Hypoglycemic Coma in Anorexia Nervosa

Case
Lisa M.

Report and Review of the Literature

Rich, MD; Marc R. Caine, MD; James W. Findling, MD; Joseph L. Shaker, MD

\s=b\ Clinically significant hypoglycemia is an unusual complication of anorexia nervosa. We describe a 44-year-old woman with a
5-year history of anorexia nervosa who presented with hypoglycemic coma and eventually experienced sudden death. Biochemical studies showed suppressed levels of insulin, C peptide, and proinsulin during hypoglycemia; appropriate elevations of growth hormone and cortisol levels were observed,
suggesting that the hypoglycemia was related to severe malnutrition. Nine previously reported cases of severe hypoglycemia in
anorexia nervosa are reviewed (six of the patients involved also
died). The presence of severe hypoglycemia in anorexia nervosa
implies a grave prognosis and mandates aggressive medical and
nutritional therapy to improve the chance of survival.
(Arch Intern Med. 1990;150:894-895)

01 evere hypoglycemia is an uncommon manifestation of an

orexia nervosa. Although hypoglycemia does occur to a
moderate degree in protein calorie malnutrition,12 it is not
usually severe. We describe a woman with anorexia nervosa
who died after presenting with hypoglycmie coma. In addi
tion, we review nine previously reported cases of severe
hypoglycemia associated with anorexia nervosa.**
REPORT OF A CASE
A 44-year-old woman with a 5-year history of anorexia nervosa was
found unconscious in her home. Paramedics found her to have a blood
pressure of 60/42 mm Hg, a pulse rate of 40 beats per minute, and a
capillary blood glucose level of 1.1 mmol/L. After she was given 50%
dextrose intravenously, she rapidly regained consciousness. Her
hypotension resolved with administration of intravenous fluids.
Her family stated that for 2 months prior to admission she had
refused to eat solid food and that during the month prior to admission
she had become weak. Two months prior to admission she was
diagnosed with Mycobacterium avium-intracellulare. She was ini
tially treated with isoniazid, rifampin, and ethambutol hydrochloride;
however, because of hepatotoxicity, treatment with these medica
tions was discontinued and streptomycin sulfate therapy was
initiated.
On physicial examination, the patient was lethargic and markedly
emaciated, and appeared much older than her 44 years. Her tempera
ture was 32C, her pulse rate was 42 beats per minute, and her blood
pressure was 90/50 mm Hg. Her weight was 39 kg and her height was
168 cm. Her skin had a yellow tinge and multiple ecchymotic areas.
There was marked pitting edema in her lower extremities up to her

thighs.
The electrocardiogram revealed sinus bradycardia, low voltage,
and nonspecific T-wave changes. Routine laboratory studies revealed
the following values: sodium, 133 mmol/L; potassium, 3.8 mmol/L;
chloride, 93 mmol/L; carbon dioxide content, 27 mmol/L; creatinine,
44.2 pmol/L; albumin, 22 g/L; aspartate transaminase, 143 U/L (nor
mal, <45 U/L); alanine transaminase, 73 U/L (normal, <45 U/L);
alkaline phosphatase, 150 U/L (normal range, 50 to 136 U/L) ; biliru
bin, 24 pmol/L (normal, <26 pmol/L); prothrombin time, 13.6 sec-

Accepted for publication June 19, 1989.

From the Department of Medicine, St Luke's Medical Center and The
Medical College of Wisconsin, Milwaukee.
Reprint requests to Department of Medicine, St Luke's Medical Center, 2901
W Kinnickinnic River Pkwy, Suite 503, Milwaukee, WI 53215 (Dr Shaker).

onds (normal range, 11 to 13 seconds); and partial thromboplastin

time, 23.2 seconds (normal range, 19 to 33 seconds). Thyroid function
testing revealed the following values: serum thyroxine, 112 nmol/L
(normal range, 67 to 142 nmol/L); triiodothyronine resin uptake, 0.47
(normal range, 0.35 to 0.45); thyrotropin, 1.6 mU/L (normal range,
0.4 to 7.0 mU/L); and triiodothyronine, less than 4 nmol/L (normal
range, 0.6 to 2.8 nmol/L). The patient's serum cortisol level was 745
nmol/L and increased to 1490 nmol/L 30 minutes after 250 pg of
cosyntropin (Cortrosyn) was administered intravenously. A urine
screen for sulfonylureas was negative. Eight days after admission,
the patient's fasting serum insulin level was 30 pmol/L (normal range,
70 to 145 pmol/L) and her C peptide concentration was less than 85
pmol/L, at a time when her serum glucose level was 1.6 mmol/L Her
serum proinsulin level was less than 20 pmol/L. Her insulin autoanti
body levels were negative. Her serum growth hormone level was 10
pg/L. Her fasting serum acetone level was negative, and her hydroxybutyrate level was 100 pmol/L (normal, <400 pmol/L).
She was initially treated with 10% dextrose infusion, hydrocortisone, and warmed intravenous fluids. After her serum glucose level
peaked at 42.3 mmol/L, the 10% dextrose in water was changed to 5%
dextrose in saline and the patient was encouraged to eat on her own.
She refused treatment throughout her hospitalization. Nasogastric
feeding was attempted, but the patient removed a feeding tube and
refused further attempts at enterai or parenteral nutritional support.
She continued to have early morning bouts of severe but asymptom
atic hypoglycemia, with glucose levels of 0.56 to 2.28 mmol/L. She
died suddenly of cardiorespiratory arrest. A postmortem examina
tion was refused.
.

