziotti G, Bianchi A, Bonadonna S, et al. Prevalence of vertebral
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3. Jialal I, Nathoo BC, Joubert S, et al. The clinical presentation and
biochemical diagnosis of acromegaly and gigantism. S Afr Med J. 1982;
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4. Killinger Z, Kužma M, Sterančáková L, Payer J. Osteoarticular changes
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References
1. Saad F, Gooren LJ. Late onset hypogonadism of men is not equivalent
to the menopause. Maturitas. 2014 Jun 30. pii: S0378-5122(14)00212-6.
2. Rochira V, Balestrieri A, Madeo B, et al. Osteoporosis and male age-
related hypogonadism: role of sex steroids on bone (patho)physiology. Eur J
Endocrinol. 2006;154(2):175-85.
3. Scovell JM, Ramasamy R, Wilken N, et al. Hypogonadal symptoms in
young men are associated with a serum total testosterone threshold of
400ng/dL. BJU Int. 2014 Oct 23.
4. Gregerman RI. Selected endocrine problems: disorders of pituitary,
adrenal, and parathyroid glands; pharmacologic use of steroids;
hypocalcemia and hypercalcemia; water metabolism; hypoglycemia; and
hormone use of unproven value. In: Barker LR, Burton JR, Zieve PD,
Finucane TE (eds.). Principles of Ambulatory Medicine. 5th ed. Baltimore,
MD: Williams & Wilkins. 1999, pp. 1096-121.
5. Tuck SP, Francis RM. Testosterone, bone and osteoporosis. Front
Horm Res. 2009;37:123-32.
6. Riggs BL, Melton LJ. Medical progress. Involutional osteoporosis. N Engl J
Med. 1986;314:1676-86.
7. Miller PD. Musculoskeletal diseases. Osteoporosis and other metabolic
bone diseases. In: Schrier RW (ed.). Geriatric Medicine. St Louis Mo: W.B.
Saunders. 1990, pp. 324- 40.
8. Morley JE. Andropause: is it time for the geriatrician to treat it ? J
Gerontol Medical Sci. 2001;56A(5):M263-5.
9. Morley JE, Kaiser FE, Perry P, et al. Longitudinal changes in testosterone,
luteinizing hormone, and follicle-stimulating hormone in healthy older men.
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10. Harman SM, Metter EJ, Tobin JD, et al. Longitudinal effects of aging on
serum total testosterone levels in healthy men. J Clin Endocrinol & Metab.
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11. Yassin AA, Saad F. Improvement of sexual function in men with late-
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Hyperparathyroidism
References
1. Moore TJ. Hypercalcemia. In: Branch WT (ed.). Office Practice of
Medicine. 2nd ed. St. Louis, MO: W.B. Saunders. 1987; pp. 752-63.
2. Rude PK. Hyperparathyroidism. Otolaryngol Clin North Am. 1996;
29:663-79.
3. Mosekilde L. Primary hyperparathyroidism and the skeleton. Clin
Endocrinol (Oxf). 2008;69(1):1-19.
4. Alcaraz MJ, Lorente R, Del Valle Y, et al. Primary hyperparathyroidism:
current role of bone densitometry. Radiologia. 2008;50:37-45.
5. Souza ER, Scrignoli JA, Bezerra FC, et al. Devastating skeletal effects of
delayed diagnosis of complicated primary hyperparathyroidism because of
ectopic adenoma. J Clin Rheumatol. 2008;14:281-4.
6. Siddiqui NI, Miah AG, Khan NK, et al. Primary hyperparathyroidism: a
case report. Mymensingh Med J. 2014;23(2):375-9.
7. Lachungpa T, Sarawagi R, Chakkalakkoombil SV, Jayamohan AE.
Imaging features of primary hyperparathyroidism. BMJ Case Rep. 2014 Mar
10;2014. pii: bcr2013203521.
Paget's disease
References
1. Brown EM. Osteoporosis and Paget’s disease of bone. In: Branch WT
(ed.). Office Practice of Medicine. 2nd ed. St Louis, MO. W.B. Saunders.
1987, pp. 952-64.
2. Whitehouse RW. Paget's disease of bone. Semin Musculoskelet Radiol.
2002;6(4):313-22.
3. Noor M, Shoback D. Paget's disease of bone: diagnosis and treatment
update. Curr Rheumatol Rep. 2000;2(1):67-73.
4. Sieghart S. Osteitis deformans - Paget's disease. Wien Med
Wochenschr. 2004;154(5-6):97-101.
5. Chrétien J. Vertebral localizations of Paget disease. Ann Radiol (Paris).
1995;38(4):169-76.
6. Anjali Thomas N, Rajaratnam S, Shanthly N, et al. Paget's disease of
bone: experience from a centre in southern India. J Assoc Physicians India.
2006;54:525-9.
7. Kannan S, Mahadevan S, Sathya A, Sriram U. A tale of three disease of
the bone. Singapore Med J. 2008;49(10):e263-5.
8. Abelson A. A review of Paget's disease of bone with a focus on the
efficacy and safety of zoledronic acid 5 mg. Curr Med Res Opin. 2008;
24(3):695-705.
9. Scutellari PN, Giorgi A, De Sario V, Campanati P. Correlation of
multimodality imaging in Paget's disease of bone. Radiol Med. 2005;110(5-
6):603-15.
References
1. Newcomer AD, Hodgson SF, McGill DB, Thomas PJ. Lactase deficiency:
prevalence in osteoporosis. Ann Intern Med. 1978; 89:218-20.
2. Savaiano D. Lactose intolerance: an unnecessary risk for low bone
density. Nestle Nutr Workshop Ser Pediatr Program. 2011;67:161-71.
3. Savaiano D. Lactose intolerance: a self-fulfilling prophecy leading to
osteoporosis? Nutr Rev. 2003;61(6 Pt 1):221-3.
4. Matthews SB, Waud JP, Roberts AG, Campbell AK. Systemic lactose
intolerance: a new perspective on an old problem. Postgrad Med J. 2005;
81(953):167-73.
5. Scheuner M, Yang H, Totter JI. Gastrointestinal manifestations of
specific genetic disorders. In: Yamada T (ed.) Textbook of Gastroenterology.
2nd ed. Philadelphia, PA: J.B. Lippincott. 1995, pp. 2419-81.
6. Laroche M, Bon E, Moulinier L, et al. Lactose intolerance and
osteoporosis in men. Rev Rhum Engl Ed. 1995;62(11):766-9.
characterizing the hip fracture risk is the measure of the BMD of the
proximal femur. The treatment of osteoporosis in patients with PBC
is largely based on trials of patients with postmenopausal
osteoporosis as there are a few and smaller studies of osteoporotic
patients with PBC. Bisphosphonates seem to be effective in biliary
disease and are more tolerated (8).
The aims were 1] to compare the prevalence of osteoporosis (T-
score <-2.5 SD) between PBC patients and a group of age-and sex-
matched controls consisting of healthy subjects from the general
population; and 2] to identify the main risk factors for the
development of bone loss. Thirty-three women with PBC (mean age,
47.3 +/- 10.4 years) and 66 healthy subjects were enrolled in the
study. BMD was assessed at the lumbar spine by DXA. Bone
metabolism was evaluated by measuring serum calcium corrected for
serum albumin, 25-OH vit. D, PTH, and osteocalcin. Vertebral
fractures were analyzed using vertebral fracture assessment. The
mean T-score was lower in the PBC group compared to healthy
controls, with a significant statistical difference (-2.39 +/- 0.93 and -
1.47 +/- 0.99 in lumbar spine and total hip, respectively, in the PBC
group vs. -0.99 +/- 0.51 and -0.56 +/- 1.14 in healthy controls,
p<0.001). The prevalence of osteoporosis was 51.5% in the PBC group
vs. 22.7% in healthy controls with a statistically significant difference
(p=0.004). BMD of the PBC group was significantly correlated
positively with BMI and 25-OH vit. D, and negatively with menopausal
status, duration of disease, and PTH levels. Vertebral fractures were
present in 9% of the patients. Osteoporosis is more prevalent in
women with PBC than in the general population. BMI, menopausal
status, duration of the disease, and vitamin D deficiency are the main
risk factors for osteoporosis in this liver disease (6.
References
1. Podolsky DK, Isselbacher KJ. Cirrhosis and alcoholic liver disease. In:
Harrison’s Principle of Internal Medicine. 14th ed. New York, NY: McGraw-
Hill. 1998, pp. 1704-9.
2. Hohenester S, Oude-Elferink RP, Beuers U. Primary biliary cirrhosis.
Semin Immunopathol. 2009;31(3):283-307.
3. Selmi C, Bowlus CL, Gershwin ME, Coppel RL. Primary biliary cirrhosis.
Lancet. 2011;377(9777):1600-9.
4. Rosenblum AL. Connective tissue disorder in diabetes. In: Alberti
K.G.M.M, Zimmet P, DeFronzo R.A, Keen H (eds.). International Textbook
of Diabetes. Vol. 2. 2nd ed. New York, NT: John Wiley & Sons. 1997, pp.
1517-29.
5. Bonjour J-P, Schurch M-A, Rizzoli R. Nutritional aspects of hip
fractures. Bone. 1996;18:139S-44S.
6. Mounach A, Ouzzif Z, Wariaghli G, et al. Primary biliary cirrhosis and
osteoporosis: a case-control study. J Bone Miner Metab. 2008;26(4):379-84.
7. Raszeja-Wyszomirska J, Miazgowski T. Osteoporosis in primary biliary
cirrhosis of the liver. Prz Gastroenterol. 2014;9(2):82-7.
8. Wariaghli G, Allali F, El Maghraoui A, Hajjaj-Hassouni N. Osteoporosis
in patients with primary biliary cirrhosis. Eur J Gastroenterol Hepatol. 2010;
22(12):1397-401.
diarrhea are the most common symptoms and are preceded in three-
quarters of cases by arthritis for a mean of six years. Long-term,
unexplained, seronegative oligoarthritis or polyarthritis of large joints
with a palindromic or relapsing course is typical. In most patients,
periodic acid-Schiff staining of proximal small bowel biopsy
specimens reveals inclusions within the macrophages, corresponding
to bacterial structures. However, patients may have no G-I
symptoms, negative jejunum biopsy results and negative PCR tests.
Even in the absence of G-I symptoms, Whipple's disease should be
considered in case of negative blood culture endocarditis, and
unexplained central neurological manifestations or unexplained
arthritis. Identification of the causative bacterium, T. whipplei, has
led to the development of PCR as a diagnostic tool, particularly useful
in patients in the early stages of the disease or with atypical disease.
The recent cultivation of T. whipplei and the complete sequencing of
its genome should improve our understanding and treatment of the
disease. The future development of an assay for detection of specific
antibodies in the serum and generalization of the
immunohistochemical detection of antigenic bacterial structures may
allow earlier diagnosis, thereby preventing the development of the
severe late systemic and sometimes fatal forms of this disease (6).
References
1. Ghitoni G, Valentini G, Spada C, et al. Whipple's disease: progress in
the diagnosis and review of the literature. Minerva Med. 2002;93:447-51.
2. Ratnaike RN. Whipple's disease. Postgrad Med J. 2000;76(902):70-6.
3. Schijf LJ, Becx MC, de Bruin PC, van der Vegt SG. Whipple's disease:
easily diagnosed, if considered. Neth J Med.2008;66:392-5.
4. Eriksen R, Westre B, Bergh K, Qvigstad G. Whipple's disease. Tidsskr
Nor Laegeforen. 2008;128:1406-9.
5. Dancygier H, Scharnke W. Whipple disease - a rare systemic disease.
Praxis (Bern 1994). 2002;91:1691-8.
306
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References
1. Diaz-Guzman E, Mannino DM. Epidemiology and prevalence of
chronic obstructive pulmonary disease. Clin Chest Med. 2014;35(1):7-16.
3. Kessler R, Weitzenblum E. COPD: from early symptoms to chronic
respiratory failure. Rev Prat. 2004;54(13):1414-8.
4. Nicholson D, Bower AD. Pulmonary Medicine. In: Rakel RE (ed.).
Textbook of Family Practice. 3rd ed. St. Louis, MO: W.B. Saunders. 1984, pp.
363-400.
5. Romme EA, Smeenk FW, Rutten EP, Wouters EF. Osteoporosis in
chronic obstructive pulmonary disease. Expert Rev Respir Med. 2013;
7(4):397-410.
6. Lehouck A, van Remoortel H, Troosters T, et al. COPD and bone
metabolism: a clinical update. Rev Mal Respir. 2010;27(10):1231-42.
7. Lehouck A, Boonen S, Decramer M, Janssens W. COPD, bone
metabolism, and osteoporosis. Chest. 2011;139(3):648-57.
8. Balzarini L, Mancini C, Mouzakiti P, et al. Osteoporosis associated with
chronic obstructive pulmonary disease and other respiratory diseases.
Recenti Prog Med. 2011;102(9):359-66.
309
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References
1. Maruotti N, Corrado A, Cantatore FP. Osteoporosis and rheumatic
diseases. Reumatismo. 2014;66(2):125-35.
2. Franck H; Kommission Osteologie der Deutschen Gesellschaft für
Rheumatologie, Braun J, Buttgereit F, Demary W, et al. Bone densitometry in
inflammatory rheumatic diseases: characteristics of the measurement site
and disease-specific factors. Z Rheumatol. 2009;68(10):845-50.
310
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Rheumatoid arthritis
References
1. Alamanos Y, Drosos AA. Epidemiology of adult rheumatoid arthritis.
Autoimmun Rev. 2005;4(3):130-6.
313
L. Ben-Nun King David
References
1. Montalcini T, Romeo S, Ferro Y, et al. Osteoporosis in chronic
inflammatory disease: the role of malnutrition. Endocrine. 2013;43(1):59-64.
2. Rizzoli R, Bonjour JP. Malnutrition and osteoporosis. Z Gerontol
Geriatr. 1999;32 Suppl 1:I31-7.
3. Bonjour J-P, Schurch M-A, Rizzoli R. Nutritional aspects of hip
fractures. Bone. 1996;18:139S-44S.
4. Riggs BL, Melton LJ. Medical progress. Involutional osteoporosis. N Engl J
Med. 1986;314:1676-86.
5. Lipschitz DA. Nutritional assessment in interventions in the elderly. In:
Buerhardt P, Heaney RP (eds.). Nutritional Aspects of Osteoporosis 94.
Challenges of Modern Medicine. Rome: Ares-Seromo Symposia Publications.
1995, pp. 177-91.
6. MacIntosh C, Morley JE, Chapman IM. The anorexia of aging. Nutrition.
2000;16:983-95.
7. Munro HN, Suter PM, Russell RM. Nutritional requirements of the
elderly. Ann Rev Nut. 1987;7:23-49.
References
1. De Nijs RN. Glucocorticoid-induced osteoporosis: a review on
pathophysiology and treatment options. Minerva Med. 2008;99:23-43.
2. Devogelaer JP, Goemaere S, Boonen S, et al. Evidence-based
guidelines for the prevention and treatment of glucocorticoid-induced
osteoporosis: a consensus document of the Belgian Bone Club. Osteoporos
Int. 2006;17:8-19.
3. Civitelli R, Ziambaras K. Epidemiology of glucocorticoid-induced
osteoporosis. J Endocrinol Invest. 2008;31(7 Supp):2-6.
4. Ensrud KE, Walczak TS, Blackwell TL, et al. Antiepileptic drug use and
rates of hip bone loss in older men: a prospective study. Neurology. 2008;
71:723-30.
5. Pack AM, Walczak TS. Bone health in women with epilepsy: clinical
features and potential mechanisms. Int Rev Neurobiol. 2008;83:305-28.
6. Greenspan SL, Greespan FS. The effect of thyroid hormone on skeletal
integrity. Ann Intern Med. 1999;130:750-8.
7. Vestergaard P. Skeletal effects of central nervous system, active drugs:
anxiolytics, sedative, antidepressants, lithium and neuroleptics. Curr Drug
Saf. 2008;3:185-9.
8. Bruyère O, Reginster JY. Osteoporosis in patients taking selective
serotonin reuptake inhibitors: a focus on fracture outcome. Endocrine. 2014
Aug 5. [Epub ahead of print]
9. Rizzoli R, Cooper C, Reginster JY, et al. Antidepressant medications and
osteoporosis. Bone. 2012 Sep;51(3):606-13.
318
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10. Yun H, Delzell E, Saag KG, et al. Fractures and mortality in relation to
different osteoporosis treatments. Clin Exp Rheumatol. 2014 Jul 28. [Epub
ahead of print]
11. Svalheim S, Røste LS, Nakken KO, Taubøll E. Bone health in adults
with epilepsy. Acta Neurol Scand Suppl. 2011;(191):89-95.
Assessment
1. Gennari L, Bilezikian JP. Idiopathic osteoporosis in men. Curr
Osteoporos Rep. 2013;11(4):286-98.
2. Peris P, Martinez-Ferre A, Monegal A, et al. Aetiology and clinical
characteristics of male osteoporosis. Have they changed in the last few
years? Clin Exp Rheumatol. 2008;26:582-8.
3. Ostertag A, Collet C, Chappard C, et al. A case-control study of
fractures in men with idiopathic osteoporosis: fractures are associated with
older age and low cortical bone density. Bone. 2013;52(1):48-55.
4. Laroche M. Pattern of bone mineral density in idiopathic male
osteoporosis. Rheumatol Int. 2012;32(10):3093-6.
ONCOHAEMATOLOGICAL
DISORDERS
The immunosecretory disorders are a diverse group of diseases
associated with proliferation of an abnormal clone of
immunoglobulin (Ig)-synthesizing, terminally differentiated B cells.
These disorders include MM and its variants, plasmacytoma, WM,
MGUS, and monoclonal Ig deposition diseases, the latter including
primary amyloidosis and nonamyloidotic types. These disorders are
histologically composed of plasma cells, or plasmacytoid cells which
produce Ig that is synthesized and usually secreted and can be
deposited in some diseases. The Ig can be complete or can be
321
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References
1. Shaheen SP, Talwalkar SS, Medeiros LJ. Multiple myeloma and
immunosecretory disorders: an update. Adv Anat Pathol. 2008;15(4):196-
210.
MULTIPLE MYELOMA
MM is the second most common hematologic malignancy, with
approximately 16.000 new cases per year, and accounts for 11.000
deaths in the USA. It is the most common cancer to metastasize to
the bone, with up to 90% of patients developing bone lesions (1).
MM is a tumor of terminally differentiated plasma cells that home
to and expands in the bone marrow (1). It is a hemato-oncological
disease in the elderly population, with a peak incidence in the eight
decade, and represents a malignant bone marrow neoplasia in which
a monoclonal strain of atypical plasma cells proliferates and may
result in bone destruction. Skeletal metastases represent the most
common malignant bone tumor and are the third most common
location for distant metastases. They occur predominantly in adults,
especially in the elderly population (2,3).
MM is characterized by the accumulation more than 10% of
monoclonal plasma cells in the bone marrow and the production of
large amounts of a monoclonal immunoglobulin or paraprotein (4,5);
322
L. Ben-Nun King David
Multiple myeloma
References
1. Esteve FR, Roodman GD. Pathophysiology of myeloma bone disease.
Best Pract Res Clin Haematol. 2007;20:613-24.
2. Nau KC, Lewis WD. Multiple myeloma: diagnosis and treatment. Am
Fam Physician. 2008;78:853-9.
3. Baur-Menyk A, Reiser M. Oncohaematologic disorders affecting the
skeleton in the elderly. Radiol Clin North Am. 46:786-98, vii.
4. Caers J, Vande broek I, De Raeve H, et al. Multiple myeloma – an
update on diagnosis and treatment. Eur J Haematol. 2008;81:329-43.
5. George ED, Sadovsky R. Multiple myeloma: recognition and
management. Am Fam Physician. 1999;59:1885-94.