COMMENT

This report describes profound hypoglycemia and death in

with anorexia nervosa. The hypoglycemia in our
patient was not associated with hyperinsulinemia. Immuno
reactive insulin and C peptide levels were appropriately sup
pressed.7 Other causes of hypoglycemia, such as adrenal or
pituitary insufficiency, were excluded. Although there was
evidence of liver dysfunction, this did not seem severe enough
to explain profound hypoglycemia. The low triiodothyronine
level observed in our patient is consistent with decreased
conversion of thyroxine to triiodothyronine as seen in starva
tion or acute illness and does not suggest hypothyroidism.8
The hypercortisolemia seen in our patient is a consistent
finding in anorexia nervosa.9"11
To our knowledge, there have been nine previous reports of
anorexia nervosa with severe hypoglycemia. The data from
these cases and our case (patient 10) are summarized in the
Table. Hyperinsulinemia and hypoadrenalism were excluded
in four of the previously reported cases. None of the patients
had any tumors of endocrine glands on autopsy. The mean age
of the patients at presentation was 34 years, while the mean
age at onset was 23 years. On average, these patients were
older at onset of anorexia nervosa than those previously
described (age range at onset, 13 to 17 years).81112 Seven ofthe
10 patients died. Of note is that the three survivors were 16,
23, and 14 years of age at onset, while the average age ofthose
who died was 26 years at onset and 38 years at death. Eight of
a woman

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Clinical Data on Patients With Anorexia Nervosa and Severe Hypoglycemia

Source, y
Elias and Gwinup,31982

Ratcliffe and Bevan,41982

Patient No./Age, y/
Age at Onset, y/Sex/Weight, kg

Outcome

Glucose,
mmol/L

1/23/18/F/38.0

Death: respiratory
arrest

0.8

2/60/30/F/25.0

Death:
Death:

pneumonia
pneumonia

0.8

3/32/30/F/24.0
6/18/16/F/29.5

Survived:

1.4

Albumin,

g/L

Cortisol,
nmol/L

Insulin,

pmol/L

29

"Low"

1020

30

770

<30

<1.0

35

>1340

Undetectable

<1.0

24

>1340

Undetectable

1.2

24

1.0

20

pneumonia,
congestive heart
failure

Zalin and Lant,51984

Copeland and Herzog,61987

Present case

7/27/24/M/38.5

Death: pulmonary
edema

4/57/27/F/22.5

Death: miliary
tuberculosis

5/27/23/F/26.5

Survived:

8/28/14/F/19.0

Survived:

9/26/13/F/31.4

Death:

0.8

28

Death: sudden

1.1

22

10/44/39/F/39.0

sepsis

pneumonia
pneumonia

the 10 had bouts of serious infection, and in four infection was

the cause of death. Three others died of cardiorespiratory
causes. These patients were usually hypoalbuminemic. Al
though hypoalbuminemia is not common in patients with
anorexia nervosa, hypoalbuminemia and fatal hypoglyce
mia213 are seen in kwashiorkor. Presumably this reflects the
severity of malnutrition.
Hypoglycemia appears to be a poor prognostic indicator in
anorexia nervosa. This is not surprising in view of similar
findings in malnourished children with kwashiorkor.2" In
1967 Kerpel-Fronius and Kaiser14 reported that "low fasting
sugar levels reflect the severity and the prognosis of malnu
trition with higher fidelity than do changes in any other
metabolic parameter. " Wharton2 reported that moderate hy
poglycemia is common in kwashiorkor, and of little clinical
significance, but profound hypoglycemia (glucose, <1.1
mmol/L) is rare, may be fatal, and is often associated with
hypothermia, coma, and infections. Several other factors,
including length of illness, lower body weight, and older age,
are also associated with a poor prognosis in anorexia ner

vosa.1518

The precise cause of severe hypoglycemia in the setting of

starvation is still uncertain. The profound hypoglycemia im
plies that hepatic glycogen reserves as well as gluconeogenic
substrates are depleted. This statement is supported by the
lack of stainable glycogen in the liver on autopsy4 and by the
sensitivity to short-term fasts in our patient and in malnour
ished children.2 Alternatively, these patients may be unable
to mobilize gluconeogenic substrates. In addition, the lack of
ketosis in our patient is consistent with markedly depleted fat
stores. Interestingly, there is evidence that starvation leads
to low insulin levels that are insensitive to both glucose and
amino acid infusion.19"21 Also, carbohydrate intolerance has
been noted in anorexia nervosa and starvation.1 This effect
may account for the hyperglycemia that occurred when our
patient was given 10% dextrose. We believe that the presence
of severe hypoglycemia in patients with anorexia nervosa
suggests a grave prognosis and mandates aggressive psychi
atric, medical, and nutritional therapy in an attempt to im
prove the chance of survival.

0.4

740

30

References
1. Hadden DR, Belf MD. Glucose, free fatty acids and insulin interrelations
in kwashiorkor and marasmus. Lancet. 1967;2:589-592.
2. Wharton B. Hypoglycemia in children with kwashiorkor. Lancet.

1970;1:171-173.

3. Elias AN, Gwinup G. Glucose-resistant hypoglycemia in inanition. Arch

Intern Med. 1982;142:743-746.
4. Ratcliffe PJ, Bevan JS. Severe hypoglycemia and sudden death in anorexia nervosa. Psychol Med. 1982;15:679-681.
5. Zalin AM, Lant AF. Anorexia nervosa presenting as reversible hypoglycemic coma. J R Soc Med. 1984;77:193-195.
6. Copeland PM, Herzog DB. Hypoglycemia and death in anorexia nervosa.

Psychother Psychosom. 1987;48:146-150.

7. Fajans SS, Floyd J. Fasting hypoglycemia

in adults. N

Engl

J Med.

1976;294:766-772.
8. Schwabe AD, Lippe BM, Chang RJ, Pops MA, Yager J. Anorexia nervosa. Ann Intern Med. 1981;94:371-381.
9. Gold PW, Gwirtsman H, Avgerinos PC, et al. Abnormal hypothalamic\x=req-\
pituitary-adrenal function in anorexia nervosa. N Engl J Med. 1986;314:1335\x=req-\
1342.
10.

Nakagawa K, Matsubara M, Obara T, Kubo M, Akikawa K. Responses of

pituitary and adrenal medulla to insulin-induced hypoglycemia in patients with
anorexia nervosa. Endocrinol Jpn. 1985;32:719-724.
11. Warren MP, Vandewiele RL. Clinical and metabolic features of anorexia
nervosa. Am J Obstet Gynecol. 1973;117:435-448.
12. Herzog DB, Copeland DM. Eating disorders. N Engl J Med.
1985;315:295-302.
13. Kahn E, Wayburne S. Hypoglycaemia in patients suffering from advanced protein malnutrition (kwashiorkor). Proc Nutr Soc S Afr. 1960;1:21-23.
14. Kerpel-Fronius E, Kaiser E. Hypoglycemia in infantile malnutrition.
Acta Paediatr Scand Suppl. 1967;172:119-127.
15. Theander S. Anorexia nervosa: a psychiatric investigation of 94 female
patients. Acta Psychiatr Scand Suppl. 1970;214:1-194.
16. Hsu LKG, Crisp AH, Harding B. Outcome of anorexia nervosa. Lancet.
1979;1:61-65.
17. Halmi K, Brodland G, Loney J. Prognosis in anorexia nervosa. Ann

Intern Med. 1973;78:907-909.

18. Morgan HG, Purgold J, Melbourne J. Management and outcome in
anorexia nervosa: a standardized prognostic study. Br J Psychiatry.

1983;143:282-287.
19. Vara E, Tamarit-Rodriguez J. Glucose stimulation of insulin secretion in

islets of fed and starved rats and its dependence on lipid metabolism. Metabolism. 1986;35:266-271.
20. Blickle JF, Reville P, Stephan F, Meyer P, Demangeat C, Sapin R. The
role of insulin, glucagon, and growth hormone in the regulation of plasma
glucose and free fatty acid levels in anorexia nervosa. Horm Metab Res.

1984;16:336-340.

21. Brodows RG. Starvation enhances the ability of insulin to inhibit its own
secretion. Metabolism. 1985;34:53-56.
22. Slone D, Taitz LS, Gilchrist GS. Aspects of carbohydrate metabolism in
kwashiorkor. Br MedJ. 1961;1:32-34.
23. Kanis JA, Brown P, Fitzpatrick K, et al. Anorexia nervosa: a clinical
psychiatric and laboratory study. Q J Med. 1974;43:321-338.

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blog.mycology.cornell.edu

http://blog.mycology.cornell.edu/2006/11/22/i-survived-the-destroying-angel/

I survived the Destroying Angel

This memoir of a near-fatal mushroom poisoning was written by our most fortunate guest, Richard Eshelman. Happy
Thanksgiving, all.