6. Yeh HS, Berenson JR. Myeloma bone disease and treatment options.
Eur J Cancer. 2006;42:1554-63.
7. Berenson JR, Rajdev L, Broder M. Bone complications in multiple
myeloma. Cancer Biol Ther. 2006;5:1082-5.
8. Itse M, Takagi T. Bone lesions in multiple myeloma. Nuppon Rinsho.
2007;65:2224-8.
9. Huff CA, Matsui W. Multiple myeloma cancer stem cells. J Clin Oncol.
2008;26:2895-900.
10. Abe M. Bone and Calcium Abnormalities in Malignancy. Myeloma
bone disease. Clin Calcium. 2014;24(8):1159-68. .
11. Seckinger A, Hose D. Interaction between myeloma cells and bone
tissue. Radiologe. 2014;54(6):545-50.
12. Epstein J, Walker R. Myeloma and bone disease:"the dangerous
tango". Clin Adv Hematol Oncol. 2006;4:300-6.
13. Siemionov K, Lieberman IH. Vertebral augmentation in osteoporosis
and bone metastasis. Curr Opin Support Palliat Care. 2007;1:323-7.
14. Harousseau JL, Dreyling M. Multiple myeloma: ESMO clinical
recommendations for diagnosis, treatment and follow-up. Ann Oncology.
2008;19 (Supplement 2):ii55-57.
15. Hansmann HJ, Wunsch C, Schneider B, et al. Radiologic diagnosis of
bone metastases. Orthopade. 1998;27:224-30.
327
L. Ben-Nun King David
16. Kyle RA. Diagnostic criteria of multiple myeloma. Hematol Onco Clin
North Am. 1992;6:347-58.
17. Minter AR, Simpson H, Weiss BM, Landgren O. Bone disease from
monoclonal gammopathy of undetermined significance to multiple
myeloma: pathogenesis, interventions, and future opportunities. Semin
Hematol. 2011;48(1):55-65.
18. Pangalis GA, Kyrtsonis MC, Kontopidou FN, et al. Differential
diagnosis of Waldenstrom's macroglobulinemia and other B-cell disorders.
Clin Lymphoma. 2005;5:235-40.
19. Kyle RA, Rajkumar SV. Monocolonal gammopathy of undetermined
significance and smouldering multiple myeloma: emphasis on risk factors for
progression. Br J Haematol. 2007;139:730-43
MONOCLONAL GAMMOPATHY OF
UNDETERMINED SIGNIFICANCE
References
1. Shirota T, Kondo M, Uchida H, Ito H. Benign monoclonal gammopathy.
Nippon Rinsho. 1995;53:720-4.
2. Kyle RA. Monoclonal gammopathy of undetermined significance and
solitary plasmocytoma. Implications for progression to overt multiple
myeloma. Hematol Oncol Clin North Am. 1997;11:71-87.
3. Kyle RA, Rajkumar SV. Monocolonal gammopathy of undetermined
significance and smouldering multiple myeloma: emphasis on risk factors for
progression. Br J Haematol. 2007;139:730-43.
4. Monoclonal Gammopathy of Undetermined Significance (MGUS).
Available 30 December 2014 at mayomedicallaboratories.com
/.../transcripts/2011/03-mgus/21.html.
WALDENSTROM MACROGLOBULINEMIA
WM is a B-cell neoplasm characterized by lymphoplasmacytic
infiltration of the bone marrow and/or other tissues. The symptoms
of WM are attributable to the extent of tumor infiltration and
elevated IgM levels (1,2).
WM is a distinct clinicopathologic entity defined as a B-cell
neoplasm characterized by lymphoplasmacytic infiltrate in the bone
marrow, with an associated immunoglobulin (Ig) M paraprotein.
Clinical manifestations are due to deposition of IgM in the liver,
spleen, and/or lymph nodes, so it presents with anemia,
hyperviscosity, lymphadenopathy, hepatomegaly, splenomegaly and
neurologic symptoms. The main diagnostic criteria are a typical peak
on serum protein electrophoresis and malignant cells in bone
marrow biopsy samples (3).
In the past 36 months, new developments have occurred both in
the understanding of the biology of WM and in therapeutic options
for WM. The symptoms of WM are attributable to the extent of
tumor infiltration and to elevated IgM levels (1,4). The most
common symptom is fatigue attributable to anemia (4). Aside from
uncommon patients with idiopathic IgM peaks, most patients have
329
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References
1. Pangalis GA, Kyrtsonis MC, Kontopidou FN, et al. Differential diagnosis
of Waldenstrom's macroglobulinemia and other B-cell disorders. Clin
Lymphoma. 2005;5:235-40.
2. Leleu X, Roccaro AM, Moreau AS, et al. Waldenstrom
macroglobulinemia. Cancer Lett. 2008;270:95-107.
3. Budimir I, Nikolid M, Pusid MS, et al. Waldenström's
macroglobulinemia as a diagnostic challenge: case report. Acta Clin Croat.
2014;53(1):94-7.
4. Vijay A, Gertz MA. Waldenström macroglobulinemia. Blood.
2007;109(12):5096-103.
5. Alexanian R. Plasma cell neoplasms and related disorders. In:
Petersdorf RG, Adams RD, Braunwald E, et al (eds). Harrison's Principles of
Internal Medicine. 10 ed. McGrawn-Hill, New York, St Louis. 1983, pp. 362-
371.
330
L. Ben-Nun King David
References
1. Witzig TE, Wahner-Roedler D. Heavy chain disease. Curr Treat Options
Oncol. 2002;3:247-54.
2. Seligman M. Heavy chain diseases. Rev Prat. 1993;43:317-20.
3. Wahner-Roedler DL, Kyle RA. Heavy chain diseases. Best Pract Res Clin
Haematol. 2005;18(4):729-46.
4. Nomura S, Kanoh T. Heavy chain disease. Nihon Rinsho.
1995;53(3):730-5.
5. Fermand JP, Brouet JC, Danon F, Seligmann M. Gamma heavy chain
"disease": heterogeneity of the clinicopathologic features. Report of 16
cases and review of the literature. Medicine (Baltimore). 1989;68:321-35.
332
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References
1. Pangalis GA, Angelipoulou MK, Vassilakopoulos TP, et al. B-chromic
lymphocytic leukemia, small lymphocytic lymphoma, and lymphoplasmacytic
lymphoma, including Waldenström's macroglobulinemia: a clinical, morphologic,
and biologic spectrum of similar disorders. Semin Hematol. 1999; 36:104-14.
2. Ghia P, Ferreri AM, Galigaris-Cappio F. Chronic lymphocytic leukemia. Crit
Rev Oncol Hematol. 2007;64:234-46.
3. Vitolo U, Ferreri AJ, Montoto S. Lymphoplasmacytic lymphoma-
Waldenstrom's macroglobulinemia. Crit Rev Oncol Hematol. 2008;67(2):172-85.
4. Alley CL, Wang E, Dunphy CH, et al. Diagnostic and clinical considerations
in concomitant bone marrow involvement by plasma cell myeloma and chronic
lymphocytic leukemia/monoclonal B-cell lymphocytosis: a series of 15 cases and
review of literature. Arch Pathol Lab Med. 2013;137(4):503-17.
335
L. Ben-Nun King David
OSTEOMYELOFIBROSIS
Osteomylofibrosis and sclerosis are chronic myeloproliferative
diseases of the elderly, with a peak incidence in the sixth and seventh
decade of life (1), in which fibrosis and sclerosis finally lead to bone
marrow obliteration (2). Bone marrow fibrosis, anemia,
splenomegaly and a leuko-erythrobastic blood picture generally
characterize idiopathic MF. Apart from minor hemorrhage and
peripheral thrombosis, patients with early stage of idiopathic MF
present with non-specific symptoms including varying degrees of
leukocytosis (51%), anemia (38%), a platelet count exceeding 600 x
10(9)/l (86%), splenomegaly (15%), increase in LAP (24%) and serum
LDH (20%) (3).
Primary MF is a myeloproliferative neoplasm characterized by
stem cell-derived clonal myeloproliferation, abnormal cytokine
expression, bone marrow fibrosis, anemia, splenomegaly,
extramedullary hematopoiesis, constitutional symptoms, cachexia,
leukemic progression, and shortened survival. Diagnosis is based on
bone marrow morphology. The presence of JAK2, CALR, or MPL
mutations is supportive but not essential for diagnosis;
approximately 90% of patients carry one of these mutations and 10%
are "triple-negative." None of these mutations is specific to primary
MF and are also seen in essential thrombocythemia. Prefibrotic
primary MF mimics essential thrombocythemia in its presentation
and the distinction, enabled by careful bone marrow morphological
examination, is prognostically relevant. Differential diagnosis includes
chronic myeloid leukemia, myelodysplastic syndromes, chronic
myelomonocytic leukemia, and acute myeloid leukemia. The DIPSS-
plus uses eight predictors of inferior survival: age >65 years, Hg <10
g/dL, leukocytes >25 × 10(9) /L, circulating blasts ≥1%, constitutional
symptoms, red cell transfusion dependency, platelet count <100 ×
10(9) /L, and unfavorable karyotype (i.e., complex karyotype or sole
or two abnormalities that include +8, -7/7q-, i(17q), inv(3), -5/5q-,
12p-, or 11q23 rearrangement). The presence of 0, one, two or three,
and ≥ four adverse factors defines low, intermediate-1, intermediate-
2, and high-risk disease with median survivals of approximately 15.4,
6.5, 2.9, and 1.3 years, respectively. High risk disease is also defined
by CALR(-)/ASXL1(+) mutational status. Observation alone is
adequate for asymptomatic low/intermediate-1 risk disease,
especially with CALR(+)/ASXL1(-) mutational status. Stem cell
336
L. Ben-Nun King David
Osteomyelofibrosis
the absence of severe intractable bone pain the King suffered from,
and appropriate investigation the diagnosis of osteomylofibrosis
seems unlikely.
References
1. Baur-Menyk A, Reiser M. Oncohaematologic disorders affecting the
skeleton in the elderly. Radiol Clin North Am. 2008;46:786-98.
2. Böhner H, Rötzscher VM, Tirier C, et al. Splenectomy in
osteomyelofibrosis. Indications and outcome. Chirurg. 1996;67:1016-9.
3. Thiele J. Kvasnicka HM, Zankovich R, Diehl V. Early-stage idiopathic
(primary) myelofibrosis- current issues of diagnostic features. Leuk Lymphoma.
2002;43:1035-41.
4. Tefferi A. Primary myelofibrosis: 2014 update on diagnosis, risk-
stratification, and management. Am J Hematol. 2014;89(9):915-25.
5. Thiele J, Kvasnicka HM. Grade of bone marrow fibrosis is associated
with relevant hematological findings-a clinicopathological study on 865
patients with chronic idiopathic myelofibrosis. Ann Hematol. 2006;
85(4):226-32.
6. Thiele J, Kvasnicka HM. Hematopathologic findings in chronic
idiopathic myelofibrosis. Semin Oncol. 2005;32(4):380-94.
7. Mitra D, Kaye JA, Piecoro LT, et al. Symptom burden and splenomegaly
in patients with myelofibrosis in the United States: a retrospective medical
record review. Cancer Med. 2013;2(6):889-98.
8. Thiele J, Kvasnicka H-M, Werden C, et al. Idiopathic Primary Osteo-
myelofibrosis: A Clinico-Pathological Study on 208 Patients with Special
Emphasis on Evolution of Disease Features, Differentiation from Essential
Thrombocythemia and Variables of Prognostic Impact. Leukemia &
Lymphoma. 1996;22(3-4):303-17.
9. Guillot X, Moldovan M2, Vidon C1, Wendling D1. Myelofibrosis-
related arthritis successfully treated with hydroxyurea. Case Rep Rheumatol.
2014;2014:869743.
AMYLOIDOSIS
Amyloid is a pathologic fibrillar aggregation of polypeptides in a
cross-beta-sheet conformation. More than 29 different amyloid
proteins have been identified. Analysis of a Congo red-stained tissue
section by polarization microscopy is the gold standard for diagnosing
amyloid. Subsequent classification of the amyloid is mandatory and is
increasingly supported by molecular biological analyses (1).
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References
1. Röcken C, Eriksson M. Amyloid and amyloidoses. Pathologe.
2009;30(3):182-92.
2. Dhawan R, Herbert S Diamond ed. AA (Inflammatory) Amyloidosis -
Medscape Reference. Available 10 December 2014 at medicine.medscape.
com/article/335559-overview
3. Amyloidosis. Wikipedia, the free encyclopedia. Available 10 December
2014 at wikipedia.org/wiki/Amyloidosis.
4. Sheppard MR, Vinay K, Abul KA, Nelson F. Robbins Basic Pathology.
Philadelphia: Saunders. 2007. 8th edition ISBN 1-4160-2973-7.
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PLASMACYTOMA
Solitary plasmacytoma is characterized by a mass of neoplastic
monoclonal plasma cells in either bone or soft tissue without
evidence of systemic disease attributing to myeloma. Biopsy
confirmation of a monoclonal plasma cell infiltration from a single
site is required for diagnosis. The common presentation of solitary
plasmacytoma of bone is in the axial skeleton, whereas the
extramedullary plasmacytoma is usually seen in the head and neck.
The ratio of solitary plasmacytoma seen at males to females is 2:1
and the median age of patients is 55 years. The incidence rate of
solitary plasmacytoma in black race is approximately 30% higher than
the white race. Incidence rate increases exponentially by advancing
age. Solitary plasmacytoma of bone has a significant higher risk for
progression to myeloma, and the choice of treatment is radiotherapy
with curative intent at min. 4000 cGy. By only radiotherapy
application, long-term disease-free survival is possible for
approximately 30% of patients with solitary plasmacytoma of bone
and 65% of patients with extramedullary plasmacytoma (1).
Intracranial plasmacytomas are a rare abnormality in a
neurosurgeon's practice. The plasmacytomas may originate from the
skull bones or soft tissue intracranial structures; they may be solitary
or occur as a manifestation of MM, this type being typical of most
intracranial plasmacytomas. Progression of solitary plasmacytoma to
MM is observed in a number of cases. The final diagnosis of
plasmacytoma is based on a morphological study (2-5).
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Plasmacytoma
Solitary plasmacytoma of the skull is rare and few cases have been
reported in the English literature. Plasmacytoma of the skull has a
wide spectrum of pathology, including a quite benign, solitary
plasmacytoma, and an extremely malignant, MM at the two ends of
the spectrum. The prognosis for solitary plasmacytoma of the skull
appears to be good when it can be diagnosed on strict criteria. The
clinical features of solitary plasmacytoma of the skull are complex
and not easily identified, resulting in a high misdiagnosis rate. A
comprehensive examination and analysis which includes radiological
examination, immunoglobulin, biochemistry, test for Bence Jones
protein in the urine and bone marrow is needed for correct diagnosis.
If the skull lesion is isolated, with accompanying marked swelling in
the area and tenderness, plasmacytoma must be considered as a
possibility for the cause of solitary skull masses. Two cases of solitary
plasmacytoma of the skull lesions were retrospectively reviewed, in
which a comprehensive examination was used in order to predict the
clinical course of solitary plasmacytoma of the skull. The patients
received postoperative radiation and/or chemotherapy. Survival
following surgery was longer than two years for patient one, and
patient two is alive at the 18-month follow-up (7).
Solitary osseous plasmacytoma rarely involves the distal
extremities. A 64-year-old man presented with swelling, mild pain
and a deformed right index finger. The workup led to the diagnosis of
solitary osseous plasmacytoma and the patient eventually required
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References
1. Kilciksiz S, Karakoyun-Celik O, Agaoglu FY, Haydaroglu A. A review for
solitary plasmacytoma of bone and extramedullary plasmacytoma.
ScientificWorldJournal. 2012;2012:895765.
2. Belov AI, Gol'bin DA. Intracranial plasmocytomas: biology, diagnosis,
and treatment. Zh Vopr Neirokhir Im N N Burdenko. 2006;3:43-7.
3. Tanaka M, Shibui S, Nomura K, Nakanishi Y. Solitary plasmocytoma of
the skull: a case report. Jpn J Clin Oncol. 1998; 28:626-30.
4. Bret P, Stan H, Streichenberg N, Sebban C, Guyotat J. Solitary
plasmocytoma of the sphenoid. A case report. Neurochirurgie. 2002;48:431-
5.
5. McLaughlin DM, Gray WJ, Jones FG, et al. Plasmacytoma: an unusual
cause of a pituitary mass lesion. A case report and a review of the literature.
Pituitary. 2004;7:179-81.
6. Georgie a B, Goergiev G. Bone manifestations of multiple
plasmocytoma. Vutr Boles.1980;19:79-81.
7. Dong L, Zhang X, Zhang H, et al. Solitary plasmacytoma of the skull:
Two case reports. Oncol Lett. 2013;5(2):479-482.
8. Daneshbod Y, Nowshadi PA, Negahban S, et al. Solitary plasmacytoma
of the index finger. J Clin Pathol. 2014 Jun 24. pii: jclinpath-2014-202413.
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TO SUM UP: the medical record of the King, that is the biblical
text, documents the patient's complains: “...my strength failed..., and
my bones are consumed” (Psalm 31:11), and “My bones wasted away
through my anguished roaring all day long” (Psalm 32:3). The
anamnestic findings indicate a very serious and lethal disease that
caused the King severe intractable bone pain and a great suffering.
Among the all diagnoses, as presented above, the most likely is MM.
LUNG CANCER
Lung cancer is currently one of the most common malignant
diseases and is responsible for substantial mortality worldwide.
Compared with never smokers, former smokers remain at relatively
high risk for lung cancer, accounting for approximately half of all
newly diagnosed cases in the US. Screening offers former smokers
the best opportunity to reduce their risk of advanced stage lung
cancer and there is evidence that annual screening using LDCT is
effective in preventing mortality. Studies are being conducted to
evaluate whether the benefits of LDCT screening outweigh its costs
and potential harms and to determine the most appropriate workup
for patients with screen-detected lung nodules. Program efficiency
would be optimized by targeting high-risk current smokers, but low
uptake among this group is a concern. Former smokers may be
invited for screening; however, if fewer long-term current smokers
and more former smokers with long quit duration elect to attend,
this could have adverse effects on cost and screening test
parameters. To illustrate this point, three possible screening
scenarios with lung cancer prevalence ranging from between 0.62%
and 5.0 % is presented. Cost-effectiveness of lung cancer screening
may be improved if linked to successful smoking cessation programs
and if better approaches are developed to reach very high-risk
patients, e.g., long-term current smokers or others based on more
accurate risk prediction models (1).
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Lung cancer
The association between COPD and lung cancer has long been a
subject of intense debate. The high prevalence of COPD in elderly
smokers inevitably strengthens their coincidence. In addition to this
contingent coincidence, recent studies have revealed a close
association between the two diseases that is independent of the
smoking history; that is, the existence of COPD is an independent risk
factor for the development of lung cancer. Molecular-based evidence
has been accumulating because of the efforts to explain the
underlying mechanisms of this association. These mechanisms may
include the following: the retention of airborne carcinogens followed
by the activation of oncogenes and the suppression of tumor
suppressor genes; the complex molecular mechanism associated with
chronic inflammation in the distal airways of patients with COPD; the
possible involvement of putative distal airway stem cells; and genetic
factors that are common to both COPD and lung cancer. The
existence of COPD in patients with lung cancer may potentially affect
the process of diagnosis, surgical resection, radiotherapy,
chemotherapy, and end-of-life care. The comprehensive
management of COPD is extremely important for the appropriate
treatment of lung cancer. Surgical resections with the aid of early
interventions for COPD are often possible, even for patients with
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L. Ben-Nun King David
References
1. Tota JE, Ramanakumar AV, Franco EL. Lung cancer screening: review
and performance comparison under different risk scenarios. Lung. 2014;
192(1):55-63.
2. Alberg AJ, Brock MV, Ford JG, et al. Epidemiology of lung cancer:
Diagnosis and management of lung cancer, 3rd ed.: American College of
Chest Physicians evidence-based clinical practice guidelines. Chest.
2013;143(5 Suppl):e1S-29S.
3. Nielsen LS1, Bælum J, Rasmussen J, et al. Occupational asbestos
exposure and lung cancer - a systematic review of the literature. Arch
Environ Occup Health. 2014;69(4):191-206.
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4. Luqman M, Javed MM, Daud S, et al. Risk factors for lung cancer in the
Pakistani population. Asian Pac J Cancer Prev. 2014;15(7):3035-9.
5. Takiguchi Y, Sekine I, Iwasawa S, et al. Chronic obstructive pulmonary
disease as a risk factor for lung cancer. World J Clin Oncol. 2014;;5(4):660-6.
6. Gonzalez-Barcala FJ, Falagan JA2, Garcia-Prim JM3, et al. Symptoms
and reason for a medical visit in lung cancer patients. Acta Med Port. 2014;
27(3):318-24.
7. Cetin K, Christiansen CF, Jacobsen JB, et al. Bone metastasis, skeletal-
related events, and mortality in lung cancer patients: A Danish population-
based cohort study. Lung Cancer. 2014 Sep 10. pii: S0169-5002(14)00367-5.
8. Metintas M, Ak G, Akcayi IA, et al. Detecting extrathoracic metastases
in patients with non-small cell lung cancer: is routine scanning necessary?
Lung Cancer. 2007;58:59-67.
9. Alpar S, Uçar N, Turgut A, et al. The correlation between the distant
metastases and organ-specific symptoms in the patients with lung cancer.
Tuberk Toraks. 2004;52(1):14-8.
10. Tsuya A, Kurata T, Tamura K, Fukuoka M. Skeletal metastases in non-
small cell lung cancer: a retrospective study. Lung Cancer. 2007;57(2):229-
32.
GASTRIC CARCINOMA
Despite a major decline in incidence and mortality over several
decades, stomach cancer is still the fourth most common cancer and
the second most common cause of cancer death in the world. There
is a 10-fold variation in incidence between populations at the highest
and lowest risk. The incidence is particularly high in East Asia, Eastern
Europe, and parts of Central and South America, and it is about twice
as high among men than among women. Prognosis is generally rather
poor, with five-year relative survival below 30% in most countries.
The best-established risk factors for stomach cancer are Helicobacter
pylori infection, the strongest established risk factor for distal
stomach cancer, and male sex, a family history of stomach cancer,
and smoking. While some factors related to diet and food
preservation, such as high intake of salt-preserved foods and dietary
nitrite or low intake of fruit and vegetables, are likely to increase the
risk of stomach cancer, the quantitative impact of many dietary
factors remains uncertain, partly due to limitations of exposure
assessment and control for confounding factors (1).
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L. Ben-Nun King David
Gastric carcinoma
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L. Ben-Nun King David
References
1. Brenner H, Rothenbacher D, Arndt V. Epidemiology of stomach
cancer. Methods Mol Biol. 2009;472:467-77.
2. Stomach (Gastric) Cancer. National Cancer Institute. Available 20
November 2014 at cancer.gov/cancertopics/types/stomach.
3. Gastric Cancer Treatment (PDQ®). National Cancer Institute. Available
20 November 2014 at http://www.cancer.gov/ cancertopics/types/stomach.
4. Hussain S, Chui S. Gastric carcinoma presenting with extensive bone
metastases and marrow infiltration causing extradural spinal haemorrhage.
Br J Radiol. 2006;79:261-3.
5. Kimura Y, Kawase T, Kawabata R, et al. Long-term efficacy of
chemotherapy for unresectable gastric cancer with multiple bone
metastases-a case report. Gan To Kagaku Ryoho. 2013;40(12):2235-7.
6. Silvestris N, Pantano F, Ibrahim T, et al. Natural history of malignant
bone disease in gastric cancer: final results of a multicenter bone metastasis
survey. PLoS One. 2013;8(10):e74402.
7. Basheer A, Daniel J, Padhi S. Compressive myeloradiculopathy from
bony metastasis as the initial presentation of poorly differentiated
adenocarcinoma stomach - a case report. Australas Med J. 2013;6(10):515-
9.
COLORECTAL CANCER
More than 1.2 million patients are diagnosed with CRC every year,
and more than 600,000 die from the disease. Incidence strongly
varies globally and is closely linked to elements of a so-called western
lifestyle. Incidence is higher in men than women and strongly
increases with age; median age at diagnosis is about 70 years in
developed countries. Despite strong hereditary components, most
cases of CRC are sporadic and develop slowly over several years
through the adenoma-carcinoma sequence. The cornerstones of
therapy are surgery, neoadjuvant radiotherapy (for patients with
rectal cancer), and adjuvant chemotherapy (for patients with stage
III/IV and high-risk stage II colon cancer). Five-year relative survival
ranges from greater than 90% in patients with stage I disease to
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References
1. Brenner H, Kloor M, Pox CP. Colorectal cancer. Lancet. 2014;383
(9927):1490-502.
2. Astin M, Griffin T, Neal RD, ET AL. The diagnostic value of symptoms
for colorectal cancer in primary care: a systematic review. Br J Gen Pract.
2011;61(586):e231-43.
3. Sundermeyer ML, Meropol NJ, Rogatko A, et al. Changing patterns of
bone and brain metastases in patients with colorectal cancer. Clin Colorect
Cancer. 2005;5:108-13.
4. Santini D, Tampellini M, Vincenzi B, et al. Natural history of bone
metastasis in colorectal cancer: final results of a large Italian bone
metastases study. Ann Oncol. 2012;23(8):2072-7.
5. Jimi S, Yasui T, Hotokezaka M, et al. Clinical features and prognostic
factors of bone metastases from colorectal cancer. Surg Today. 2013;
43(7):751-6.
HEPATOCELLULAR CARCINOMA
HCC is the most common primary malignancy of the liver. It is the
sixth most common malignancy worldwide and the third cause of
cancer-related mortality. Approximately 90% of HCCs are associated
with a known risk factor, mainly hepatitis B and cirrhosis which is a
true precancerous state, whatever its cause. The incidence of HCC in
a patient with cirrhosis is 3-5% per year. In developed countries,
hepatitis C and alcohol use are the main risk factors, and the
incidence of HCC is growing, owing probably to the hepatitis C
epidemic, the increasing incidence of non-alcoholic steatohepatitis
and the better prevention and treatment of other complications of
cirrhosis. In France, non-alcoholic steatohepatitis is currently the
second cause of cirrhosis with HCC after alcoholIn eastern Asia and
sub-saharan Africa, the dominant risk factor is chronic hepatitis B
infection (together with exposure to aflatoxin B1 in Africa). The high
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Hepatocellular carcinoma
timely treatment of bone metastases are thus called for in the follow-
up of HCC patients (4).
In Japan, the clinical records of 482 patients who had been
diagnosed as having HCC were reviewed, 1995-2001. Extrahepatic
metastases had been detected in 65 patients. The frequent
metastatic sites were lung (53.8%), bone (38.5%), and lymph node
(33.8%). Other metastatic sites were the adrenal gland, peritoneum,
skin, brain and muscle (5). Spinal cord compression was an unusual
cause of metastatic HCC (6,7).
A 65-year old man presented with bone pain and anemia. Skull X-
ray revealed multiple osteolytic lesions. The patient was evaluated
for MM but detailed workup revealed the diagnosis of primary HCC
with osteolytic bone metastases (8).
A case of solitary skull metastasis as the first symptom of HCC is
reported. A 49-year-old male patient was admitted to Jinjiang
Hospital of Quanzhou Medical College with a painless parietal-
occipital scalp mass, while he denied any history of hepatic disease. A
cranial CT demonstrated a hypervascular enhancement with
osteolytic change in the right parietal-occipital region, cranial MRI
indicated a highly enhanced and osteolytic skull tumor, and
abdominal CT showed a huge tumor in the liver. The other
examinations showed no other metastases. Laboratory data showed
no liver dysfunction while hepatitis B surface antigen was positive,
and AFP level was high. A craniectomy was performed and the mass
was totally removed. The histological diagnosis was skull metastasis
from HCC. The patient was subsequently treated by transcatheter
arterial chemoembolization. In a review of published literature, the
incidence of skull metastasis from HCC in the period between 1990
and 2011 has increased significantly. The misdiagnosis rate of skull
metastases as the first symptom from HCC was high. Therefore, it is
necessary to give each patient with a scalp mass that has invaded the
skull a liver ultrasound or CT scan. On the other hand, metastases
that occurred in the calvaria site were more frequent than those that
occurred in the skull base and facial skeleton (9).
References
1. Fares N, Péron JM. Epidemiology, natural history, and risk factors of
hepatocellular carcinoma. Rev Prat. 2013;63(2):216-7, 220-2.
2. Paul SB, Gulati MS, Sreenivas V, e al. Evaluating patients with cirrhosis
for hepatocellular carcinoma: value of clinical symptomatology, imaging and
alpha-fetoprotein. Oncology. 2007;72 Suppl 1:117-23.
3. Lai EC, Lau WY. Hepatocellular carcinoma presenting with obstructive
jaundice. ANZ J Surg. 2006;76(7):631-6.
4. Fukutomi M, Yokota M, Chuman H, et al. Increased incidence of bone
metastases in hepatocellular carcinoma. Eur J Gastroenterol Hepatol. 2001;
13(9):1083-8.
5. Natsuizaka M, Omura T, Akaike T, et al. Clinical features of
hepatocellular carcinoma with extrahepatic metastases. J Gastroenterol
Hepatol. 2005; 20:1781-7.
6. Doval DC, Bhatia A, Vaid AK, et al. Spinal cord compression secondary
to bone metastases from hepatocellular carcinoma. World J Gastroenterol.
2006;12:5247-52.
7. Melichar B, Voboril Z, Toupková M, Dvorál J. Hepatocellular carcinoma
presenting with bone metastasis. J Exp Clin Cancer Res. 2002;21:433-6.
8. Dovai DC, Bhatia K, Vaid AK, et al. Bone metastases from primary
hepatocellular carcinoma simulating multiple myeloma. Hepatobilliary
Pancrear Dis Int. 2005;4:308-10.
9. Guo X, Yin J, Jiang Y. Solitary skull metastasis as the first symptom of
hepatocellular carcinoma: case report and literature review. Neuropsychiatr
Dis Treat. 2014 Apr 28;10:681-6.
PANCREATIC CANCER
Pancreatic cancer is the fourth most common cause of cancer-
related mortality in the US, with over 38,000 deaths in 2013. The
opportunity to detect pancreatic cancer while it is still curable
depends on the ability to identify and screen high-risk populations
before their symptoms arise. Risk factors for developing pancreatic
cancer include multiple genetic syndromes as well as modifiable risk
factors. Genetic conditions include hereditary breast and ovarian
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Pancreatic tumor
References
1. Becker AE, Hernandez YG, Frucht H, Lucas AL. Pancreatic ductal
adenocarcinoma: Risk factors, screening, and early detection. World J
Gastroenterol. 2014 28;20(32):11182-11198.
2. Freelove R, Walling A. Pancreatic cancer: diagnosis and management.
Am Fam Physician. 2006;73(3):485-92.
3. Dzeletovic I, Harrison ME, Crowell MD, et al. Pancreatitis before
pancreatic cancer: clinical features and influence on outcome. J Clin
Gastroenterol. 2014;48(9):801-5.
4. Matsuda Y, Hagio M, Naito Z, Ishiwata T. Clinicopathological features
of 30 autopsy cases of pancreatic carcinoma. J Nippon Med Sch. 2012;
79(6):459-67.
5. Iguchi H, Yasuda M, Matsuo T, et al. Clinical features and management
of pancreatic cancer with bone metastases. Nippon Shokakibyo Gakkai
Zasshi. 2004;101:872-8.
6. D'Haese JG, Hartel M, Demir IE, et al. Pain sensation in pancreatic
diseases is not uniform: the different facets of pancreatic pain. World J
Gastroenterol. 2014;20(27):9154-61.
clinical and radiological findings were the same as those for benign
GCT. Wide excision of the tumor was performed in all three cases. In
two cases, knee arthrodesis was performed, and in one case a
custom-made total knee replacement was performed. PMGCT was
diagnosed on initial biopsy in one patient, in the second patient it
was diagnosed in the excised specimen, and in third case it was only
diagnosed after local recurrence six months after initial treatment. All
the patients died within five months of detection of recurrence and
metastasis. PMGCT has a poor prognosis. Histological examination is
highly significant in such cases. Awareness about this entity,
adequate biopsy, and sampling of specimen can aid in early
diagnosis, which may improve the overall prognosis (4).
References
1. Raskin KA, Schwab JH, Mankin HJ, et al. Giant cell tumor of bone. J Am
Acad Orthop Surg. 2013;21(2):118-26.
2. Gupta R, Seethalakshmi V, Jambhekar NA, et al. Clinicopathologic
profile of 470 giant cell tumors of bone from a cancer hospital in western
India. Ann Diag Pathol. 2008;12:239-48.
3. Billingsley JT, Wiet RM, Petruzzelli GJ, Byrne R. A locally invasive giant
cell tumor of the skull base: case report. J Neurol Surg Rep. 2014;75(1):
e175-9.
4. Kapoor SK, Jain V, Agrawal M, et al. Primary malignant giant cell tumor
of bone: a series of three rare cases. J Surg Orthop Adv. 2007;16(2):89-92.
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LEPTOMENINGEAL CARCINOMATOSIS
Leptomeningeal carcinomatosis is a rare complication of solid
tumors, e.g., breast, lung and G-I carcinomas. Clinical manifestations
are variable with radicular pains with or without neurological
deficiencies as well as headache and hallucinations. The case of a 57-
year-old patient with urological symptoms caused by a
leptomeningeal carcinomatosis and a spinal metastasis of an
asymptomatic signet-ring cell gastric carcinoma is reported (1).
Leptomeningeal metastasis is discovered at autopsy in
approximately 5% of patients with systemic cancer. Until recently
with the introduction of MRI, premorbid diagnosis was extremely
difficult. In particular, initial CSF cytology is diagnostic in less than
50% of autopsy-verified patients, although repeated CSF
examinations may increase the yield significantly. Leptomeningeal
metastasis in metastatic prostate cancer has been reported in only 14
patients previously. A patient was studied and a correct diagnosis
was based solely on the MRI and the presence of an elevated PSA in
CSF. Only three previous patients with leptomeningeal prostate
metastasis have undergone PSA evaluations in CSF. In conclusion, in
such patients, the combination of MRI and CSF studies can overcome
the lack of sensitivity of CSF cytology (2).
Metastatic prostate carcinoma commonly involves bones and
extrapelvic lymph nodes, with occasional visceral deposits. CNS
involvement is unusual and particularly the occurrence of
leptomeningeal metastasis is extremely rare, with few cases
described in the medical literature. The clinical presentation is
characterized by multifocal neurological deficit and the prognosis is
generally dismal, with survival ranging between three and six
months. A patient affected by leptomeningeal metastasis due to
prostate cancer was treated with a combined-modality approach
consisting of sequential chemotherapy and radiotherapy. A 70-year-
old man was referred to the group for cognitive mental disorder, left-
sided frontal headache and nausea; the patient had a previous
history of metastatic prostate cancer. Leptomeningeal metastasis
was diagnosed neuroradiologically with brain MRI and evidence of a
detectable level of PSA in the CSF. He was treated with docetaxel and
prednisone for three cycles followed by EBRT to the whole brain to a
total dose of 30 Gy in 10 fractions with a simultaneous integrated
boost to the macroscopic disease (total dose of 35 Gy in 10 fractions).
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References
1. Cresto N, Barth A, Arnold M, et al. Extraordinary manifestation of a
gastric carcinoma by leptomeningeal carcinomatosis and spinal metastasis.
Med Klin (Munich). 2007;102:255-8.
2. Cone LA, Koochek K, Henager HA, et al. Leptomeningeal
carcinomatosis in a patient with metastatic prostate cancer: case report and
literature review. Surg Neurol. 2006;65(4):372-5, discussion 375-6.
3. Cante D, Franco P, Sciacero P, et al. Leptomeningeal metastasis from
prostate cancer. Tumori. 2013;99(1):6e-10e.
disease. Metastases are typically found in the lung, soft tissue, bone,
liver, cutaneous sites, and CNS (1).
The survival rates by age (<65 and ≥65 years) and sex were evaluated.
The total number of advanced RCC patients during 2001-2009, 2001-
2005, 2006-2007 and 2008-2009 were 7,047, 4,059, 1,548 and 1,440,
respectively. During 2001-2009, the one- and three-year relative
survival rates were 26.7 ± 0.6 and 10.0 ± 0.4%, respectively. There
was insignificant difference in one-year relative survival rates for
patients diagnosed during 2006-2007 and 2008-2009 compared to
those diagnosed during 2001-2005. Similarly, the three-year survival
rates for patients diagnosed during 2006-2007 were similar to those
diagnosed during 2001-2005. In conclusion, there was insignificant
improvement in relative survival rates among advanced RCC patients
in the era of targeted agents (3).
In Japan, Nagasaki, bone scan was performed at presentation in
205 patients with confirmed RCC. Overall, bone metastasis was
present in 34 (17%) patients (4).
RCC is an uncommon tumor in adults. Metastasis in the nasal
fossa is rare, and can become apparent because of repeated
epistaxis. A patient with RCC presented epistaxis secondary to a
metastasis in the right nasal fossa. The primary tumor was treated
with nephrectomy and the nasal fossa metastasis was treated
successfully with embolization, chemoimmunotherapy, surgery, and
radiotherapy. The presence of repeated epistaxis may occasionally be
the first symptom of RCC, and systemic treatment combined with
local treatment may enable adequate control the disease (5).
This study utilizes a large contemporary patient cohort to examine
patterns of RCC presentation and their clinical implications.
Retrospective analysis was performed on 721 patients (260 women,
461 men) who underwent 750 nephrectomies for treatment of RCC
between 7/1/89 and 12/31/97; 29 patients required two operations
for bilateral RCC. Median age and follow-up were 63 years and 41
months, respectively. Indicators of symptomatic presentation
included flank pain, flank mass, hematuria, varicocele, constitutional
symptoms, paraneoplastic syndromes, and bone pain related to
metastatic disease. Incidental and symptomatic presentation
occurred in 57% and 42% of cases, respectively. When compared to
incidental cases, symptomatic presentation was predominantly
detected in younger patients (mean age, 59 years, p<0.001), in males
(p<0.04), and in tumors with conventional (clear cell) histology
(p<0.001), larger size (mean, eight cm, p<0.001), and non-organ
confined pathology (p<0.001). In univariate analysis, symptomatic
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References
1. Kumar RM, Aziz T, Jamshaid H, et al. Metastatic renal cell carcinoma
without evidence of a primary renal tumour. Curr Oncol. 2014;21(3):e521-4.
2. Shah BK, Ghimire KB. Survival Trends among Patients with Advanced
Renal Cell Carcinoma in the United States. Urol Int. 2014 Aug 19. [Epub
ahead of print].
3. Corgna E, Betti M, Gatta G, et al. Renal cancer. Crit Rev Oncol
Hematol. 2007;64:247-62.
4. Koga S, Tsuda S, Nishikido M, et al. The diagnosis of bone scan in
patients with renal cell carcinoma. J Urol. 2001;166:2126-8.
5. Cobo-Dols M, Alés-Díaz I, Villar-Chamorro E, et al. Solitary metastasis
in a nasal fossa as the first manifestation of a renal carcinoma. Clin Transl
Oncol. 2006;8(4):298-300.
6. Lee CT, Katz J, Fearn PA, Russo P. Mode of presentation of renal cell
carcinoma provides prognostic information. Urol Oncol. 2002;7(4):135-40.