I. That Fateful day July 18th, 2006

Tuesday, July 18th, 2006. It was a balmy day in Ithaca, New York. I went for a walk after work to sit and meditate at
my favorite spot near a waterfall in Upper Buttermilk State Park. Its really nice to have such a huge backyard cared
for by the public like Upper Buttermilk. I feel privileged.
Before I left my private meditation area I did a standing STARS (Somatics Transformation and Restorative Systems)
exercise called Aligning the Three Tan Tiens. Something inside me made me feel invincible. You know that feeling
you have when you are young and feel invincible? Well, as I walked out of the wooded area I was in, I found some
young mushrooms. Their caps were hanging down like closed umbrellas. I mistook them for inky caps (Coprinus
spp.) even though I spotted an Amanita nearbyits cap was fully open, and not hanging down. Thinking back, I
should have been more suspicious as mushrooms do grow in colonies.
I took three home with me. I couldnt find my Mushroom book, was in a hurry,
so I trusted my judgment, fried them up in olive oil, and ate them as a side
dish. I should have recognized then that they werent inky caps, because
inky caps exude a black substance when you fry them.
They honestly did not taste that good, rather bland in my opinion. I thought to
myself, Gee, I dont think Ill ever pick and eat these again. (Little did I know
the truth of my thought at the time).
I went dancing afterward, and bragged to my friends that I had picked and
eaten some wild mushrooms for dinner. A friend asked me Were they all
white?
I said Yes.
She scolded me, saying, My mother told me never to eat an all white
mushroom.
At that point, I got concerned. I covered it up by saying, Im OK, I know what
Im doing and I dont feel sick.
I got home. I was hungry, so I ate some nachos and humus and drank some
apple juice before going to bed around 11 p.m. I still felt fine, so I wasnt
worried.
The crack of dawn that time of year is early, sometime between 4:30 and
5:00. Its a really neat time if youve never experienced itthe silence is
almost unbearable. To most busy people it is unbearable. There is nothing to
drown out the chatter in the head. City folks usually find it uncomfortable in
contrast to the noise of the city. Ive become accustomed to awakening with the light. This morning I woke a little
earlier than usual. I couldnt quite tell whether it was still night or just breaking into the day.
I felt queasy. It was the same feeling I had when I had food poisoning. Before I had any more time to assess my state,
I realized I needed to get to the bathroom. I barely made it to the royal throne when I started heaving my guts out. The

vomiting reflex was strong. The pressure of the strong contractions forced stuff out both ends of the GI tract,
uncontrollably. I had a severe case of vomiting and diarrhea. At that point, deep down I knew I had made the big
mistake: I HAD EATEN AMANITA VIROSA, AKA, THE DESTROYING ANGEL. 1
For the next three hours, I was making trips constantly from my bed to the
bathroom. I was still in denial. My housemate asked me the first time I was
up Are you OK? I said Yes, I was just sick. By the time 7:30 had rolled
around, I had talked to my girlfriend, called in sick to work and still had not
mentioned that I thought it was Amanita poisoning. Finally, my housemate
again asked me what was going on. I responded saying I think I
accidentally poisoned myself with some bad mushrooms last night.
He said Maybe you should go get checked out at the local Convenient
Care Center.
I silently thought to myself, Yeah, If I go there, Ill be sitting and waiting and
by the time someones sees me, Ill be dead.
I found my mushroom book and looked up the symptoms for Amanita
poisoning: vomiting and diarrhea or severe constipation 6-8 hrs after
consumption.2 Oh, and by the way, its now destroying your liver and 50 to
80 percent of the people who ingest Amanita DO NOT SURVIVE! At that
point, I knew I was in deep, deep doo doo and in for the biggest fight of my
life, for my life.
I called the Poison Control Center 800-222-1222.
They suggested I go back to the area where I had picked the mushrooms
and get one to take with me for identification, then get myself to the local
emergency room. I went back to the area and picked the one mushroom I
had left because I thought it was Amanita. I also took a piece of stem I had
thrown into the garbage the night before.
At this point, as long as I didnt eat or drink anything I could get around. I
had pretty much eliminated everything from my GI tract.
I got in my car to drive myself to the emergency room. Three thoughts went
through my head as I prepared to leave:
1. Should I go back into the house and say goodbye to my cats? My response: No you idiot, you dont have time
for that!
2. If I didnt have health insurance, would I go to the emergency room knowing I was just about to wipe out my
cash reserve? Luckily I didnt have to ponder that question as I had insurance and felt very fortunate. But what
about someone who didnt? Would they deny their symptoms and just consider it food poisoning? What would
have been the end result? They probably would just start to feel better and then keel over from liver failure.
Amanita will fool you that way.
3. My last thought was Take one last look around you, because you may never be back here again. I did, and
left without telling anyone where I was going.

II. The Emergency Room

Wednesday, July 19th. I arrived at the ER of Cayuga Medical Center about 9:15 a.m. I went in and walked straight up