7. Hofbauer SL, de Martino M, Seemann C, et al. Associations between
presenting symptoms, clinicopathological parameters, and prognosis in a
contemporary series of patients with renal cell carcinoma. Korean J Urol.
2014;55(8):505-10.
PROSTATE CANCER
Prostate cancer is the second most common cancer in men and
the fifth most common cancer worldwide. In the US, it is more
common in African-American men than in Caucasian men (1).
Due to a combination of earlier detection and better treatments,
survival of adenocarcinoma of the prostate has increased
dramatically. Prostate cancer itself is associated with lower bone
density and increased fractures. This is compounded by the use of
androgen deprivation therapy, which causes dramatic falls in
circulating testosterone and estrogen, resulting in rapid falls in bone
377
L. Ben-Nun King David
Prostate cancer
References
1. Segamwenge IL, Mgori NK, Abdallahyussuf S, et al. Cancer of the
prostate presenting with diffuse osteolytic metastatic bone lesions: a case
report. J Med Case Rep. 2012;6:425.
2. Tuck SP, Hanusch B, Walker J, Datta HK. Prostate cancer and
osteoporosis. Curr Osteoporos Rep. 2013;11(1):11-20.
3. Uemura M, Nonomura N. Bone and Calcium Abnormalities in
Malignancy. Bone metastasis from prostate cancer. Clin Calcium. 2014;
24(8):1169-75.
4. Birtle AJ, Freeman A, Masters JR, et al. Clinical features of patients
who present with metastatic prostate carcinoma and serum prostate-
specific antigen (PSA) levels < 10 ng/mL: the "PSA negative" patients.
Cancer. 2003;98(11):2362-7.
5. Moslehi M, Cheki M, Salehi-Marzijarani M, et al. Predictors of bone
metastasis in pre-treatment staging of asymptomatic treatment-naïve
patients with prostate cancer. Rev Esp Med Nucl Imagen Mol. 2013;32(5):
286-9.
6. Swierz J, Stawarz B. Bone metastasis in patients with urogenital
neoplasms. Wiad Lek. 1997;50:100-5.
380
L. Ben-Nun King David
BLADDER CARCINOMA
Bladder cancer
References
1. DeSouza K, Chowdhury S, Hughes S. Prompt diagnosis key in bladder
cancer. Practitioner. 2014;258(1767):23-7, 3.
2. Mukesh M, Cook N, Hollingdale AE, et al. Small cell carcinoma of the
urinary bladder: a 15-year retrospective review of treatment and survival in
the Anglian Cancer Network. BJU Int. 2009;103(6):747-52.
3. Blick CG1, Nazir SA, Mallett S, et al. Evaluation of diagnostic strategies
for bladder cancer using computed tomography (CT) urography, flexible
cystoscopy and voided urine cytology: results for 778 patients from a
hospital haematuria clinic. BJU Int. 2012;110(1):84-94.
4. Shinagare AB, Ramaiya NH, Jagannathan JP, et al. Metastatic pattern
of bladder cancer: correlation with the characteristics of the primary tumor.
AJR Am J Roentgenol. 2011;196(1):117-22.
5. Sasaki Y, Oi H, Oyama T, Kagawa J, et al. Non-muscle invasive bladder
cancer with multiple bone metastasis without local invasion : a case report].
Hinyokika Kiyo. 2013 Oct;59(10):669-72.
References
1. Coleman RE. Metastatic bone disease: clinical features,
pathophysiology and treatment strategies. Cancer Treat Rev. 2001;7(3):165-
76.
2. Guise TA, Mohammad KS, Clines G, et al. Basic mechanisms
responsible for osteolytic and osteoblastic bone metastases. Clin Cancer
Res. 2006;12(20 Pt 2):6213s-6216s.
3. Coleman R, Heidenreich A, Bell R. Managing metastatic bone disease:
three cases studies. Semin Oncol. 2004;31(5 Suppl10):83-6.
4. Rizzoli R, Body JJ, Brandi ML, et al. International Osteoporosis
Foundation Committee of Scientific Advisors Working Group on Cancer-
Induced Bone Disease. Cancer-associated bone disease. Osteoporos Int.
2013;24(12):2929-53.
5. Mercandane S. Malignant bone pain: pathophysiology and treatment.
Pain. 1997;69:1-18.
6. Twycross RG. Management of pain in skeletal metastases. Clin Orthop
Relat Res. 1995;Mar (312):187-96.
7. Slavik E, Ivanovid S, Grujucid D. Cancer pain (classification and pain
syndromes). Acta Chi Iudosi. 2004;51:9-14.
8. Vincet S, Luis-Ravelo D, Antón I, et al. Bone metastases. An Sit Sanit
Navar. 2006'29:177-88.
9. Oremek GM, Weiss A, Sapoutzis N, Sauer-Eppel H. Diagnostic value of
bone and tumour markers in patients with malignant diseases. Anticancer
Res. 2003;23:987-90.
cancer (13.1%), breast cancer (7.4%), liver cancer (6.4%), G-I cancer
(5.7%), and unknown cancers (24.6%). The common metastatic sites
were spine (47.7%), pelvis (18.2%), femur (15.4%), and rib (12.6%).
Multiple metastases occurred in 20.5% of the patients. The main
symptoms were skeletal pain (53.3%), pathologic fractures (10.3%),
dysfunction (4.9%), and paraplegia (2.1%). Primary tumor detected
before metastasis accounted for 29.7% of the patients with a median
metastatic time of 319 days, and the metastatic intervals were
uncertain in 70.3% of the patients. Osteolytic types accounted for
80.7% of the cases in radiographic patterns, followed by
osteosclerotic (10.5%) and mixed types. In conclusion, metastatic
bone tumors most frequently occur in patients older than 41 years,
and commonly originate from lung, prostate, breast, and liver.
Vertebrae, pelvis, femur, and rib are the most common sites of
metastases. The clinical manifestation is extensive and nonspecific.
Most lesions present osteolytic patterns. Metastases with unknown
origin account for 24%. In spite of complexity, the clinical features
should be mastered for early diagnosis and treatment (4).
Pathological fracture
breast (25), kidney (18), G-I system (17), liver (12), thyroid (11),
prostate (7), bladder (2) and skin (1). Skeletal metastases occurred
more often in elderly males. Axial bones (spine and pelvis) were
usually affected (5).
The most common metastases in men are from prostate cancer
(60%) while in women from breast cancer (70%). Other tumors
responsible for bone metastases are: lung, kidney, thyroid, G-I,
bladder, and skin. The spine and pelvis are the most common
metastatic sites, due to the presence of red (hematopoietic active)
bone marrow in a high amount. Generally, the radiographic pattern is
lytic type; other aspects are osteosclerotic, mixed, lytic vs. mixed and
osteosclerotic vs. lytic patterns. The main symptom is pain, although
many bone metastases are asymptomatic. The most severe
consequences are pathological fractures and cord compression.
Clinical evaluation of patients with skeletal metastases needs
multimodal diagnostic imaging, able to detect lesions, to assess their
extension and location, and eventually to perform the biopsy (for
histo-morphological diagnosis). These techniques give different
performances in terms of sensitivity and specificity; but none of the
modalities alone seems to be adequate to yield a reliable diagnostic
outcome. Therefore, multidisciplinary cooperation is required to
optimize the screening, clinical management and follow-up of the
patients (6).
There were 124,655-fracture cases and 373,962 ages and gender
matched controls. An increased risk of fractures, primarily within the
first year after diagnosis occurred in patients with primary bone
cancer, MM, metastases to the bones, metastases to other organs
than bone, lung cancer, and cancer of the liver, gall bladder and
pancreas. For patients with prostate cancer an increase in the risk of
fractures occurred with time. Other cancer types were not associated
with an increased risk of fractures. A high-risk group regarding
fractures included cancers primarily affecting the bone, primary bone
cancer, MM, metastases to the bone, metastases to other organs
than bone, lung cancer, and cancer of the liver, gall bladder,
pancreas, and prostate cancer. The main increase in risk of fractures
in this group occurred within the first year following diagnosis. A low
risk group for fractures included all other cancer types (e.g. cancer of
the breast, colon, and skin) (7).
Tumor registry data were collected between 1994-1996 on 11
primary tumor sites and 15 metastatic sites from 4,399 patients.
391
L. Ben-Nun King David
References
1. Scutellari PN, Antinolfi G, Gaoleti R, Giganti M. Metastatic bone
disease. Strategies for imaging. Minerva Med. 2003;94:77-90.
2. Galasko CSB. Skeletal metastases. London, Butterworths. 1986; p. 99.
3. Enneking WF, Conrad EU III. Common bone tumors. Clin Sympt. 1989;
41:1.
4. Xu DL, Zhang XT, Wang GH, et al. Clinical features of pathologically
confirmed metastatic bone tumors - a report of 390 cases. Ai Zheng. 2005;
24(11):1404-7.
5. Shen DH, Guo W, Yang Y, et al. Clinicopathologic analysis of 141 cases
of metastatic carcinoma in bone. Zhonghua Bing Li Xue Zhi. 2006;35:324-7.
6. Scutellari PN, Antinolfi G, Gaoleti R, Giganti M. Metastatic bone
disease. Strategies for imaging. Minerva Med. 2003;94:77-90.
7. Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk patients with
different types of cancer. Acta Oncol. 2008;4:1-11.
8. Hess KR, Varadhachary GR, Taylor SH, et al. Metastatic patterns in
adenocarcinoma. Cancer. 2006;106:1624-33.
9. Scutellary PN, Addonisio G, Righi R, Giganti M. Diagnostic imaging of
bone metastases. Radiol Med. 2000;100:429-35.
10. Kakhki VR, Anvari K, Sadeghi R, et al. Pattern and distribution of bone
metastases in common malignant tumors. Nucl Med Rev Cent East Eur.
2013;16(2):66-9.
394
L. Ben-Nun King David
References
1. Băicuş C, Tănăsecu C, Ionescu R. Has this patient a cancer? The
assessment of weight loss, anemia and erythrocyte sedimentation rate as
diagnostic tests in cancer. A retrospective study in a secondary university
hospital in Romania. Rom J Intern Med. 1999;37:261-7.
2. Ben-Noun L. What was the disease of the bones that affected King
David? J Gerontol A Biol Med Sci. 2001;57(3):M152-4.
3. Ben-Nun L. In: Ben-Nun L. ed. Approach to a Patients with Severe Bone
Pain from Biblical to Contemporary Times. Israel. 2013.
INTRODUCTION
Elderly patients have suffered from decrease in weight that may
be associated with various diseases for thousands of years. By
studying the causes of weight loss in geriatric persons from ancient
history, modern physicians can expand their knowledge thereby
improving their professional skills.
Who suffered from loss of weight in biblical times? What is the
most likely diagnosis? What are the characteristics of the diseases
396
L. Ben-Nun King David
that caused weight loss? This report aims to answer these questions
by evaluating weight loss in geriatric patient as described in the Bible.
Reference
1. Hamerman D. Molecular-based therapeutic approaches in treatment
of anorexia of aging and cancer cachexia. J Gerontol Med Sci. 2002;57A(8):
M511-8.
CACHEXIA
The word "cachexia" comes from the Greek words "kakos" and
"hexis", meaning bad condition (1). Cachexia is a complex metabolic
status with progressive weight loss and depletion of host reserves of
adipose tissue and skeletal muscle. Cachexia should be suspected if
involuntary weight loss of greater than five percent of premorbid
weight occurs within a six-month period. Cachexia represents the
clinical consequence of a chronic, systemic inflammatory response,
with high hepatic synthesis of acute-phase proteins resulting in
depletion of essential amino acids. By contrast, in starvation only fat
metabolism is increased while the organism tries to conserve body
mass (1).
397
L. Ben-Nun King David
References
1. Tisdale MJ. Biology of cachexia. J Natl Cancer Inst. 1997;89:1763-73.
2. Tisdale MJ. Cachexia in cancer patients. Nat Rev Cancer. 2002; 2:862-
71.
400
L. Ben-Nun King David
References
1. Miller SL, Wolfe RR. The danger of weight loss in the elderly. J Nutr
Health Aging. 2008;12:487-91.
2. Rabinovitz M, Pitlik SD, Leifer M, et al. Unintentional weight loss. A
retrospective analysis of 154 cases. Arch Intern Med. 1986;146:186-7.
3. Hardy C, Wallace C, Khansur T, et al. Nutrition, cancer and aging. An
annotated review. J Am Geriatr Soc. 1986;24:219-28.
4. Schiffman S, Pasternak M. Decreased discrimination of food odors in
the elderly. J Gerontol. 1979;34:79.
403
L. Ben-Nun King David
5. Liu LJ, Bopp MM, Roberson PK, et al. Undernutrition and risk of
mortality in elderly patients within 1 year of hospital discharge. J Gerontol
Med Sci. 2002;57A(11):M741-6.
6. Lee IB, Blair SN, Allison DB, et al. Epidemiologic data on the
relationships of caloric intake, energy balance, and weight gain over the life
span with longevity and morbidity. J Gerontol Med Sci. 2001;56A(Special
Issue SI):7-19.
7. Potter JF, Schafer DF, Bohi RL. In-hospital mortality as a function of
body mass index: an age-dependent variable. J Gerontol. 1988;43:M59-63.
8. Harris T, Cook EF, Garrison R, et al. Body mass index and mortality
among nonsmoking older persons: The Framingham Heart Study. JAMA.
1988;259:1520-4.
9. Fischer DW. Low body weight and weight loss in the aged. Am Diet
Assoc. 1990;90:1697-705.
10. Loh KW, Vriens MR, Gerritsen A, et al. Unintentional weight loss is
the most important indicator of malnutrition among surgical cancer
patients. Neth J Med. 2012;70(8):365-9.
11. Gaddey HL, Holder K. Unintentional weight loss in older adults. Am
Fam Physician. 2014;89(9):718-22.
12. Shea MK, Nicklas BJ, Houston DK, et al. The effect of intentional
weight loss on all-cause mortality in older adults: results of a randomized
controlled weight-loss trial. Am J Clin Nutr. 2011;94(3):839-46.
References
1. Reife C. Involuntary weight loss. Med Clin North Am. 1995;79:299-
313.
2. Morley J. Decreased food intake with aging. J Gerontol Med Sci.
2001;56 (Special Issue 2):81-8.
3. Roberts SB, Fuss P, Heyman MB, et al. Control of food intake in older
men. JAMA. 1994;272:1601-6.
4. Bertrand PC, Roulet M. Anorexia and malnutrition. Rev Prat.
2003;53:259-62.
5. Hays NP, Robers SB. The anorexia of aging in humans. Physiol Behav.
2006;88:257-66.
406
L. Ben-Nun King David
6. Parker BA, Chapman IM. Food intake and ageing – the role of the gut.
Mech Ageing Dev. 2004;125:859-66.
7. Moss C, Dhillo WS, Frost G, Hickson M. Gastrointestinal hormones: the
regulation of appetite and the anorexia of ageing. J Hum Nutr Diet.
2012;25(1):3-15.
8. Morley JE. Pathophysiology of the anorexia of aging. Curr Opin Clin
Nutr Metab Care. 2013;16(1):27-32.
9. Geokas MC, Haverback BJ. The aging gastrointestinal tract. Am J Surg.
1969;117:881-92.
10. Hays NP, Robers SB. The anorexia of aging in humans. Physiol Behav.
2006;88:257-66.
11. Mathey MFAM, Siebelink E, de Graaf C, et al. Flavor enhancement of
food improves dietary intake and nutritional status of elderly nursing home
residents. J Gerontol Med Sci. 2001;56A(4):M200-5.
12. Langan MJ, Yaerick ES. The effect of improved oral hygiene on taste
perception and nutrition of the elderly. J Gerontol. 1976; 31:413-8.
13. Elsner RJ. Changes in eating behavior during the aging process. Eat
Behav. 2002;3:15-43.
14. Reynish W, Andrieu S, Nourhashemi F, et al. Nutritional factors and
Alzheimer’s disease. J Gerontol Med Sci. 2001;56(11):M675-80.
15. Gazewood JD, Mehr DR. Diagnosis and management of weight loss
in the elderly. J Fam Pract. 1998;47:19-25.
References
1. Schiffman S, Pasternak M. Decreased discrimination of food odors in
the elderly. J Gerontol. 1979;34:79.
2. Lankish P, Gerzmann M, Gerzmann JF, Lehnick D. Unintentional weight
loss: diagnosis and prognosis. The first prospective follow-up study from a
secondary referral centre. J Intern Med. 2001;249:41-6.
3. Metalidis C, Knockaert DC, Bobbaers H, Vanderschueren S. Involuntary
weight loss. Does a negative baseline evaluation provide adequate
reassurance? Eur J Inten Med. 2008;19:345-9.
4. Henández JL, Matorras P, Riancho JA, González-Macías J. Involuntary
weight loss without specific symptoms: a clinical prediction score for
malignant neoplasm. QJM. 2003;86:649-55.
5. Lee IB, Blair SN, Allison DB, et al. Epidemiologic data on the
relationships of caloric intake, energy balance, and weight gain over the life
span with longevity and morbidity. J Gerontol Med Sci. 2001;56A (Special
Issue SI):7-19.
6. Morley JE, Slag MF, Elson MK, et al. The interpretation of thyroid
function tests in hospitalized patients. JAMA. 1983; 249:2377-9.
7. Foster DW. Gain and loss in weight. In: Isselbacher KJ, Braunwald E,
Winson JD, et al (eds.). Harrison’s Principles of Internal Medicine, ed. 13.
New York: McGraw-Hill. 1994, pp. 221-4.
8. Reife C. Involuntary weight loss. Med Clin North Am. 1995;79:299-
313.
9. Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of
thyroid disorders in the community: a twenty-year follow-up of the
Whickham Survey. Clin Endocrinol (Oxf). 1995;43:55-68.
10. Morley J. Decreased food intake with aging. J Gerontol Med Sci.
2001;56 (Special Issue 2):81-8.
11. L. Ben-Noun. Was the biblical King David affected by hypothermia? J
Gerontol Med Sci. 2002; 57:M364-7.
12. Rabinovitz M, Pitlik SD, Leifer M, et al. Unintentional weight loss. A
retrospective analysis of 154 cases. Arch Intern Med. 1986;146:186-7.
411
L. Ben-Nun King David
INTRODUCTION
Patients have suffered from chronic weakness, which may be
associated with various diseases, for thousands of years. Who
suffered from this condition in biblical times? What were the
causes? What was the most likely diagnosis? This research aims to
answer these questions by evaluating diseases that caused chronic
weakness as described in the Bible.
King David, the second and greatest of Israel’s Kings who ruled
that country more than 3537 years ago, suffered from diminished
strength “My strength fails…, My heart palpitates, my strength fails
me” (Psalms 31:11; 38:11), “My heart fails me” (38:13), and “My
strength is dried up like a potsherd” (22:16). These passages show
that the King became very weak, and was afflicted by the loss of
energy.
412
L. Ben-Nun King David
DEFINITION
Weakness is defined as a reduction in the strength of one or more
muscles (1). It may be generalized (total body weakness) or localized
to a specific area, side of the body, limb or muscle (1,2). Thus,
according to the contemporary definition, the passages mentioned
above, indicate a generalized weakness.
References
1. Aminof MJ. Weakness and paralysis. In: Fauci A, Kasper DL, Longo DL,
Braunwald E, et al. (eds). Principles of Harrison's Internal Medicine. 17th ed.
New York: McGraw-Hill. 2008, pp. 147-150.
2. Plum F. Disorders of motor function. Weakness, asthenia, and fatigue.
In: Benet JC, Plum F. (eds.). Cecil Textbook of Medicine. Saunders.
Philadelphia, London. 1991, pp. 2027-8.
GENERALIZED WEAKNESS
Since David suffered from generalized weakness, all conditions
associated with local weakness were not analyzed. Causes for
generalized weakness include electrolyte disturbances, e.g.,
hypokalemia, hypercalcemia, hypernatremia, hypophosphatemia,
hypermagnesemia, endocrine disorders such as
hypo/hyperthyroidism, Addison’s disease, muscle disorders -
channelopathies (periodic paralyses), metabolic defects of muscle
(impaired carbohydrate or fatty acid utilization; abnormal
mitochondrial function), neuromuscular junction disorders -
myasthenia gravis, Lambert-Eaton myasthenic syndrome, CNS
disorders - transient ischemic attacks, transient global ischemia,
multiple sclerosis, toxic myopathy, fibromyalgia, any infection, such
as infectious mononucleosis, flu, poliomyelitis, botulism, pneumonia,
any serious disease, such as CHF, cirrhosis, CRF, cancer, and
psychiatric conditions, especially depression (1-4).
Did any of the factors listed above play a role in the development
of David’s weakness? The previous report shows that King David
suffered from mild hypothermia (5). It seems unlikely that this
condition led to a generalized weakness. King David also suffered
from intractable bone pains due to osteoporosis. Among the various
diseases that may be associated with osteoporosis, the most likely
413
L. Ben-Nun King David
References
1. Aminof MJ. Weakness and paralysis. In: Fauci A, Kasper DL, Longo DL,
Braunwald E, et al. (eds.). Principles of Harrison's Internal Medicine. 17th
ed. New York: McGraw-Hill. 2008, pp. 147-150.
2. Plum F. Disorders of motor function. Weakness, asthenia, and fatigue.
In: Benet JC, Plum F. (eds.). Cecil Textbook of Medicine. Saunders.
Philadelphia, London. 1991, pp. 2027-8.
3. Olney RK, Aminoff MJ. Weakness, myalgias, disorders of movement
and imbalance. In: Braunwald E, Fauci AS, Kasper DL, et al. (eds.). Harrison’s
Principle of Internal Medicine. 15th ed. New York: McGraw-Hill. 2001, pp.
118-348.
4. Fietta P. Fibromyalgia: state of art. Minerva Med. 2004;95:37.
5. Ben-Noun L. Was the biblical King David affected by hypothermia? J
Gerontol Med Sci. 2002;57A:M364-7.
6. Ben-Noun L. The disease that caused weight loss in King David the
Great. J Gerontology Med Sci. 2004 59A(2):143-5.
7. Ben-Noun L. What was the disease of bones that affected King David?
J Gerontol Med Sci. 2002;57A:M152-4.
8. Ben-Noun L. Mental disorder that afflicted King David the Great. Hist
Psychiatry. 2004;15:467-76.
9. Hjermstad MJ, Fayers PM, Bjordal K, et al. Health-related quality of life
in the general Norwegian population assessed by European Organization for
Research and Treatment of Cancer Core Quality-of-Life Questionnaire: the
QLQ-C30 (+3). J Clin Oncol 1998;16:188-96.
10. Glaus A. Fatigue in patients with cancer: analysis and assessment.
Heidelberg: Springer-Verlag, 1998.
11. Cella D, Jin-shei L, Vhang C-H, et al. Fatigue in cancer patients
compared with fatigue in the general United States population. Cancer.
2002;94:528-38.
414
L. Ben-Nun King David
References
1. Hjermstad MJ, Fayers PM, Bjordal K, et al. Health-related quality of life
in the general Norwegian population assessed by European Organization for
Research and Treatment of Cancer Core Quality-of-Life Questionnaire: the
QLQ-C30 (+3). J Clin Oncol 1998;16:188-96.
2. Glaus A. Fatigue in patients with cancer: analysis and assessment.
Heidelberg: Springer-Verlag, 1998.
3. Cella D, Jin-shei L, Vhang C-H, et al. Fatigue in cancer patients
compared with fatigue in the general United States population. Cancer.
2002;94:528-38.
4. Cella D. The functional Assessment of Cancer Therapy-Anemia (FACT-
An): a new tool for the assessment of outcomes in cancer anemia and
fatigue. Semin Hematol. 1997;34(Suppl):13-9.
5. Cella D, Peretman A, Passik S, et al. Progress toward guidelines for the
management of fatigue. Oncology 1998;12:369-77.
6. Mooney K, Ferrel B, Nail L, et al. Oncology Nursing Society research
priorities survey. Oncol Nurs Forum. 1991;18:1381-8.
7. Stetz K, Haberman M, Holcombe J, et al. 1994 Oncology Nursing
Society research priority survey. Oncol Nurs Forum. 1995;22:785-9.
8. Stone P, Richards M, Hardy J. Fatigue in patients with cancer. Eur J
Cancer. 1998;34:1670-6.
9. North American Nursing Diagnosis Association. Nursing diagnoses:
definition and classification, 1987-1998. Philadelphia: McGraw-Hill. 1996.
418
L. Ben-Nun King David
B12 and folate will detect the underlying disease in many cases,
when anemia is classified according to red blood cell MCV. Microcytic
anemia is typically for iron deficiency, but normocytic anemia can
also be found in iron deficiency or anemia of chronic disease. Anemia
due to vitamin B12 or folate deficiency is typically macrocytic. The
treatment should aim to correct the underlying cause of disorder.
Recombinant human erythropoietin is a standard treatment of
anemia associated with CRF and tumor-associated anemia, but not in
other forms of anemia. Regular blood transfusions may be required
for elderly patients with chronic anemia (1,2).
In elderly patients, underlying causes of anemia must be
investigated and treated in a similar manner to that used in younger
adults. In addition to a thorough history and physical examination,
basic investigations such as red cell indices and morphology,
reticulocyte count, haematinic assays and occasionally bone marrow
examination, will detect the underlying pathology in most cases.
Anemia may be classified, according to red blood cell MCV, into
microcytic, macrocytic and normocytic types. Anemia with an
absolute reticulocytosis is due either to acute blood loss or
haemolysis. Other anemias, more frequently encountered in elderly
patients, are hypoproliferative, and reflect depressed marrow
production or impaired erythroid maturation. Examples include ACD
and IDA and, less commonly, megaloblastic anemia and anemia due
to primary bone marrow failure. The treatment of anemia should aim
to correct the underlying cause of the disorder and/or to improve the
quality of the blood, e.g. by haematinic replacement therapy.
Recombinant human erythropoietin has revolutionised the treatment
of anemia associated with CRF, while its role in other anemias is
currently under investigation. Regular blood transfusion may be
required for some elderly patients with chronic anemia. However,
the attendant risks of this procedure, such as iron overload and viral
hepatitis transmission, must be considered (2).
Anemia is a frequent finding in the elderly. Hypochromic
microcytic anemia, usually secondary to iron deficiency, is the most
common type. Macrocytic anemia, usually caused by folic acid or
vitamin B12 deficiency, is the next most common. Both iron and
vitamin B deficiencies are easy to treat with supplements, but the
clinician must make a careful search for the cause of the deficiency.
Normochromic normocytic anemia can be caused by a number of
420
L. Ben-Nun King David
References
1. Ebnöther M. Anemia in the elderly - a diagnostic and therapeutic
challenge? Ther Umsch. 2010;67(5):257-63.
2. Murphy PT, Hutchinson RM. Identification and treatment of anaemia
in older patients. Drugs Aging. 1994;4(2):113-27.
3. Howe RB. Anemia in the elderly. Common causes and suggested
diagnostic approach. Postgrad Med. 1983;73(4):153-60.
4. Smith DL. Anemia in the elderly. Am Fam Physician. 2000;62(7):1565-
72.
5. Joosten E, Lioen P. Iron deficiency anemia and anemia of chronic
disease in geriatric hospitalized patients: How frequent are comorbidities as
an additional explanation for the anemia? Geriatr Gerontol Int. 2014 Sep 26.
References
1. Cella D, Jin-shei L, Vhang C-H, et al. Fatigue in cancer patients
compared with fatigue in the general United States population. Cancer.
2002;94:528-38.
2. Hurter B, Bush NJ. Cancer-related anemia: clinical review and
management update. Clin J Oncol Nurs. 2007;11:349-59.
424
L. Ben-Nun King David
HYPOTHERMIA
INTRODUCTION
Elderly patients have suffered from hypothermia for thousands of
years. It is defined as a core (rectal, esophageal, tympanic) body
temperature equal to or less than 350 C (950 F) (1-5).
The causes of hypothermia are either primary or secondary.
Primary, or accidental, hypothermia occurs in healthy individuals with
inadequately clothing and who are exposed to severe cooling (6).
The term accidental hypothermia is used to imply that the low body
temperature is unintentional (7), environmentally induced, and
distinguished from hypothermia that develops secondary to medical
conditions or surgical treatment (2,4,7-9). Who was the person who
suffered from hypothermia as described in the Bible? What were the
characteristics of this hypothermia? This report aims to evaluate this
subject using the biblical description of hypothermia.
References
1. Editorials. Hypothermia. Ann Intern Med. 1978;89:565-7.
2. Reuler JB. Hypothermia: pathophysiology, clinical settings, and
management. Ann Intern Med. 1978 89:519-27.
3. Davidson M, Grant E. Accidental hypothermia. A community hospital
perspective. Postgraduate Med. 1981;70: 42-9.
425
L. Ben-Nun King David
References
1. Petersdorf RG. Hypothermia. Editorials. Arch Intern Med. 1979;
139:399.
2. Navari RM, Sheehy TW. Hypothermia. In: Calkins E, Davis PJ, Ford AB
(eds.). The Practice of Geriatrics. Philadelphia, PA: W.B. Saunders. 1986, pp.
291-301.
3. Collins KJ, Exton-Smith AN, Dore K. Urban hypothermia: preferred
temperature and thermal perception in old age. BMJ. 1981;282:175-7.
4. MacMillan AL, Corbett JL, Johnson RH, et al. Temperature regulation in
survivors of accidental hypothermia of the elderly. Lancet. 1967;2:165-69.
5. Thompson MK. The care of the older patient in winter. Practitioner.
1979;223:787-91.
6. Sallis R, Chassay CM. Recognizing and treating common cold-induced
injury in outdoor sports. Med Sci Sports Exerc. 1999;31:1367-73.
TYPES OF HYPOTHERMIA
Etiologically, there are three types of hypothermia: immersion,
exhaustion, and subclinical (1). Immersion or accidental hypothermia
may result from exposure to prolonged or extreme cold from
immersion or atmospheric conditions that lead to a body heat deficit
and a fall in the core temperature to 950 F (2). Mountain climbers
inadequately clothed in cold weather and long distance swimmers
exposed to hot and cold waters are prone to this type of hypothermia
(1). Exhaustion hypothermia results from depletion of the body’s
427
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References
1. Lloyd L. Treatment of accidental hypothermia. BMJ. 1979;1:413.
2. Birrer R, Wilkerson LA. Sports injuries. Cold injuries. In: Rakel R (ed.).
Textbook of Family Practice. 3rd ed. Philadelphia, PA: W.B. Saunders. 1984,
pp. 689-91.
3. Navari RM, Sheehy TW. Hypothermia. In: Calkins E, Davis PJ, Ford AB
(eds.). The Practice of Geriatrics. Philadelphia, PA: W.B. Saunders. 1986, pp.
291- 301.
ENVIRONMENTAL HYPOTHERMIA
A variety of environmental factors such as poor heating facilities,
particularly during winter, a lack of indoor plumbing, living alone, and
being housebound contribute to hypothermia (1-4). Fox et al. (5),
however, were unable to correlate any environmental factors with
low body temperatures in the elderly. Similarly, Davidson and Grant
show that accidental hypothermia was not confined to the elderly
people, nor it was a winter phenomenon. They found that the
eventual outcome was determined more by the underlying medical
condition than by the severity of hypothermia (6).
Exposure to cold can produce a variety of injuries that occur
because of man's inability to adapt to cold. These injuries can be
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References
1. Salvosa CB, Payne PR, Wheeler BF. Environmental conditions and body
temperatures of elderly women living alone or in local authority homes.
BMJ. 1971;4:656-9.
2. Emslie-Smith D. Accidental hypothermia: a common condition with a
pathognomonic electrocardiogram. Lancet. 1958;2:492.
3. Duguid H, Simpson RG, Stowers JM. Accidental hypothermia. Lancet.
1961;2:1214-9.
4. Society and Medical Officers of Health. A pilot survey into the
occurrence of hypothermia in elderly people living at home. Public Health.
1968;82:223.
5. Fox RH, Woodward PM, Exton-Smith AN, et al. Body temperature in
the elderly: A national study of physiological, social and environmental
conditions. BMJ. 1973;1:200-3.
6. Davidson M, Grant E. Accidental hypothermia. A community hospital
perspective. Postgraduate Med. 1981;70:42-9.
rd
7. Long WB 3 , Edlich RF, Winters KL, Britt LD. Cold injuries. J Long Term
Eff Med Implants. 2005;15:67-78.
8. Jurkovitz GJ. Environmental cold-induced injury. Surg Clin North Am.
2007;87:247-67, viii.
9. Elbaz G, Etzion O, Delgado J, et al. Hypothermia in a desert climate:
severity score and mortality prediction. Am J Emerg Med. 2008; 26:683-8.
URBAN HYPOTHERMIA
Urban hypothermia is characterized by a poor temperature
discrimination and lack of precision in adjusting the thermal
environment (1). In Zagreb, University Hospital Rebro, Croatia, 18
elderly patients, 11 women and seven men, aged 66-87 years, were
afflicted by urban hypothermia. Ten patients suffered from moderate
hypothermia (rectal temperature 32-35 degrees C), and eight from
severe hypothermia (rectal temperature <32 degrees C). In the group
of patients suffering from moderate hypothermia, three were
somnolent and six in various degrees of comatose states. In the
group of patients with severe hypothermia, three patients were
somnolent or stuporous and five were in comatose states of various
degrees. In the group with severe hypothermia, three presented with
arterial hypotension and five were in a state of shock (2).
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L. Ben-Nun King David
References
1. Collins KJ, Exton-Smith AN, Dore K. Urban hypothermia: preferred
temperature and thermal perception in old age. BMJ. 1981;282:175-7.
2. Durakovid Z, Misigoj-Durakvid M, Corovid N, Cubrilo-Turek M. Urban
hypothermia and hyperglycemia in the elderly. Coll Antropol. 2000;24:405-
9.
CLINICAL STAGES
References
1. Davidson M, Grant E. Accidental hypothermia. A community hospital
perspective. Postgraduate Med. 1981;70: 42-9.
2. Navari RM, Sheehy TW. Hypothermia. In: Calkins E, Davis PJ, Ford AB
(eds.). The Practice of Geriatrics. Philadelphia, PA: W.B. Saunders. 1986, pp.
291-301.
3. Fox RH, Woodward PM, Exton-Smith AN, et al. Body temperature in
the elderly: A national study of physiological, social and environmental
conditions. BMJ. 1973;1:200-3.
4. Petersdorf RG. Hypothermia. Editorials. Arch Intern Med. 1979;
139:399.
5. Collins KJ. Effects of cold on old people. Brit J Hosp Med. 1987;38: 506-
14.
6. Editorials. Hypothermia. Ann Intern Med. 1978;89:565-7.
7. Besdine RW. Accidental hypothermia: the body’s energy crisis.
Geriatrics. 1979;34:51-9.
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ADDITIONAL SIGNS
References
1. Besdine RW. Accidental hypothermia: the body’s energy crisis.
Geriatrics. 1979;34:51-9.
2. Collins KJ. Effects of cold on old people. Brit J Hosp Med. 1987;
38:506-14.
3. Medical News. Action needed to prevent deaths from hypothermia in
the elderly. JAMA. 1980;243:407-8.
4. Vaisburg S. Accidental hypothermia in the elderly. Editorials. JAMA.
1978;18:1888.
Reference
1. Reuler JB. Hypothermia: pathophysiology, clinical settings, and
management. Ann Intern Med. 1978 89:519-27.
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EKG CHANGES
There is a pathognomonic EKG pattern - the lengthening of the
RR, PR, QRS, and corrected QT (QTC) intervals, the presence of the
typical J deflection, with or without inversion of T, in leads related to
the left ventricle (1-3), and lethal cardiac arrhythmias (VF and
asystole) (4).
References
1. Emslie-Smith D. Accidental hypothermia: A common condition with a
pathognomonic electrocardiogram. Lancet. 1958;2:492.
2. Aslam AF, Aslam AK, Vasavada BC, Khan IA. Hypothermia: evaluation,
electrocardiographic manifestations, and management. Am J Med.
2006;119: 297-301.
3. Wong FW. J wave and hypothermia. Dynamics. 2005;16:17-8.
4. Southwick FS, Dalgish PH. Recovery after prolonged asystolic cardiac
arrest in profound hypothermia. JAMA. 1980;243:1250-3.
References
1. Ben-Noun L. What was the disease of the bones that affected King
David? J Gerontol Med Sci. 2002;57A:M152-4.
2. Ben-Noun L. Was the biblical King David affected by hypothermia? J
Gerontol A Biol Sci Med Sci. 2002;57(6): M364-7.
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L. Ben-Nun King David
THERAPY
The general principals of prehospital management are: 1] prevent
further heat loss, 2] rewarm the body core temperature in advance
to shell, and 3] avoid precipitating VF (1).
Accidental hypothermia is an infrequent and under-diagnosed
pathology, which causes fatalities every year. Its management
requires thermometers to measure core temperature. An esophageal
probe may be used in a hospital situation, although in moderate
hypothermia victims epitympanic measurement is sufficient. Initial
management involves advance life support and body rewarming.
Vigorous movements can trigger arrhythmia which does not use to
respond to medication or defibrillation until the body reaches 30°C.
External, passive rewarming is the method of choice for mild
hypothermia and a supplementary method for moderate or severe
hypothermia. Active external rewarming is indicated for moderate or
severe hypothermia or mild hypothermia that has not responded to
passive rewarming. Active internal rewarming is indicated for
hemodynamically stable patients suffering moderate or severe
hypothermia. Patients with severe hypothermia, cardiac arrest or
with a potassium level below 12 mmol/l may require
cardiopulmonary bypass treatment (2).
For hypothermic victims in the prehospital setting,
cardiopulmonary resuscitation, removing wet clothes, insulating the
victim, stabilization with warmed air/oxygen and IV fluids constitute
the initial treatment modalities (3-7). Individuals with only mild
symptoms of hypothermia may be rewarmed with external active
and passive rewarming techniques such as heating blankets, hot wet
towels, warmed water mattresses, warm packs, warm baths, hot
water bottles, and warm enemas (3,4,8). Hospital management
should include, if necessary, central line replacement, pleural lavage
with warm saline, heated humified oxygen (5), warmed peritoneal
dialysis, and extracorporeal blood warming with partial bypass (4,5).
Post resuscitation complications should be monitored; they include
pneumonia, pulmonary edema, cardiac arrhythmias, myoglobinuria,
disseminated intravascular thrombosis, and seizures (5).
References
rd
1. Long WB 3 , Edlich RF, Winters KL, Britt LD. Cold injuries. J Long Term
Eff Med Implants. 2005;15:67-78.
2. Soteras Martínez I, Subirats Bayego E, Reisten O. Accidental
hypothermia. Med Clin (Barc). 2011;137(4):171-7.
3. Besdine RW. Accidental hypothermia: the body’s energy crisis.
Geriatrics. 1979;34:51-9.
4. Part IV. Guidelines for cardiopulmonary resuscitation and emergency
cardiac care. Special resuscitation situations. JAMA. 1992; 268:2242-9.
5. Weinberg AD. Hypothermia. Ann Emerg Med. 1993;22:370-7.
6. Arcangeli A, Cavaliere F, Pennisi MA, et al. Physiology and treatment
of accidental hypothermia. Receti Prog Med. 1990; 81:356-60.
7. Kjaergaard B, Rudolph SF, Lucas A, Holdgaard HO. Treatment of the
hypothermic patients. Ugeskr Laeger. 2008;170:2005-10.