to the receptionist. She was on the phone with someone. She obviously was in a discussion with someone about
some problem and it wasnt going to be anytime soon that she could get off the phone. I waited patiently thinking, I
dont want to make a scene. Nevertheless, I didnt understand why she couldnt put the person on hold while she
addressed a new emergency room client.Finally, around 9:30, she got off the phone and asked What can I do for
you? I explained to her that I felt I had accidentally poisoned myself with some poisonous mushrooms. She asked
whether my records were at the hospital. I said yes. She checked my name and found I indeed was registered and
my insurance information was current. She asked me to be seated and informed me that someone would be with me
shortly.
I expected that someone would be out to see me within a minute or so since I had informed them that I suspected
mushroom poisoning. Instead, time dragged on. I kept thinking, just stay calm and collected. Finally, after waiting
another 20 minutes, someone came to get me.
Its amazing to me. Most people when they know they are dying think of what they didnt do or what they should have
done. In this case, all I could do was watch and monitor time like a hawk. My concern was I needed help NOW!
ASAP! But, I also knew I needed to stay calm so as not to create a panic situation.
I dont remember much once I was admitted other than them taking vital signs and getting the info they needed
regarding the poisoning and making sure that I was the only one involved. They kept me comfortable while someone
took the mushroom to Cornell for identification. They started an IV to replenish my fluids.
While waiting, I finally took the time to write down some phone numbers for people to call in case I didnt make it. I
also made a few more trips to the restroom.
The Emergency room staff came back saying a Cornell Mycologist (Kathie Hodge) had identified it. It was definitely
Amanita virosa mushroom poisoning.1
The first thing they did was make me drink a milk shake size container of charcoal. Have you ever seen a charcoal
drink? It is as black as you can imagine. I often practice the Bates palming eye improvement exercise. During this
exercise you rub your palms together, then place them over your eyes, and imagine the blackest black you can
imagine. This was the blackest black I had ever seen! It was really hard to get past the thought and just drink it. It had
a chalky flavor.
About a half hour later. The ER staff informed me they had called Bangs Ambulance and they were present, waiting to
transport me to Strong Memorial Hospital in Rochester, New York.
Needless to say, the charcoal drink did not stay down long. It would be at least another half hour before we left
because I had to first go to the restroom to honor the vomiting reflex. My body was still reacting to anything put into
my stomach and was rejecting the charcoal drink. Its probably a good thing I made the ambulance crew wait and
went to the bathroom when I did or I would have been upchucking in the ambulance all the way to Rochester.
Before leaving, I also made a few phone calls; to work, letting them know what was going on and that I probably
wasnt going to be available to work the weekend, to my housemate, and to my girlfriend Julie. Then I was strapped in
a gurney, loaded in the ambulance and on my to Rochester.
The trip to Rochester from Ithaca was uneventful. The attending ambulance technician comforted me all the way.
What I do remember the most was watching the clock above the rear doors. We left Ithaca around 3:00 p.m. in the
afternoon and arrived at Strong Memorial in Rochester around 5:37 p.m.
I was being sent to Strong Memorial because they had the only liver transplant unit in upstate New York. The
treatment of choice is often liver transplantation. With early diagnosis, another experimental treatment includes
massive doses of penicillin to stimulate the livers defenses. This was the treatment I would receive with the option to
transplant if my liver failed.

III. Strong Memorial Hospital

Upon our arrival at the Emergency Room, I was surprised to find they were ready to accept me without any
paperwork. All the information about me had already been transmitted to them and I was admitted directly to the
Emergency Room.The ER room there is impressive. It has a semicircular console area facing individual double
occupancy booths. I was in the first one upon entering the ER room. I called Julie on my cell to let her know what had
happened. She wanted to come up then, but, I insisted she wait till the next day. She insisted on letting my family
know.
I was having blood drawn every 2 hours to monitor the buildup of toxins in my liver and kidneys. They hooked me up
to a transfusion stand and monitors. They were preparing to run me through all the tests they needed in order to
prepare me for a transplant in case my liver failed. They were giving me huge dose of penicillin plus fluids to rehydrate
me.
Being sick as a dog with constant vomiting and diarrhea is no fun! I had a diaper on. I felt helpless. I felt humbled.
I was given a bed in the transplant unit. Taken for x-rays. Back to the room. Given a drink in order to do a CAT scan. It
was a liter of pink liquid. I drank it in small amounts and even though they had given me something to shut down the
vomiting, it just wasnt working. Shortly after getting it all down, it came right back up. They gave me another liter.
Again, I slowly started sipping an 8 oz glass every 15-20 minutes. Eventually, I almost got it all down and felt I could
not drink another glass without vomiting again. They wheeled me down to the CAT scan machine and transferred me
onto the bed that slides into the large instrument. As they started to roll me in, I yelled Back me out, back me out! Im
going to throw up again!
They pulled me out of the cylinder and got me a bedpan just in time. Im glad I didnt ruin their large instrument puking
inside it.
After the CAT scan, I was taken back to my room in the transplant unit. There was a constant droning sound that I
couldnt figure out and constant announcements over the PA system. It was really difficult sleeping with the noise and
being awakened all the time for blood work. (They were drawing blood every 4 hours to monitor my liver and kidneys).
Its not a place conducive to good sleep. I just couldnt get a decent nights sleep.
My girlfriend Julie and my housemate Mark visited the next day. Julie had sent out an email to the dance community
informing them of my situation, and had let my family know of my happenstance. Everyone was praying for me. My
sister even had a bus load of kids praying for me while on their way to a youth conference in Colorado. All were
worried about me. The focus was on me. I felt embarrassed. I had made a critical error in judgment and everyone
knew about it.
Eileen, my friend who had first alerted me to my possible dilemma, saw the email and discussed it with her friends.
One of them had just read about an alternative treatment. She went home at lunch and brought it to Eileen, who faxed
it to the Doctors in Rochester. The doctors say they never received it.
The treatment uses Lipoic Acid. 3 It has also been shown to be useful in the treatment of liver problems such as
hepatitis B and C, autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholagitis. The article is from
Dr Whitakers health newsletter Vol.16, No.7, p6.
By now the doctors were coming around asking me questions in order to assess my mental capacity. If my liver went
into failure, I would not be lucid. Without sleep, I found it hard to remember what day it was as everything seemed to
blend into one long event.
I work as an accelerator operator in high energy physics and am an avid amateur dancer, a certified massage
therapist and Hanna Somatic Educator. When they asked me about this and I told them, they thought I had lost my
sanity. They had to ask Julie and Mark if I was telling them the truth. How many people do you know that earn their

living as an accelerator operator?