8. Bristow G, Smith R, Lee J, et al. Resuscitation from cardiopulmonary
arrest during accidental hypothermia due to exhaustion and exposure. CMA.
1977;117:247-9.
PRESSURE ULCERS
Elderly patients have suffered from pressure ulcers for thousands
of years. This is indicated by the presence of pressure ulcers found
on Egyptian mummified bodies (1). Even today, pressure ulcers
remain a common problem in all health care settings.
Patients with pressure ulcers had significantly more pain,
immobility, lack of energy, more restrictions regarding their social
functioning, less vitality, and limitations with respect their emotional
roles. Other problem areas include restrictions in work capacity,
recreation, social interaction, psychological well-being, as well as
problems caused by treatment regiments, worries and frustrations
and a lack of self-esteem (2-4).
Pressure ulcer in an otherwise sick patient is a matter of concern
for the caregivers as well as the medical personnel. A lot has been
done to understand the disease process. So much so, that US and
European countries have established advisory panels in their
respective continents. Since the establishment of these
organizations, the understanding of the pressure ulcer has improved
significantly. The well-documented and well-publicized definition of
pressure ulcer is somewhat lacking in the correct description of the
disease process. Hence, a modified definition has been presented.
This disease is here to stay. In the process of managing these ulcers,
the basic pathology needs to be understood well. Pressure ischemia
is the main reason behind the occurrence of ulceration. Different
extrinsic and intrinsic factors have been described in detail with
review of literature. There are a large number of risk factors causing
ulceration. The risk assessment scales have eluded the surgical
literature and mostly remained in nursing books and websites. These
scales have been reproduced for completion of the basics on
decubitus ulcer. The classification of the pressure sores has been
given in a comparative form to elucidate that most of the
classifications are the same except for minor variations. The
management of these ulcers is ever evolving but the old age saying of
"prevention is better than cure" suits this condition the most (5).
By studying the causes that led to the development of pressure
ulcers in a case taken from ancient history, modern physicians can
expand the horizons of their knowledge and thereby make their
approach more comprehensive. Who suffered from pressure ulcers
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in the Bible? What were the most likely causes? This research aims
to answer these questions using a biblical description of pressure
ulcers.
References
1. Clarke M, Kadhom H. The nursing prevention of pressure sores in
hospital and community patients. J Adv Nurs. 1988;13:365-73.
2. Herber OR, Schnepp W, Rieger MA. A systematic review on the impact
of leg ulceration on patient's quality of life. Health Qual Outcomes. 2007;
5:44.
3. Hopkins A, Dealey C, Bale C, et al. Patient stories of living with a
pressure ulcer. J Adv Nurs. 2006;56:345-53.
4. Persoon A, Heinen MM, van der Vleuten CJ, et al. Leg ulcers: a review
of their impact on daily life. J Clin Nurs. 2004;13:341-54.
5. Agrawal K, Chauhan N. Pressure ulcers: Back to the basics. Indian J
Plast Surg. 2012;45(2):244-54.
DEFINITION
Pressure sores are complex wounds with clinical appearances
ranging from mild redness of the skin to severe necrosis (1-4). Some
patients develop pressure sores due to many intrinsic and extrinsic
factors (2,5-7), the extent of which may not be apparent on initial
assessment. Intrinsic factors include limited mobility, poor nutrition,
comorbidities, and aging skin while extrinsic factors include pressure,
friction, shear, and moisture (8).
There are many terms used to describe pressure ulcers: pressure
sores, decubitus ulcers, bedsores, pressure necrosis, and ischemic
ulcers (9). Of these terms, the most commonly used was once
“decubitus ulcer.” This term is related to the Latin word meaning “to
lie down” (10) since it was thought that “decubitus ulcers” resulted
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L. Ben-Nun King David
References
1. Banks V. An educational initiative in pressure area management for
nursing staff. J Wound Care. 1997a;6;9:438441.
2. Banks V. Pressure sore education. J Wound Care. 1997b. 6;10:506507.
3. Dealey C. The care of wounds. Blackwell Scientific Publications:
London. 1994.
4. Maklebust J, Sieggreen M. Pressure Ulcers. Guidelines for prevention
nd
and nursing management. 2 ed. Springhouse Corporation. Springhouse
Pennsylvania, 1996.
5. Bridel J. The aetiology of pressure sores. J Wound Care. 1993;
40:23238.
6. Jones KR, Fennie K. Factors influencing pressure ulcer healing in adults
over 50: an exploratory study. J Am Med Dir Asoc. 2007;8:347-8.
7. Bader DL. Pressured sores. Clinical Practice and Scientific Approach.
Macmillan Press: London. 1990.
8. Bluestein D, Javaheri A. Pressure ulcers: prevention, evaluation, and
management. Am Fam Physician. 2008;78:1186-94.
9. Clinical practice guidelines for the prediction and prevention of
pressure ulcers. Stedman’s Medical Dictionary. 24th ed. Baltimore: Williams
& Wilkins. 1982.
10. Kahn, L.F, Van B, Wilking, S, Phillips T. Pressure ulcers. Am Acad
Dermatol. 1998;8:517-38.
11. Shea JD. Pressure sores: classification and management. Clin Orthop.
1975;112:89-100.
MECHANISM OF DEVELOPMENT
References
1. Bluestein D, Javaheri A. Pressure ulcers: prevention, evaluation, and
management. Am Fam Physician. 2008;78:1186-94.
2. Bergstrom N, Allman R, Alvarez O, et al. Treatment of pressure ulcers.
Clinical Practice Guidelines No. 15. Rockville, M: Agency for Health Care
Policy and Research, Public Health Service, US Department of Health and
Human Services; 1994;AHCPR No. 95-0652.
3. National Pressure Ulcer Advisory Panel. Pressure ulcers: incidence,
economics, risk assessment. Consensus development conference statement.
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L. Ben-Nun King David
Decubitus. 1989;2:24-8.
4. Bauer J, Philips LG. MOC-PSSM CME article: Pressure sores. Plast
Reconstr Surg. 2008;121(1Sup-pl):1-10.
5. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;
289:223-6.
6. Norton D, McClaren R, Exton-Smith AN. An investigation of geriatric
nursing problems in hospital. Edinburgh: Churchill-Livingstone. 1975, pp.
193-236.
7. Odom RB, James WD, Berger TG. Mechanical injuries to the skin.
Pressure ulcers (decubitus). In: Odom RB, James WD, Berger TG (eds.).
Andrews’ Diseases of the Skin. Clinical Dermatology. Philadelphia: W.B.
Saunders. 2000, pp. 41-48.
8. Shea JD. Pressure sores: classification and management. Clin Orthop.
1975;112:89-100.
9. Clarke M, Grace P. Understanding the underlying causes of the chronic
leg ulceration. J Wound Care. 2004;13:215-8.
10. Djarmarajan TS, Ahmed S. The growing problem of pressure ulcers.
Postgrad Med. 2003;113:77- 88.
11. Allman R. Pressure ulcers among the elderly. New Engl J Med. 1989;
320:850-3.
12. Bliss DZ, Gurvich O, Savik K, et al. Are there racial-ethnic disparities in
time to pressure ulcer development and pressure ulcer treatment in older
adults after nursing home admission? J Aging Health. 2014 Sep 25. pii:
0898264314553895. [Epub ahead of print]
EPIDEMIOLOGY
During each of nine surveys conducted between 1989 and 2005,
clinical teams in participating facilities predominantly in the US (some
facilities in Canada, Saudi Arabia, and Australia participated after
2003) assessed admitted on assigned study dates. For this study,
trends using all records (n=447.930; average, 49.770) were reviewed.
The majority of facilities in each survey were in the US (99%) overall.
Nosocomial pressure ulcer prevalence rates ranged from 9.2% and
5.6% in 1989 to 15.5% and 10% in 2003 and 2004, respectively. The
highest prevalence was documented in long-term acute care (27.3%
overall, and 8.5% nosocomial) (1).
In Maryland, 2015 residents aged 65 years and older admitted to
59 long-term-care facilities were studied. Of these residents, 208
(10.3%) had one or more pressure ulcers on admission to a long-
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L. Ben-Nun King David
References
1. Valginger C, Macfarlane GD, Meyer S. Results of nine international
pressure ulcer prevalence surveys: 1989 to 2005. Ostomy Wound Manage.
2008;54:40-54.
2. Baumgarten M, Margolis D, Gruber-Baldini AL, et al. Pressure ulcers
and the transition to long-term care. Adv Skin Wound Care. 2003;16:299-
304.
3. Woodbury MG, Houghton PE. Prevalence of pressure ulcers in
Canadian Healthcare settings. Ostomy Wound Management. 2004;50:22-
4,26,28,30,32,34,36-8.
4. Vanderwee K, Clark M, Dealey C, et al. Pressure ulcer prevalence in
Europe: a pilot study. J Eval Clin Pract. 2007;13:227-35.
5. Lahman NA, Halfens RJ, Dassen T. Prevalence of pressure ulcers in
Germany. J Clin Nurs. 2005;14:165-72.
6. Shanin ES, Dassen T, Halfens RJ. Pressure ulcer prevalence and
incidence in intensive care patients: a literature review. Nurs Crit Care.
2008;13:71-9.
7. Bours GJ, De Laat E, Halfens RJ, Lubbers M. Prevalence, risk factors
and prevention of pressure ulcers in Dutch intensive care units. Results of a
cross-sectional survey. Intensive Care Med. 2001;27:1599-605.
8. Bours GJ, Halfens RJ, Lubbers M, Haaboom JR. The development of a
national registration form to measure the prevalence of pressure ulcers in
the Netherlands. Ostomy Wound Manage. 1999;45:28-33,36-8, 40.
9. Gunninberg L. Risk, prevalence and prevention of pressure ulcers in
three Swedish healthcare settings. J Wound Care. 2004;13:286-90.
10. Jiang Q, Li X, Qu X, et al. The incidence, risk factors and
characteristics of pressure ulcers in hospitalized patients in China. Int J Clin
Exp Pathol. 2014; 7(5):2587-94. eCollection 2014.
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L. Ben-Nun King David
HOSPITAL COST
Incident pressure ulcers were associated with significantly higher
mean unadjusted hospital costs ($7.288 vs. $13.924, p<0.0001) and
length of stay (30.4 vs. 12.8 days, p=0.0001). Compared with those
who did not develop pressure ulcers, patients who developed
pressure ulcers were more likely to develop nosocomial infections,
and other hospital complications. Length of state for those who
developed pressure ulcers remained significantly greater than for
those who did not develop pressure ulcers ($14,260 vs. $12,382,
p=0.03, and 16.9 vs. 12.9 days, p=0.02, respectively). Incident
pressure ulcers were associated with substantial and significant
increases in hospital costs and length of stay. Nosocomial infections
and other hospital complications were additional significant
independent predictors of health care utilization among patients at
risk for pressure ulcers (1).
Reference
1. Allman RM, Goode PS, Burst N, et al. Pressure ulcers, hospital
complications, and disease severity: impact on hospital costs and length of
stay. Adv Wound Care. 1999;12:22-30.
CLASSIFICATION
Reference
1. EPUAP. European Pressure Ulcer Advisory Panel: Review 1.
1999;2:31.
Reference
1. Maklebust J, Sieggreen M. Pressure Ulcers. Guidelines for prevention
and nursing management. 2nd ed. Springhouse Corporation. Springhouse
Pennsylvania, 1996.
sore, bed sore, and pain and then culled to English-language, clinical
publications. Of the 417 articles recovered, 26 met the study inclusion
criteria, six specifically identified pain prevalence (ranging from 37%
and 100%), and none documented the incidence of pain in patients
with pressure ulcers. Measurement tools used to assess pain included
the Visual Analogue Scale, the Verbal Rating Scale, the Wong-Baker
Facial Recognition Scale, the McGill Pain Questionnaire-Short Form, the
Numerical Rating Scale, and the Present Pain Intensity scale. Pressure
ulcer pain was described as a burning sensation and reported as both
constant and transient. Contrary to often-held clinical opinion, the
studies reviewed suggest that pain increases with pressure ulcer stage.
Although a number of intrinsic and extrinsic factors were studied (e.g.,
age, ulcer stage, and bed surfaces), no conclusions could be drawn from
the available research. Because pain is an issue for individuals with
pressure ulcers and may present a different profile than other sources
of pain, pain assessment should become an integral part of pressure
ulcer care and documented to guide pressure ulcer management (1).
The aim of this study was to estimate the prevalence of UPAR pain
which was defined as pain, soreness or discomfort reported by
patients, on an "at risk" or pressure ulcer skin site, reported at a patient
level. Pain prevalence surveys in two large UK teaching hospital NHS
Trusts (six hospitals) and a district general hospital NHS Trust (three
hospitals) during their routine annual pressure ulcer prevalence audits
were conducted. The hospitals provide secondary and tertiary care
beds in acute and elective surgery, trauma and orthopedics, burns,
medicine, elderly medicine, oncology and rehabilitation. Anonymised
individual patient data were recorded by the ward nurse and pressure
ulcer prevalence team. In nine acute hospitals, 3,397 patients were
included in routine pressure ulcer prevalence audits and, of these, 2010
(59.2%) patients participated in the pain prevalence study. UPAR pain
prevalence was 16.3% (327/2010); 1,769 patients had no pressure
ulcers and of these 223 patients reported UPAR pain, a prevalence of
12.6%. Of the 241 people with pressure ulcers, 104 patients reported
pain, an UPAR pain prevalence of 43.2% (104/241). In conclusion, one
in six people in acute hospitals experience UPAR pain on 'at risk' or
pressure ulcer skin sites; one in every eight people without pressure
ulcers and, more than two out of every five people with pressure
ulcers. The results provide a clear indication that all patients should be
asked if they have pain at pressure areas even when they do not have a
pressure ulcer (2).
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L. Ben-Nun King David
References
1. Girouard K, Harrison MB, VanDenKerkof E. The symptom of pain with
pressure ulcers: a review of the literature. Ostomy Wound Manage.
2008;54(5):30-40, 42. Erratum in Ostomy Wound Manage. 2008;54(6):8.
2. Briggs M, Collinson M, Wilson L, et al. The prevalence of pain at pressure
areas and pressure ulcers in hospitalised patients. BMC Nurs. 2013;12(1):19.
MALODOROUS WOUNDS
Infection may present with increased local pain, cellulitis, local
abscess, necrotizing fasciitis, osteomyelitis, bacteremia, or sepsis (1).
Factors that lead to odor formation include necrotic tissue/slough,
infection that multiplies and thrives in necrotic tissue/slough, and
exudates (2-4).
The smell of the exudates is embarrassing to the patient. If the
pressure ulcer is covered with black necrotic tissue, it is difficult to
establish depth of the tissue damage (5). Infections in non-healing
wounds contain a mixture of organisms, including gram-positive
cocci, gram-negative bacilli, and anaerobes.
Necrotizing soft tissue infections are serious complications that
may arise from pressure ulcers. However, there are few studies on
this important issue. In addition, diagnostic criteria for necrotizing
soft tissue infections developing from pressure ulcers and infected
pressure ulcers are not well established. Necrotizing soft tissue
infections developing from pressure ulcers based on clinical findings
were defined. Based on the definition, the medical records of 24
elderly patients with this condition were retrospectively analyzed to
determine patient age, gender, comorbid disease, laboratory
findings, wound location, bacteriology, and treatment outcomes. In
the examined population, necrotizing soft tissue infections
developed primarily from pressure ulcers over the sacrum. Dementia
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L. Ben-Nun King David
References
1. Ebright JR. Microbiology and chronic leg and pressure ulces: clinical
significance and implications for treatment. Nurs Clin North Am. 2005;40:
207-16.
2. Hack A. Malodorous wounds-taking the patient’s perspective into
account. J Wound Care. 2003;12:319-21.
3. Haugton W, Young T. Common problems in wound care: malodorous
wounds. Br J Nurs. 1995;4:959-63.
4. Bowler PG, Davies BJ, Jones SA. Microbial involvement in chronic
wound order. J Wound Care. 1999;8:216-8.
5. Russel L. Pressure ulcer classification: defining early skin damage. Br J
Nurs. 2002;11(16 Suppl):S33-4, S36,S40-1.
6. Mizokami F, Furuta K, Isogai Z. Necrotizing soft tissue infections
developing from pressure ulcers. J Tissue Viability. 2014;23(1):1-6.
7. Dowd SE, Sun Y, Secor PR, et al. Survey of bacterial diversity in chronic
wounds using pyrosequnecing, DGGE, and full ribosome shotgun
sequencing. BMC Microbiol. 2008;8:43.
8. Heym B, Rimareix F, Lorta-Jacob A, et al. Bacteriological investigation
of infected pressure ulcers in spinal cord-injured patients and impact on
antibiotic therapy. Spinal Cord. 2004;42:230-4.
9. Soldera J, Nedel WL, Cardoso PR, d'Azevedo PA. Bacteremia due to
Staphylococcus cohnii ssp. urealyticus caused by infected pressure ulcer:
case report and review of the literature. Sao Paulo Med J.2013;131(1):59-61.
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L. Ben-Nun King David
References
1. Collier M. Effective prevention requires accurate risk assessment. J
Wound Care. 2004;13:3-7.
2. Torpy MJ, Lynn C, Glass E. Pressure ulcers. JAMA. 2003;289:254.
3. Finucane TE. Malnutrition, tube, feeding and pressure sores: data are
incomplete. J Am Geriatr Soc. 1995;43:447-51.
4. Allman RM, Goode PS, Burst N, et al. Pressure ulcers, hospital
complications, and disease severity: impact on hospital costs and length of
stay. Adv Wound Care. 1999;12:22-30.
5. Makleburst J, Magnam M. Risk factors associated with having a
pressure ulcer: a secondary data analysis. Adv Wound Care. 1994;7:25-34.
6. Clinical practice guidelines for the prediction and prevention of
pressure ulcers. Stedman’s Medical Dictionary. 24th ed. Baltimore: Williams
& Wilkins. 1982.
7. Margolis DJ, Knauss J, Bilker, W, et al. Medical conditions as risk
factors for pressure ulcers in an outpatient setting. Age Ageing.
2003;32:259-62.
8. Berlowitz DR, Wilking VB. Risk factors for pressure sores. A
comparison of cross-sectional and cohort-derived data. J Am Geriatr Soc.
1989;37:1943-50.
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L. Ben-Nun King David
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of pressure ulcers includes: ischemic
ulcers, neuropathic ulcers, vasculitides, skin cancers such as
squamous cell carcinoma, basal cell carcinoma, malignant melanoma
(1), radiation injury, RA, infectious diseases that lead to tissue
necrosis and ulceration by microorganisms such as -haemolytic
Streptococcus pyogenes, necrobiosis lipoidica, pyoderma
gangrenosum (2), venous leg ulcers, diabetic foot ulcer, gangrenous
wounds and fungating malignant wounds (3-6).
References
1. Grace P. (ed.). Guidelines for the Management of Leg Ulcers in Ireland.
Smith and Nephew. 2002.
2. Moloney C. Understanding the underlying causes of chronic leg
ulceration. J Wound Care. 2004;13(6):213-7.
3. Trémezaygues L, Schmaltz R, Vogt T, Reichrath J. Management of
pyoderma gangrenosum. An update on clinical features, diagnosis and
therapy. Hautarzt. 2010;61(4):345-53; quiz 354-5.
4. Baltzis D, Eleftheriadou I, Veves A. Pathogenesis and Treatment of
Impaired Wound Healing in Diabetes Mellitus: New Insights. Adv Ther. 2014;
31(8):817-36.
5. Misciali C, Dika E, Baraldi C, et al. Vascular leg ulcers: histopathologic
study of 293 patients. Am J Dermatopathol. 2014;36(12):977-83.
6. Allman R. Pressure ulcers among the elderly. New Engl J Med.
1989;20: 20: 850-3.
ERECTILE DYSFUNCTION
INTRODUCTION
References
1. Swendsen KO, Schultz A. Sexual dysfunction in men. Tidsskr Nor
Largeforen. 2008;128:448-52.
2. Camacho ME, Reyese-Otiz CA. Sexual dysfunction in the elderly: age or
disease? Int J Impot Res. 2005;17 Suppl 1:S52-6.
456
L. Ben-Nun King David
King David, the second and greatest of Israel’s Kings who ruled the
country more than 3537 years ago, was about 70 years old at the end
of his reign. When the King reached old age, he suffered from ED:
“Now King David was old, advanced in years; and they covered him
with clothes, but he could not become warm” (Kings 1:1). David’s
servants decided to summon “ a young virgin; and let her lie in thy
bosom, that my lord the king may become warm” (I Kings 1:2). They
“...found Avishag the Shunammite, and brought her to the king. And
the maiden was very fair, and she cherished the king, and ministered
to him: but the king knew her not” (I Kings 1:3-4). These words
indicate that the old King was unable to have sexual relations with
this pretty young woman. We have here the case of an old man,
from a high socioeconomic stratum, who had loved many women
during his long life, had wives, concubines and many children, but in
his old age was afflicted by some type of ED.
In King David’s case the relevant information has been extracted
from the patient’s medical file, the biblical text, recorded more than
3000 years ago. In this case, the pertinent biblical passages studied
should be regarded as the patient’s interview.
DEFINITION
ED is defined by a consistent or recurrent inability to attain and/or
maintain penile erection sufficient for sexual activity (1-3).
References
1. NIH Consensus Development Panel on Impotence. NIH consensus
conference: impotence. JAMA. 1993;270:83-90.
2. Korenman SG. Advances in the understanding and management of
erectile dysfunction. J Clin Endocrinol Metab. 1995;60:1985-8.
3. Giuliano F, Droupy S. Erectile dysfunction. Prog Urol. 2013;23(9):629-
37.
457
L. Ben-Nun King David
EPIDEMIOLOGY
ED prevalence is less than 10% in men aged below 50, while 20%
for men over 60 (1). The prevalence of sexual dysfunction increases
with age; about 20-30% of adult men have at least one manifested
sexual dysfunction (2,3). Sexual dysfunction is common among
individuals with chronic illnesses and is associated with distress and
reduced QOL (4).
The aim of this study was to estimate, by race/ethnicity in the US,
the prevalence of ED and the impact of sociodemographic, health,
relationship, psychological, and lifestyle variables. This cross-
sectional, population-based, nationally representative probability
survey conducted between May 2001 and January 2002 in the
general community setting facilitated equivalent representation
among US non-Hispanic white (n=901), non-Hispanic black (n=596),
and Hispanic (n=676) men aged 40 and older by using targeted phone
lists to oversample the minority populations. Estimated prevalence
of moderate or severe ED, defined as a response of "sometimes" or
"never" to the question "How would you describe your ability to get
and keep an erection adequate for satisfactory intercourse?" The
estimated prevalence was 22.0% (95% CI 19.4-24.6) overall, 21.9%
(95% CI 18.8-24.9) in whites, 24.4% (95% CI 18.4-30.5) in blacks, and
19.9% (95% CI 13.9-25.9) in Hispanics, and increased with increasing
age. The OR increased with increasing age. Probability also increased
with DM, hypertension, and moderate or severe LUTS overall; age
≥70 years and DM in whites; severe LUTS in blacks; and age ≥60
years, moderate LUTS, hypertension, and depression in Hispanics. It
decreased with exercise and college vs. less than high school
education overall; with exercise, good relationship quality, and
according to alcohol intake in blacks; and with high school or college
education in Hispanics. In conclusion, the odds of ED increased with
increasing age across race/ethnicity when controlling for
sociodemographic, health, relationship, psychological, and lifestyle
variables (5).
The inability to achieve or sustain an erection satisfactory for
intercourse in at least 75% of attempts is estimated to affect at least
10 million American men (6). Prevalence increases dramatically in
men over 50 years of age, with at least a quarter of older men being
affected (7). In men aged 40 to 70 years, 52% report some degree of
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L. Ben-Nun King David
References
1. Giuliano F, Droupy S. Erectile dysfunction. Prog Urol. 2013;23(9):629-
37.
2. Camacho ME, Reyese-Otiz CA. Sexual dysfunction in the elderly: age or
disease? Int J Impot Res. 2005;17 Suppl 1:S52-6.
3. Lewis RW, Fugl-Meyer KS, Bosch R, et al. Epidemiology/risk factors for
sexual dysfunction. J Sex Med. 2004;1:35-9.
4. Barsky JL, Friedman MA, Rosen RC. Sexual dysfunction and chronic
illness: the role of flexibility in coping. J Sex Marit Ther. 2006;32:235-53.
5. Laumann EO, West S, Glasser D, et al. Prevalence and correlates of
erectile dysfunction by race and ethnicity among men aged 40 or older in
460
L. Ben-Nun King David
the United States: from the male attitudes regarding sexual health survey. J
Sex Med. 2007;4(1):57-65.
6. Morley JE. Impotence. Am J Med. 1986;80(5):897-905.
7. Slag ME, Morley JE, Elson MK, et al. Impotence in medical clinic
outpatients. JAMA. 1983; 249:1736-40.
8. Feldman HA, Goldstein I, Hatzichriston DG, et al. Impotence and its
medical and psychological correlates: results of the Massachusetts male
ageing study. J Urol. 1994; 151:54-61.
9. Wylie K. Erectile dysfunction. Adv Psychosom Med. 2008;29:33-49.
10. Bacon CG, Mittelman MA, Kawachi I, et al. Sexual function in men
older than 50 years of age: results from the health professionals follow-up.
Ann Intern Med. 2003;139:161-8.
11. Hosain GM, Latini DM, Kauth M, et al. Sexual dysfunction among
male veterans returning from Iraq and Afghanistan: prevalence and
correlates. J Sex Med. 2013;10(2):516-23.
12. Chew KK, Stuckey B, Bremner A, et al. Male erectile dysfunction: its
prevalence in Western Australia and associated sociodemographic factors. J
Sex Med. 2008;5(1):60-9.
ETIOLOGY
Normal erectile function requires the coordination of
psychological, hormonal, neurological, vascular and cavernosal
factors (1,2). Alteration in any of these factors, or their combination,
is sufficient to cause ED (3). Organic causes are the main factor in
90% of cases in men over age 50, while in younger men psychogenic
causes are more common (4). ED often has multiple causes (5-7).
Diagnostic evaluation should include psychosexual, endocrinological,
neurological, vascular, traumatic, and iatrogenic (drugs and surgery)
factors (7).
ED is a sentinel marker for several reversible conditions including
peripheral and coronary vascular disease, hypertension, and DM.
Endothelial dysfunction is a common factor between the disease
states. Concurrent conditions such as depression, late-onset
hypogonadism, Peyronie's disease, and LUTS may significantly
worsen erectile function, other sexual and relationship issues, and
pen's dysmorphobia (8).
Major causes of ED include: vascular diseases such as C-V
problems, particularly hypertension, peripheral vascular diseases,
atherosclerotic disease of the penile artery, and the venous leakage
461
L. Ben-Nun King David
Even though treatable C-V risk factors were quite prevalent in the
study group, 45.2% of men suffered from dyslipidemia, 4.2% from
essential hypertension, 1.6% from DM, and 25.6% smoked. ED was
significantly associated with age and DM alone (p<0.0001). In
conclusion, there is a high prevalence of ED and associated treatable
C-V risk factors in Israeli men aged 25-55 years, especially in those
with DM (40).
The medical record of the King, that is the biblical text, gives no
details about the existence of C-V risk factors such as dyslipidemia,
hypertension, DM, or smoking.
References
1. Wagner G, Saenz De Tejada S. Update on erectile dysfunction. BMJ.
1998;316: 678-82.
2. Lue TF. Erectile dysfunction. New Engl J Med. 2000; 342:1802-13.
3. Krane RJ, Goldstein I, Saenz de Tejada I. Impotence. N Engl J Med.
1989;321:1648-9.
4. Morley JE. Management of impotence. Diagnostic considerations and
therapeutic options. Postgrad Med. 1993;93:65-72.
5. NIH Consensus Development Panel on Impotence. NIH consensus
conference: impotence. JAMA. 1993;270:83-90.
6. Morley JE. Impotence in older men. Hosp Pract. 1988;23:139-42, 145-
6.
7. Kirby RS. Impotence: diagnosis and management of male erectile
dysfunction. BMJ. 1994;308:957-60.
8. Wylie K. Erectile dysfunction. Adv Psychosom Med. 2008;29:33-49.
9. Giuliano F, Droupy S. Erectile dysfunction. Prog Urol. 2013;23(9):629-
37.
10. Wagner G, Mulhan J. Pathophysiology and diagnosis of male erectile
dysfunction. BJU Int. 1991;88(Suppl)3:3-10.
11. Feldman HA, Goldstein I, Hatzichriston DG, et al. Impotence and its
medical and psychological correlates: results of the Massachusetts male
ageing study. J Urol. 1994;151:54-61.
12. Morley JE, Kaiser FE. Sexual function with advancing age. Geriatr
Med. 1989;73:1483-95.
13. Korenman SG, Morley JE, Mooradian AD, et al. Secondary
hypogonadism in older men: its relation to impotence. J Clin Endocrinol
Metab. 1990;71:963-9.
14. Nephra A, Moreland RB. Neurologic erectile dysfunction. Urol Clin
North Am. 2001;28:289-305.
15. Sullivan, ME, Keoghane SR, Miller MAW. Vascular risk factors and
erectile dysfunction. BJU Int. 2001;87:838-45.
466
L. Ben-Nun King David
16. Phanjoo AL. Sexual dysfunction in old age. Adv Psychiat Treat.
2000;6:270-7.
17. Parmet S, Lynm C, Glass RM. Male sexual dysfunction. JAMA.
2004;291:307
18. Camacho ME, Reyese-Otiz CA. Sexual dysfunction in the elderly: age
or disease? Int J Impot Res. 2005;17 Suppl 1:S52-6.
19. Lewis RW, Fugl-Meyer KS, Bosch R, et al. Epidemiology/risk factors
for sexual dysfunction. J Sex Med. 2004;1:35-9.
20. Nicolai MP, van Bavel J, Somsen GA, et al. Erectile dysfunction in the
cardiology practice - a patients' perspective. Am Heart J. 2014;167(2):178-
85.
21. Ludwig W, Phillips M. Organic causes of erectile dysfunction in men
under 40. Urol Int. 2014;92(1):1-6.
22. Martin CE. Factors affecting sexual functioning in 60-79 year old
married males. Arch Sex Behav. 1981;10:399-420.
23. Pan LJ, Xia XY, Huang YF. Androgen deficiency and erectile
dysfunction. Zhonghua Nan Ke Xue. 2006;12:1030-4.
24. Traish A, Kim N. The physiological role of androgens in penile
erection: regulation of corpus cavernosum structure and function. J Sex
Med. 2005;2:759-70.
25. Traish AM, Guay AT. Are androgens critical for penile erections in
humans? Examining the clinical and preclinical evidence. J Sex Med. 2006;
3:382-404.
26. Caretta N, Ferlin A, Palego PF, Foresta C. Erectile dysfunction in aging
men: testosterone role in therapeutic protocols. J Endocrinol Invest. 2005;
28(11 Suppl Proceedings):108-11.
27. Morellli A, Corona G, Filippi S, et al. Which patients with sexual
dysfunction are suitable for testosterone replacement therapy? J Endocrinol
Invest. 2007;30:880-8.
28. Shabsigh R, Rajfer J, Aversa A, et al. The evolving role of testosterone
in the treatment of erectile dysfunction. Int J Clin Pract. 2006;60:1087-92.
29. Shabsigh R. Testosterone therapy in erectile dysfunction and
hypogonadism. J Sex Med. 2005;2:786-92.
30. Stanworth RD, Jones TH. Testosterone for the aging male; current
evidence and recommended practice. Clin Interv Aging. 2008;3:25-44.
31. Blute M, Hakimian P, Kashanian J, et al. Erectile dysfunction and
testosterone deficiency. Front Horm Res. 2009;37:108-22.
32. Buvat J, Bou Jaoudé G. Significance of hypogonadism in erectile
dysfunction. Words J Urol. 2006;24;657-67.
33. Fine SR. Erectile dysfunction and comorbid diseases, androgen
deficiency, and diminished libido. JAOA. 2004;104(1Suppl 1):S9-15.
34. Morley J. Endocrine factors in geriatric sexuality. Clin Geriatr Med.
1991;7:85-93.
467
L. Ben-Nun King David
35. Gottfried LA, Richie JP. Sexual problems. Premature ejaculation. In:
Branch WT (ed.). Office Practice of Medicine. Philadelphia, Toronto: W.B.
Saunders. 1987, pp.1407-14.
36. Briganti A, Salonia A, Deho F, et al. Peyronie’s disease: a review. Curr
Opin Urol. 2003;13:417-22.
37. Hellstrom WJ. History, epidemiology, and clinical presentation of
Peyronie's disease. Int J Impot Res. 2003; Suppl 5:S91-2.
38. Hellstrom WJ. Medical management of Peyronie's disease. J Androl.
2009;30:397-405.
39. Wagner G, Mulhan J. Pathophysiology and diagnosis of male erectile
dysfunction. BJU Int. 1991;88(Suppl)3:3-10.
40. Heruti RJ, Steivil A, Shochat T, et al. Screening for erectile dysfunction
and associated cardiovascular risk factors in Israeli men. Isr Med Assoc J.
2008;10;686-90.
TO SUM UP: the elderly have suffered from ED since the dawn of
history. The main objective of this research was to evaluate from a
contemporary perspective the biblical description of a geriatric
patient who suffered from ED. This report analyzes the sexual
disorder that affected the biblical King David, the second and
greatest of Israel’s Kings, who ruled the country more than 3537
years ago. A passage “And the maiden was very fair, and she
cherished the king, and ministered to him: but the king knew her not”
(I Kings 1:4) indicates ED that afflicted the biblical King David. Among
various types of sexual dysfunction, ED combined with low or absent
libido was most likely responsible. The numerous possible causes of
King David’s ED include malignancy such as MM, or RCC, or prostate
cancer, or gastric carcinoma, or CRC with metastases to the bones,
MDD and various social problems such as loneliness, lack of close
relationships with friends on whom the King could rely, feelings of
neglect, and loss of power and control over his people. The story of
King David unfolds as possibly the earliest description of an elderly
patient who suffered from ED.
References
1. Phanjoo AL. Sexual dysfunction in old age. Adv Psychiat Treat. 2000;
6:270-7.
2. Ben-Noun L. Was the biblical King David affected by hypothermia? J
Gerontol Med Sci. 2002;57A:M364-7.
3. Ben-Noun L. What was the disease of the bones that affected King
David? J Gerontol A Biol Sci Med Sci. 2002; 57A:M152-4.
4. Ben-Noun L. The disease that caused weight loss in King David the
Great. J Gerontol A Biol Sci Med Sci. 2004;59A: M143-5.
470
L. Ben-Nun King David
MENTAL DISORDER
INTRODUCTION
Patients have suffered from mental disorders since the dawn of
history. There is an indication of this in the book of Deuteronomy,
which talks of God’s punishment for those who violate divine
commands: “The Lord shall smite thee with madness, and blindness,
and astonishment of heart” (Deuteronomy 28: 28). Thus, we learn
that even in those ancient times there was a negative attitude
towards some mental illnesses.
Contemporary interpretation of the currently available literature
on mental disorders is important since it may give us a better
understanding of the roots of modern psychiatry. By studying the
mental disorder of a patient from ancient history, modern physicians
can expand their knowledge and thus improve their professional
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L. Ben-Nun King David
HISTORICAL BACKGROUND
King David, who ruled Israel more than 3537 years ago, was
“...the son of Ephrathite of Beth-lehem-judah, whose name was Jesse;
and he had eight sons” (I Samuel 17:12). David was the youngest and
tended his father’s sheep. He was a ruddy and handsome young man
(17:42), and even in his youth was already very strong, showing his
skills by killing a lion and a bear. Subsequently, David killed Goliath, a
terrifying giant from the area of Gat, and defeated the Philistines.
Participating in numerous wars, he built a great empire located
between Mesopotamia and Anatolia in the north and Egypt in the
south. King David was an enigmatic warrior, whose name evokes a
mystical power almost like that of a deity (1). Even today, after
thousands of years, King David continues to live in the heart of the
Israeli people. One very popular song proclaims that “David, the King
of Israel, lives, lives and exists.” We can assume that medical
information relating to this great leader is important to many people.
In his old age King David began to suffer from a number of
physical ailments (2,3). Was he also afflicted by some mental
disorder? This article aims to answer this question by studying all
biblical passages relating to the King’s mental state.
The passages “....My soul in distress...” (Psalm 31:8), “...having
agony in my heart daily” (13:3), “My soul is alarmed..” (6:4), “...Heal
my soul ; because I sinned..” (41:5), and “The troubles of my heart are
widened;. bring thou me out of my distress” (25:17) indicate that the
King had some mental problem. What was the mental disorder that
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L. Ben-Nun King David
afflicted King David in his old age? Are mental disorders prevalent in
contemporary days?
References
1. David. In: Encyclopedia of Tanach. The Jerusalem Publishing House
Ltd. 1987, pp. 172-74.
2. Ben-Noun L. What was the disease of the bones that affected King
David? J Gerontol A Biol Sci Med Sci. 2002; 57:M152-4.
3. Ben-Noun, L. Was the biblical King David affected by hypothermia? J
Gerontol A Biol Sci Med Sci. 2002;57: M364-7.
PSYCHIATRIC EPIDEMIOLOGY
US population estimates, based on combined site data, indicate
that 15.4% of the population 18 years of age and over fulfilled criteria
for at least 1 alcohol, drug abuse, or other mental disorder during the
period one month before interview. Men had higher rates of
substance abuse and antisocial personality, whereas women had
higher rates of affective, anxiety, and somatization disorders (1). In
addition, men have a significantly higher rate of cognitive impairment
than women did after controlling for the effects of age, race or
ethnicity, marital status and socioeconomic status (2).
The objective of this study was to present estimates of the
lifetime prevalence of DSM-IV mental disorders with and without
severe impairment, their comorbidity across broad classes of
disorder, and their sociodemographic correlates. The National
Comorbidity Survey-Adolescent Supplement (NCS-A) is a nationally
representative face-to-face survey of 10,123 adolescents aged 13 to
18 years in the continental US. DSM-IV mental disorders were
assessed using a modified version of the fully structured WHO CIDI.
Anxiety disorders were the most common condition (31.9%),
followed by behavior disorders (19.1%), mood disorders (14.3%), and
substance use disorders (11.4%), with approximately 40% of
participants with one class of disorder meeting criteria for another
class of lifetime disorder. The overall prevalence of disorders with
severe impairment and/or distress was 22.2% (11.2% with mood
disorders, 8.3% with anxiety disorders, and 9.6% behavior disorders).
The median age of onset for disorder classes was earliest for anxiety
(six years), followed by 11 years for behavior, 13 years for mood, and
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L. Ben-Nun King David
References
1. Regier DA, Boyd JH, Burke JD Jr, et al. One-month prevalence of
mental disorders in the United States. Based on five Epidemiology
Catchment Area sites. Arch Gen Psychiatry. 1988;45:977-86.
2. Regier DA, Farmer ME, Rae DS, et al. One-month prevalence of mental
disorders in the United States and sociodemographic characteristics: the
Epidemiologic Catchment Area study. Acta Psychiatr Scand. 1993;88:35-47.
3. Merikangas KR, He JP, Burstein M, et al. Lifetime prevalence of mental
disorders in U.S. adolescents: results from the National Comorbidity Survey
Replication - Adolescent Supplement (NCS-A). J Am Acad Child Adolesc
Psychiatry. 2010;49(10):980-9.