At one point a doctor came in and asked me What is Pi? I wasnt quite sure how to respond as I didnt know if he
was asking about Pi, or pie. My question to him was Which pi/pie, pi the mathematical term or pie the thing you eat?
His response, Pi the mathematical term. I proceeded to tell him about its relationship to a circle and its origins. I
stumbled a little and thought maybe I really was losing my sanity.
Thursday, Julie was with me most of the day. I was taken for tests of my cardiovascular system. The stress test. They
had to do it chemically as I was unable to do it physically on the treadmill. A friend from my mediation group visited,
who ironically worked with the wife of the transplant surgeon, Dr. Peter Abt.
Thursday evening they took me into intensive care. Before wheeling me into intensive care, Dr Abt visited me. I had to
sign papers giving Julie power of attorney etc. He informed me they were ready to give me a transplant if I needed it. I
remember grabbing the cross on my neck chain and praying silently to myself, Dear Lord, let me keep my liver. I do
not want to live with someone elses liver the rest of my life and have to deal with the medical expenses to keep my
body from rejecting it.
I had put my fate in the hands of my Lord and Savior Jesus Christ. The 23rd psalm was running through my mind as
well. The Sunday morning meditation group I attend had just recited it the previous Sunday.
The thought that these guys might be trying to get my liver for someone else did cross my mind. I let it go. Instead, I
did a visualization exercise. I imagined my liver. I saw the color black (it should have been green). My kidneys, ocean
blue. I smiled to both of them. (For more info on visualization, I recommend you read Awaken the Healing Light of the
Tao by Mantak and Maneewan Chia.)
Somehow, in the middle of the night my liver numbers peaked and started coming down. I wasnt out of the woods yet,
but it looked like I was going to recover without a liver transplant. I was wheeled back to my room in the liver
transplant unit Friday morning.
Members of my family visited that day: Jim, my oldest brother, Tim and his wife Kim, and my baby sister Betty Sue.
They brought flowers and balloons wishing me well and a happy birthday balloon as my birthday was coming up. We
all held hands and my sister in law, Kim, prayed for my recovery. I was also receiving prayers and get well wishes
from the dance community.
All along, I had hoped to be out of the hospital by Friday to work my weekend shift. All along, the doctors told me I was
going to be there for a while. It was clear I wasnt getting out Friday.
My liver and kidneys had taken a big insult, as had my gastrointestinal tract. Although my liver numbers were coming
down, the kidney numbers still hadnt peaked. I would be in the hospital another week to make sure I would not need
kidney dialysis.
They took the tube out of my nose going to my stomach on Friday. It had been quite annoying as it gave me the
hiccups. I could almost predict when the next one would come along. It was that periodic. Even after removing the
tube, the hiccups lingered for another couple hours.
By Sunday, all the tubes in me had been removed. Julie was there for me as well. She got me out of bed that evening
and we took a short walk around the nurses station. We did a little salsa together. I was dancing again! The nurses
applauded.
I still found it hard to sleep. Now, at least, they were only drawing blood every 4 hours. That night another patient was
in my room who was there to receive a transplant. He was constantly yelling out for help from the nurses.
Sunday night/Monday morning I finally fell into a deep dream sleep. I saw a white church glistening in white light. A

power cord glowing red was feeding power to keep it lit up. I was riding in a black limo and sparks flew from behind
the car as we drove over the power cord. The next thing I knew, I was next to my grandfathers grave. I was
wondering why I was there when I was awakened by the nurse for another blood sample.
When people ask me whether I had any near-death experiences, I usually relay my dream to them. I am here by the
grace of God! I feel so lucky and yet fortunate. I found out that of three people admitted in 2006 to Strong Memorial
with Amanita poisoning, I am the only one to have survived; 66% died.
Why did I live and the rest not live?
Was it the amount of toxin?
Was it that I knew what had happened to me and sought care and help quickly?
Was it my meditation/visualization and somatic self care/self help practice?
Was it the prayers of my friends and family and my faith?
Was it the doctors care? One of them said it was a miracle!
Simply said, I dont know that it was any individual thing, but a combination of everything.
Monday, July 24th was my birthday. I could not have received a better gift than the gift of life. Throughout my life, I
have been traumatized. I was born a blue baby, fell out of a silo at the age of 12, etc. I could go on, but the important
thing is, I am a survivor. I love catsmaybe I have nine lives!
How did I get in such a mess? In retrospect, I considered the possibility that I had subconsciously poisoned myself.
But in reality, the mistake I made was just not taking the time to positively identify the mushrooms I had picked
before ingesting them.

The Truth
Most victims of life-threatening mushroom poisoning in North America are people from Southeast Asia;
Laos, Cambodia, Thailand, Viet Nam. They apparently mistake Amanita for edible Paddy-Straw
(Volvariella volvacea) mushrooms. The two are similar in several ways; cap color, size, and the white
cup around the base of the stalk, but different in others (for example, the Paddy-Straw has a pink
spore print, the Amanita*, a white spore print; and the Amanita* has a partial veil). The Paddy Straw
mushroom occurs in tropical and temperate areas worldwide, and is especially common in Southeast
Asia; the Amanita, alas, does not occur in Southeast Asia, so folks from that part of the world are
unaware of the lethal look-alike.
Millions of North Americans pick and eat wild mushrooms every year, without as much as a belly ache.
Are they experts? Yes! At least, they are experts on the edible wild mushrooms they know. Either
their parents or grandparents taught them how to identify morels, or puffballs, or meadow mushrooms,
or they have a good field guide and they read it or both.
No one with a reasonable understanding of the importance of properly identifying mushrooms with a
serious awareness that some species are fatally toxic falls victim to the Destroying Angel*. The folks
who eat Destroying Angel* do not use field guides: they just pick the damned things and eat them. No
trip to the library. No reading. No spore prints. No idea what a partial veil is or what gill attachment
means.
So Is it really dangerous to eat wild mushrooms?
How dangerous is it to drive a car? If youre drunk or careless, it is VERY dangerous; if youre sensible
and pay attention, it is reasonably safe.

Consider this: Would you pick and eat an unfamiliar berry simply because it looked good? Of course
not. Finding, identifying, preparing, and eating wild mushrooms can be a delightful pastimeIF it is
done intelligently.
Otherwise, it is a terrible accident waiting to happen.
* I took the liberty of changing the name from deathcap to destroying angel or Amanita in the text
above. Its worth noting that Amanita phalloides most closely resembles the paddy-straw mushroom;
A. virosa less so.
Excerpted with permission from David Fischers American Mushrooms.

Epilogue
It was another week after leaving of the hospital before I felt comfortable eating and not being close to a bathroom. I
was back to work within two weeks of being released from the hospital. A month later, I was pretty much back to full
strength. My liver numbers normalized early, pretty much by the time I had left the hospital. It would be another month
and a half before my kidney numbers normalized.The liver is a remarkable organ. It is the only organ that can
regenerate itself. The kidneys are a different story. There is probably some permanent damage there but not sufficient
to require any long term care. People often donate and live with just one kidney.
I did have some strange thoughts during my recovery at home. Im assuming they were just lingering effects of the
toxins in my system. In general, Ive made a complete recovery and expect no long term effects. I am grateful to be
alive and feel very lucky. Im also grateful for my training in Hanna Somatic Education. It felt great to get back home
and in the routine of practicing my somatic exercises, exploring, and able to be comfortable in my body again. It was
like coming home to my body as well. I encourage everyone to get a copy of Thomas Hannas book: Somatics:
Reawakening the Minds Control of Movement, Flexibility, and Health or to visit the Hanna Somatics website.
Richard Eshelman can be contacted via phone at 607-280-6788, or by email at re16@cornell.edu or
upstatehse@aol.com.
A Special Thanks to Kathie Hodge for encouraging me to write this.
1. Editors Note: Amanita virosa and Amanita bisporigera are treated as two separate species by most
mycologists, but their appearance and effects are quite similar, and the names have sometimes been used
interchangeably. The Editor follows the authoritative example of Rod Tulloss and Zhu-liang Yang in treating
northeastern North American destroying angels as Amanita bisporigera, whereas Amanita virosa is a strictly
European species. There is some satisfaction in this, since A. bisporigera was described from the Ithaca area
exactly 100 years ago by my predecessor at Cornell, George F. Atkinson. This is a centennial poisoning!
2. Editors Note: For more on Amanita toxicity and recognition please see our Destroying Angels post.
3. Editors Note: Alpha-lipoleic acid, also known as thioctic acid, was advocated for treatment of Amanita
poisoning in the 1950s and 1960s, but subsequent studies failed to find a therapeutic effect, according to D.R.
Benjamin (1995, Mushrooms: Poisons and Panaceas. W.H. Freeman).
Photos: K.T. Hodge (young Amanita), and K.E. Loeffler (the mature Amanita that Richard brought with him to the
hospital for identification).

CASE STUDY

35-YEAR-OLD FEMALE WITH HIGH BLOOD CHOLESTEROL

AND FAMILY HISTORY OF HEART DISEASE

Roger S. Blumenthal, MD

HISTORY
Mrs. Gordon is a 35-year-old woman whose
mother died from heart disease at the age of 55.
She currently has 2 children and is planning a
pregnancy in the near future. On evaluation,
blood pressure is 130/80 mm Hg and body mass
index is 27.

LABORATORY RESULTS
Mrs. Gordons fasting lipid profile includes a total
cholesterol level of 300 mg/dL; the low-density
lipoprotein (LDL) level is 220 mg/dL, the high-density lipoprotein (HDL) level is 40 mg/dL, and the
triglyceride level is 200 mg/dL. Fasting blood glucose
level is 110 mg/dL. Liver enzyme assessment reveals an
alanine aminotransferase value of 25 U/L and an
aspartate aminotransferase value of 30 U/L.
INTERVENTION
Mrs. Gordons LDL level is more than double the
goal of 100 mg/dL recommended in the clinical
guidelines issued in May 2001 by the National
Cholesterol Education Program (NCEP) Adult
Treatment Panel (ATP III). The HDL level is low,
and below the cutpoint of 40 mg/dL. Moreover, her
family history of heart disease further increases her
own risk for coronary heart disease. Clearly, treatment for her hypercholesterolemia is warranted.
However, because Mrs. Gordon is considering
another pregnancy, the use of statins is contraindi-

Advanced Studies in Medicine

cated. In an effort to achieve NCEP goals, Mrs.