4. Melzer D, Buxton J, Villamil E. Decline in common mental disorder
prealence in men during the sixth decade of life. Evidence from the national
psychiatric morbidity survey. Soc Psychiatry Psychiatr Epidemiol. 2004;
39:33-8.
5. Cohidon C, Imberson E, Goldberg M. Prevalence of common mental
disorders and their work consequences in France, according to occupational
category. Am J Ind Med. 2008;52:178.
6. Rothenhäusler HB, Stepan A, Kreiner B, et al. Patterns of psychiatric
consultation is an Austrian tertiary care center - results of a systematic
analysis of 3.307 referrals over 2 years. Psychiatr Danub. 2008;20:301-9.
7. Rothenhäusler HB. Mental disorders in general hospital patients.
Psychiatr Danub. 2006;18:183-92.
8. Abou–Saleh MT, Ghubash R, Daradkeh TK. A1 Ain Community Survey.
I. Prevalence and sociodemographic correlates. Soc Psychiatry Psychiatric
Epidemiol. 2001;36:20-8.
9. Trollor JN, Andeson TM, Sachdev PS, et al. Prevalence of mental
disorders in the elderly: the Australian National Mental Health and Well-
Being Survey. Am J Geriatr Psychiatry. 2007;15:455-66.
10. Kohn R, Vicente B, Salvidivia S, et al. Psychiatric epidemiology of the
elderly population in Chile. Am J Geriatr Psychiatry. 2008;16:1020-8.
11. Gureje O, Lasebikan VO, Kola L, Makanjuola VA. Lifetime and 12-
month prevalence of mental disorders in the Nigerian Survey of Mental
Health and Well-Being. Br J Psychiatry. 2006;188:465-71.
12. Silove D, Bateman C, Brooks RT, et al. Estimating clinically relevant
mental disorders in a rural and an urban setting in postconflict Timor Leste.
Arch Gen Psychiatry. 2008;65:1205-12.
13. Hossain M, Ahmed H, Chowdhury W, et al. Mental disorders in
Bangladesh: a systematic review. BMC Psychiatry. 2014;14(1):216.
477
L. Ben-Nun King David
increased (21% to 29%), but there was insignificant change in the use
of appropriate counseling (19% to 23%) (6).
In a community-based study, Amsterdam, The Netherlands, the
prevalence of depressive symptomatology and risk indicators were
assessed in 2,850 participants aged 75 years or more. The
prevalence of depressive symptoms was 31.1% (7).
The aim of this study was to determine the association between
physical fitness and depressive symptoms among young adults. The
study population consisted of 5,497 males and females, members of
the Northern Finland birth cohort of 1966, who at age 31 completed
fitness tests and filled in a questionnaire including questions about
depressive symptoms (Hopkins' Symptom Checklist-25) and physical
activity. Cardiorespiratory fitness was measured by a four-min step
test and muscular fitness by tests of maximal isometric handgrip and
isometric trunk extension. The OR with 95% CI for having depressive
symptoms were calculated for quintiles groups of physical fitness
using the third, median quintile as reference group, and the results
were adjusted for potential confounding variables. Depressive
symptoms were most common among males and females in the
lowest quintile group of trunk extension test (OR 1.58, 95% CI 1.07-
2.32 for males and OR 1.43, 95% CI 1.03-2.0 for females) and among
males in the lowest quintile group of handgrip strength (OR 1.64, 95%
CI 1.11-2.42) compared to the reference group. Level of self-reported
physical activity was inversely associated with depressive symptoms
both for males (OR 1.74, 95% CI 1.25-2.36) and for females (OR 1.36,
95% CI 1.05-1.75). The cardiorespiratory fitness was not associated
with depressive symptoms (OR 1.01, 95% CI 0.68-1.49 for males and
0.82, 95% CI 0.57-1.16 for females). In conclusion, low level of
isometric endurance capacity of trunk extensor muscles is associated
with high level of depressive symptoms in both sexes. In males, also
poor handgrip strength is associated with increased levels of
depressive symptoms. The physical activity level is inversely
associated with the prevalence of depressive symptoms among
young adults (8).
This cross-sectional study was conducted to determine prevalence
of current depressive, anxiety, and stress-related symptoms on a
Dimensional and Categorical basis among young adults in Ranchi city
of India. A stratified sample of 500 students was selected to be
representative of the city's college going population (n=50,000) of
which 405 were taken up for final analysis. Data were obtained using
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L. Ben-Nun King David
References
1. Trivedi MH, Lin EH, Katon WJ. Consensus recommendations for
improving adherence, self-management, and outcomes in patients with
depression. CNS Spectr. 2007;12(8 Suppl 13):1-27.
2. Von Korff M, Katon W, Unützer J, et al. Improving depression care:
barriers, solutions, and research needs. J Fam Pract. 2001;50(6):E1.
3. Wells K.B, Burman M.A. Caring for depression in America: lessons
learned from early findings of the Medical Outcomes Study. Psychiatr Med.
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4. Katon W, Schulberg H. Epidemiology of depression in primary care.
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6. Young AS, Klap R, Shoai R, Wells KB. Persistent depression and anxiety
in the United States: prevalence and quality of life. Psychiatr Serv. 2008;
59:1391-8.
7. van't Veer-Tazelaar PJ, van Marwijk HW, Jansen AP, et al. Depression
in old age (75+), the Piko study. J Affect Disord. 2008;106:295-9.
8. Suija K, Timonen M, Suviola M, et al. The association between physical
fitness and depressive symptoms among young adults: results of the
Northern Finland 1966 birth cohort study. BMC Public Health. 2013 Jun 3;
13:535.
9. Sahoo S, Khess CR. Prevalence of depression, anxiety, and stress
among young male adults in India: a dimensional and categorical diagnoses-
based study. J Nerv Ment Dis. 2010;198(12):901-4.
10. Qadir F, Haqqani S, Khalid A, et al. A pilot study of depression among
older people in Rawalpindi, Pakistan. BMC Res Notes. 2014 Jun 28;7:409.
11. Chung S. Residential status and depression among Korean elderly
people: a comparison between residents of nursing home and those based
in the community. Health Soc Care Community. 2008;16(4):370-7.
12. Georgotas, A. Affective disorders in the elderly: diagnostic and
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The verse “..All the night make I my bed to swim; I water my couch
with my tears” (6:7) points to insomnia during which the King wept
so much that his bed was wet with tears (Criterion 4).
The passages “Fearfulness and trembling are come upon me...”
(55:6), “My heart is shivering within me ..” (55:5) and “..Like a deaf
man I would not hear and like a mute I would not speak..” (38:14)
indicate psychomotor agitation or retardation that are compatible
with criterion 5.
The verse ”My strength failed because of mine iniquity...” (31:11)
indicates fatigue or loss of energy (criterion 6).
The subsequent passages “But I am a worm, and no man; a
disgrace of men, and despised of the people” (22:7) and “I am
forgotten as a dead man out of mine mind: I am like a lost tool”
(31:13) express feelings of worthlessness (criterion 7).
Fear of death and recurrent thoughts of death (criterion 9) are
found in numerous passages: ”...has brought me into the dust of the
earth to death” (22:16), “... the terrible fears of death had fallen
upon me” (55:5), “The sorrows of death compassed me...” (18:5) and
“...The mines of death preceded me..” (18: 6).
This study found 7 criteria for major depression in King David.
Criterion 3 can be related either to depression or to physical illness
such as bone diseases, with the diagnosis of malignancy as the most
probable (1). Since cancer may have a link to depression, this
criterion is removed. Criterion 6 can also be attributed to physical
illness, for example anemia. If criteria 3 and 6 are dropped, there are
still sufficient criteria (5) for a diagnosis of major depression.
References
1. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
2. American Psychiatric Association. Practice Guideline for the Treatment
of Patients with Major Depressive Disorder (Revision). Am J Psychiatry.
2000;157:1-45.
References
1. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
2. Goodwin FK, Bunney, W.E Jr. Depressions following reserpine: a
reevaluation. Sem Psychiatry. 1971;3:435-8.
3. Kronke, K. A 75-year-old man with depression. JAMA. 2002;287:1568-
76.
4. Lewis DA, Smith, R.E. Steroid-induced psychiatric syndromes: a report
of 14 cases and a review of the literature. J Affect Disord. 1983;5:319-32.
5. Pope HG Jr, Katz DL. Affective and psychotic symptoms associated
with anabolic steroid use. Am J Psychiatry. 1988;145:487-90.
6. Uzych L. Anabolic-androgenic steroids and psychiatric-related effects:
a review. Can J Psychiatry. 1992;37(1):23-8.
References
1. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
2. Kronke, K. A 75-year-old man with depression. JAMA. 2002;287:1568-
76.
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L. Ben-Nun King David
DYSTHYMIC DISORDER
This disorder refers to a chronic mild depressive syndrome, with
insidious onset often commencing in childhood or adolescence,
characterized by less acute, less severe, and less disabling depressive
symptoms, symptomatically subsyndromal and psychologically
intractable to change, which are present for at least two years and
may last for many years (1-5). Dysthymic disorder is a chronic
condition with a protracted course and a high risk of relapse. Almost
all patients with dysthymic disorder eventually develop
superimposed MDD. Although patients with dysthymic disorder
show mild to moderate symptoms, from a longitudinal perspective,
the condition is severe (6,7).
The diagnosis of dysthymic disorder was created in DSM-III and
maintained in DSM-IV to describe a depressive syndrome of mild to
moderate severity of at least two years' duration that did not meet
criteria for MDD. The prevalence of dysthymic disorder is
approximately 2% in the elderly population where subsyndromal
depressions of lesser severity are more common. Dysthymic disorder
was replaced in DSM-V by the diagnosis of "persistent depressive
disorder" that includes chronic major depression and dysthymic
disorder. In older adults, epidemiological and clinical evidence
supports the use of the term "dysthymic disorder." In contrast to
young adults with dysthymic disorder, older adults with dysthymic
disorder commonly present with late age of onset, without major
depression and other psychiatric disorders, and with a low rate of
family history of mood disorders. They often have stressors such as
loss of social support and bereavement, and some have
cerebrovascular or neurodegenerative pathology. A minority has
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References
1. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
2. Akiskal HS. Dysthymic disorder: psychopathology of proposed chronic
depressive subtypes. Am J Psychiatry. 1983;140:11-20.
3. Akiskal HS. Mood disorders: clinical features. In: Sadock B J, Sadock
VA (eds.). Comprehensive Textbook of Psychiatry, 7th ed. Philadelphia:
Lippincott Williams & Wilkins. 2000, pp. 1338-44.
4. Lehmann, H.E. Affective disorders. In: Kaplan HI and Sadock BJ (eds.).
Comprehensive Textbook of Psychiatry, 4th edn. Baltimore: Williams &
Wilkins. 1985, pp. 786- 811.
5. McCullough JP, Kasnetz MD, Braith JA, et al. A longitudinal study of an
untreated sample of predominantly late onset characterological dysthymia.
J Nerv Mental Dis. 1988;176:658-67.
6. Klein DN, Schwartz JE, Rose S, Leader JB. Five-year course and
outcome of dysthymic disorder: a prospective naturalistic follow-up study.
Am J Psychiatry. 2000;157:931-9.
488
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MINOR DEPRESSION
Did King David suffer from minor depression? Subsyndromal
subthreshold (minor) depression is common and associated with
symptoms of impairments of clinical importance (1). This depression
is a condition in which a person has depressive symptoms but does
not meet the criteria for a depressive disorder. Subthreshold
depression has serious consequences for the QOL, but not as serious
as in the case of a depressive disorder. Subthreshold depression has
considerable economic consequences for the individual concerned,
although again less severe than if the individual had a MDD (2).
Major depression, defined according to DSM IV TR criteria, is less
common in older subjects, while other types of depression are two to
three times more prevalent. This heterogeneous group of
disturbances has received different names: depression not otherwise
specified, minor depression, subthreshold or subsyndromal
depression. Moreover, each condition has been defined using
heterogeneous criteria by different authors. The term of
subthreshold depression will be adopted in this position statement.
Subthreshold depression has been associated with the same negative
consequences of major depression, including reduced well being and
QOL, worsening health status, greater disability, increased morbidity
and mortality. Nevertheless, there is a dearth of clinical trials in this
area, and therefore older patients with subthreshold depression are
either not treated or they are treated with the same non-
pharmacological and pharmacological therapies used for major
depression, despite the lack of supporting scientific evidence. There
is an urgent need to reach a consensus concerning the diagnostic
criteria for subthreshold depression as well as to perform clinical
trials to identify effective and safe therapies in this too long
neglected patient group (3).
DSM-IV criteria for this disorder include two to four depressive
symptoms, such as depressed mood or anhedonia, causing significant
impairment in social, occupational or other important areas of
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L. Ben-Nun King David
References
1. Lyness JM, Kim J, Tang W, et al. The clinical significance of
subsyndromal depression in older primary care patients. Am J Geriatr
Psychiatry. 2007;15:214-23.
2. Cuijpers P, Smit F. Subclinical depression: a clinically relevant
condition? Tijdscr Psychiatr. 2008;50:519-28.
3. Cherubini A, Nisticò G, Rozzini R, et al. Subthreshold depression in
older subjects: an unmet therapeutic need. J Nutr Health Aging.
2012;16(10):909-13.
4. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
5. Williams JW, Hitchcock P, Cordes JA, et al. Is this patient clinically
depressed? JAMA. 2002;287:1160-70.
6. Pincus HA, Davis WW, McQueen LE. “Subthreshold” mental disorders:
a review and synthesis of studies on minor depression and other “brand
names”. Br J Psychiatry. 1999;174:288-96.
7. Marangell. LB. The importance of subsyndromal symptoms in bipolar
disorder. J Clin Psychiatry. 2004;65 Suppl 10:24-7.
8. Altshuler LL, Gitlin MJ, Mintz J, et al. Subsyndromal depression is
associated with functional impairment in patients with bipolar disorder. J
Clin Psychiatry. 2002;63:807-11.
9. Cuijpers P, Smit F. Subclinical depression: a clinically relevant
condition? Tijdscr Psychiatr. 2008;50:519-28.
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L. Ben-Nun King David
References
1. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
2. Koenig HG, George, L.K., Peterson, B.L, et al. Depression in medically ill
hospitalized older adults: prevalence, characteristics, and course of
symptoms according to six diagnostic schemes. Am J Psychiatry.
1997;154:1376-83.
3. Cohen-Cole S, Stoudemire A. Major depression and physical illness:
special considerations in diagnosis and biologic treatment. Psychiat Clin
North Am. 1987;10:1-17.
4. Kronke, K. A 75-year-old man with depression. JAMA. 2002;287:1568-
76.
5. Williams JW, Hitchcock P, Cordes JA, et al. Is this patient clinically
depressed? JAMA. 2002;287:1160-70.
6. Koenig HG, George LK, Peterson BL, et al. Depression in medically ill
hospitalized older adults: prevalence, characteristics, and course of
symptoms according to six diagnostic schemes. Am J Psychiatry. 1997;154:
1376-83.
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L. Ben-Nun King David
References:
1. Bebbington P, Tennant C, Hurry J. Adversity and the nature of
psychiatric disorder in the community. J Affect Disord. 1981; 3:345-66.
2. Roy A, Breier A, Doran AR, Pickar D. Life events in depression:
relationships to subtypes. J Affec Disord. 1985;9:143-8.
3. Shrout, P, Link B, Dohrenwend B, et al. Characterizing life events as
risk factors for depression: the role of fateful loss events. J Abnorm Psychol.
1989;95:460-67.
4. Mazure CM, Bruce ML, Maciejewski PK, et al. Adverse life events and
cognitive-personality characteristics in the prediction of major depression
and antidepressant response. Am J Psychiatry. 2000;157:896-903.
5. Beck AT. Cognitive model of depression. Journal Cogn Psychother.
1987;1:2-27.
497
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OUTCOME
perceived health, finding life not satisfying, and looking back over life
and finding it unhappy. Treatment options include antidepressants
(alone or in combination) and psychotherapy (4).
Screening surveys of depressive symptoms were conducted
among primary care patients at six sites in different countries.
Subjects aged 18 to 75 were recruited from participating primary
care facilities in Beer Sheva (Israel), Porto Alegre (Brazil), Melbourne
(Australia), Barcelona (Spain), St Petersburg (Russian Federation) and
Seattle (USA). Depressive symptoms were measured by CES-D. A
total of 18,489 patients were screened, of whom 37% overall (range
24-55%) scored ≥16 on the CES-D and 28% (range 17-42%) scored ≥
20. Overall, 13% reported current treatment for depression (range 4-
23%). Patients with higher depressive symptoms scores had worse
health, functional status, QOL, and greater use of health services
across all sites. Among those with a CES-D score ≥16, subjects
reporting treatment for depression were more likely than those
reporting no treatment to be satisfied with their health (except St
Petersburg), and have higher depressive scores. Higher depressive
symptom scores in primary care patients were consistently
associated with poorer health, functional status and QOL, and
increased health care use, but not with demographic variables (5).
An association between major and subsyndromal depression on
QOL and attitudes toward aging was examined in a large
international sample. A cross-sectional study assessed 4,315
responders in 20 countries from five continents. The study used the
WHOQOL Assessment for Older Adults, known as the WHOQOL-OLD;
the brief version of the WHOQOL instrument, known as WHOQOL-
BREF; and the Attitudes to Ageing Questionnaire. Even relatively
minor levels of depression were associated with a significant
decrease in all QOL domains and with a pattern of a negative
attitudes toward aging (overall WHOQOL-OLD R(2) change = 0.421).
QOL and attitudes toward aging scores were lower as depression
intensity is increased, even in subsyndromal levels (overall WHOQOL-
OLD mean scores of 97.7 vs. 86.4, p<0.001). This phenomenon
happened not only for clinically depressed individuals but also for
subsyndromic individuals (6).
QOL in depression could be of great value as an outcome
measure, especially in determining the effectiveness of treatment
strategies. However, for this aim to be accomplished, it is important
to clarify the relationship between QOL and a number of potentially
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L. Ben-Nun King David
References
1. Melartin TK, Rytsälä HL, Leskelä US, et al. Severity and comorbidity
predict episode duration and recurrence of DSM-IV major depressive
disorder. J Clin Psychiatry. 2004;65:810-9.
2. O'Leary D, Costello F, Gormley N, Webb M. Remission onset and
relapse n depression. A 18-month prospective study of course for 100 first
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L. Ben-Nun King David
References
1. Flint AJ. Generalized anxiety disorder in elderly patients:
epidemiology, diagnosis and treatment options. Drugs Aging. 2005;22:101-
14.
2. Kroenke K, Spitzer RL, Williams JB, et al. Anxiety disorders in primary
care: prevalence, impairment, comorbidity, and detection. Ann Intern Med.
2007;146(5):317-25.
3. Roy-Byrne PP, Wagner A. Primary care perspectives on generalized
anxiety disorder. J Clin Psychiatry. 2004;65 Suppl 13:20-6.
4. APA. Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Washington, DC: American Psychiatric Association, 1994.
5. Ben-Noun L. Mental disorder that afflicted King David the Great. Hist
Psychiatry. 2004;15(4):467-76.
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ABBREVIATIONS
VA Visual acuity
VEGF Vascular endothelial growth factor
VF Ventricular fibrillation
VI Visual impairment
VLBW Very low birth weight
WBC White blood cell
WHO World Health Organization
WHOQOL World Health Organization Quality of Life
WM Waldenström's macroglobulinemia
WMH-CIDI World Mental Health version of the
Composite International Diagnostic Interview
WWII World War Two
ZOL Zoledronic acid
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L. Ben-Nun King David
PICTURES
Boaz meets Ruth. Julius Schnorr von Carolsfeld. German, 1794 – 1872. Due to this
marriage, a son, Obed, the grandfather of King David, was born.