Gordon is advised to begin a regular exercise program, to adopt a low-fat diet, and to substitute a
plant sterol enriched margarine (Benecol or Take
Control) for butter. In addition, she is to start therapy with colesevelam at a dose of three 625-mg
tablets twice daily. At the 6-week checkup, the
patients LDL has decreased to 170 mg/dL but the
HDL and triglyceride levels remain unchanged.
FOLLOW-UP
After 2 months of the prescribed interventions,
Mrs. Gordon comes in for a follow-up examination.
At this visit, the LDL level is further decreased to 130
mg/dL, and the HDL level is increased from 40 mg/dL
to 50 mg/dL. Triglycerides are decreased from 200
mg/dL to 160 mg/dL. Total cholesterol is now 216
mg/dL, a considerably improved lipid profile. She is
maintained on the current drug regimen and advised
to increase exercise to brisk walking 4 times a week and
to make additional dietary changes.
DISCUSSION
Mrs. Gordon presents with hypercholesterolemia.
Lipid altering systemic drugs are not advisable because
she is considering another pregnancy. With a family
history of heart disease, optimization of the lipid profile is highly desirable.
Numerous clinical studies have demonstrated the
efficacy of bile acids in reducing LDL, particularly in
individuals who have heterozygous familial hypercholesterolemia. Although the combination of a statin and
a bile acid resin have been shown to slow the progression of coronary disease in clinical trials such as the
Familial Atherosclerosis Treatment Study and the

167

CASE STUDY

Cholesterol Lowering Atherosclerosis Study, such

combination therapy was not feasible for this patient
because she was planning a pregnancy. Therefore, a
bile acid resin was prescribed to achieve an improved
cholesterol profile. The conventional bile acid resins,
cholestyramine and colestipol, are frequently accompanied by gastrointestinal side effects, which would
be particularly undesirable during pregnancy; therefore, a newer formulation was prescribed for this
patient. Colesevelam, a bile acid-binding polymer,

168

has better gastrointestinal tolerance at full dose (3.8 g

daily) and is expected to achieve a 15% to 20% reduction in the LDL level. For Mrs. Gordon, colesevelam
reduced total cholesterol levels to 216 mg/dL, with the
LDL 130 mg/dL, the HDL 50 mg/dL, and the triglyceride level 160 mg/dL.
Following her pregnancy and lactation period, she
will be further evaluated. At that point, a low-dose of
a statin may be added in combination with her current
colesevelam therapy. She will likely need lifelong lipidlowering therapy to achieve her target values.

Vol. 2, No. 5

March 2002

NOTES

Advanced Studies in Medicine

169

PATIENT NO. 3: PLE IN THE SETTING OF LYMPHOMA

A 68-year-old man was in good health until December 2006 when he developed generalized fatigue associated
with a 10-pound weight loss. The following month, his weight began to rise and he developed progressive
abdominal distension. An evaluation by his local physician demonstrated the presence of ascites. He was begun on
diuretics and referred to our institution for further evaluation. He was found to have ascites with substantial
peripheral edema and muscle wasting. Laboratory evaluation revealed a mildly increased serum creatinine and
mild proteinuria. Both serum albumin and total protein were decreased at 2.4 and 5.1g per 100ml, respectively. A
computed tomography scan of his chest, abdomen, and pelvis demonstrated a large left pleural effusion, a moderate
amount of ascites, and extensive mesenteric lymphadenopathy that was felt not to be pathologically enlarged.
Diagnostic paracentesis was notable for a serum-ascites albumin gradient of 0.9g per 100ml. Additional testing
did not demonstrate a renal, cardiac, or liver cause of the anasarca and severe hypoalbuminemia; however, he was
noted to have a markedly elevated CA-125 level (5,310U/ml; normal, <35U/ml). This prompted the performance
of a diagnostic laparoscopy with peritoneal and mesenteric biopsies. The laparoscopy was normal as were the
biopsies.

Despite an absence of gastrointestinal complaints, colonoscopy, upper endoscopy, and video capsule endoscopy
were then performed, all of which were normal including random biopsies from the duodenum and colon. Fecal
A1AT clearance was found to be markedly abnormal at 299mg per 100ml (normal, <54mg per 100ml),
consistent with PLE. Fat malabsorption was also found to be present (29g/day; normal, 27g/day). Numerous
micronutrient deficiencies were identified including copper, zinc and selenium, and vitamins A and D. Given the
finding of PLE without a defined cause, an excisional lymph node biopsy was performed and revealed chronic
lymphocytic leukemia/small lymphocytic lymphoma. This was confirmed on a subsequent bone marrow
examination. He was subsequently treated with chemotherapy and his ascites and edema were gradually resolved.
At his last follow-up visit in May 2008, his ascites and edema were absent, albumin level was normal, previous
micronutrient deficiencies were resolved, and a repeat fecal fat collection was nearly normal at 10g/day. Fecal
A1AT clearance was not repeated.