Professional Documents
Culture Documents
Asthma
Classification and external resources
Despite this, with proper control of asthma with step down therapy, prognosis is generally good.
[13]
Contents
[hide]
1 Classification
o 1.1 Brittle asthma
o
1.5 Occupational
3 Causes
o
3.1 Environmental
3.2 Genetic
3.4 Exacerbation
4 Diagnosis
o
5 Prevention
6 Management
o
6.2 Medications
6.3 Other
7 Prognosis
8 Epidemiology
o
8.2 Variability
9 History
10 References
11 External links
[edit] Classification
Asthma is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the
airways in which many cells and cellular elements play a role. The chronic inflammation is
associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing,
breathlessness,chest tightness and coughing particularly at night or in the early morning. These
episodes are usually associated with widespread, but variable airflow obstruction within the lung
that is often reversible either spontaneously or with treatment".[14]
Clinical classification of severity[3]
Severity in
patients 12
years of age [15]
Symptom
frequency
Nighttime
symptoms
Intermittent
2 per week
2 per month
Mild persistent
Moderate
persistent
Daily
Severe persistent
Throughout
the day
>30%
Daily
<60%
>30%
Several times
per day
While asthma is classified based on severity, at the moment there is no clear method for
classifying different subgroups of asthma beyond this system. [16] Within the classifications
described above, although the cases of asthma respond to the same treatment differs, thus it is
clear that the cases within a classification have significant differences.[16] Finding ways to
identify subgroups that respond well to different types of treatments is a current critical goal of
asthma research.[16]
Although asthma is a chronic obstructive condition, it is not considered as a part of chronic
obstructive pulmonary disease as this term refers specifically to combinations of disease that are
irreversible such as bronchiectasis, chronic bronchitis, and emphysema.[15] Unlike these diseases,
the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic
inflammation of the lungs during asthma can become irreversible obstruction due to airway
remodeling.[17] In contrast to emphysema, asthma affects the bronchi, not the alveoli.[18]
Status asthmaticus is an acute exacerbation of asthma that does not respond to standard
treatments of bronchodilators and steroids. Nonselective beta blockers (such as Timolol) have
caused fatal status asthmaticus.[26]
[edit] Occupational
Main article: Occupational asthma
Asthma as a result of (or worsened by) workplace exposures is a commonly reported
occupational respiratory disease. Still most cases of occupational asthma are not reported or are
not recognized as such. Estimates by the American Thoracic Society (2004) suggest that 1523%
of new-onset asthma cases in adults are work related.[29] In one study monitoring workplace
asthma by occupation, the highest percentage of cases occurred among operators, fabricators,
and laborers (32.9%), followed by managerial and professional specialists (20.2%), and in
technical, sales, and administrative support jobs (19.2%). Most cases were associated with the
manufacturing (41.4%) and services (34.2%) industries.[29] Animal proteins, enzymes, flour,
natural rubber latex, and certain reactive chemicals are commonly associated with work-related
asthma. When recognized, these hazards can be mitigated, dropping the risk of disease.[30]
Common symptoms of asthma include wheezing, shortness of breath, chest tightness and
coughing, and use of accessory muscle. Symptoms are often worse at night or in the early
morning, or in response to exercise or cold air.[31] Some people with asthma only rarely
experience symptoms, usually in response to triggers, whereas other may have marked persistent
airflow obstruction.[32]
[edit] Causes
Asthma is caused by environmental and genetic factors.[5] These factors influence how severe
asthma is and how well it responds to medication.[35] The interaction is complex and not fully
understood.[36]
Studying the prevalence of asthma and related diseases such as eczema and hay fever have
yielded important clues about some key risk factors.[37] The strongest risk factor for developing
asthma is a history of atopic disease;[38] this increases one's risk of hay fever by up to 5x and the
risk of asthma by 3-4x.[39] In children between the ages of 3-14, a positive skin test for allergies
and an increase in immunoglobulin E increases the chance of having asthma.[40] In adults, the
more allergens one reacts positively to in a skin test, the higher the odds of having asthma.[41]
Because much allergic asthma is associated with sensitivity to indoor allergens and because
Western styles of housing favor greater exposure to indoor allergens, much attention has focused
on increased exposure to these allergens in infancy and early childhood as a primary cause of the
rise in asthma.[42][43] Primary prevention studies aimed at the aggressive reduction of airborne
allergens in a home with infants have shown mixed findings. Strict reduction of dust mite
allergens, for example, reduces the risk of allergic sensitization to dust mites, and modestly
reduces the risk of developing asthma up until the age of 8 years old.[44][45][46][47] However, studies
also showed that the effects of exposure to cat and dog allergens worked in the converse fashion;
exposure during the first year of life was found to reduce the risk of allergic sensitization and of
developing asthma later in life.[48][49][50]
The inconsistency of this data has inspired research into other facets of Western society and their
impact upon the prevalence of asthma. One subject that appears to show a strong correlation is
the development of asthma and obesity. In the United Kingdom and United States, the rise in
asthma prevalence has echoed an almost epidemic rise in the prevalence of obesity.[51][52][53][54] In
Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each
20% increase in body-mass index.[55] Several factors associated with obesity may play a role in
the pathogenesis of asthma, including decreased respiratory function due to a buildup of adipose
tissue (fat) and the fact that adipose tissue leads to a pro-inflammatory state, which has been
associated with non-eosinophilic asthma.[56]
Asthma has been associated with ChurgStrauss syndrome, and individuals with
immunologically mediated urticaria may also experience systemic symptoms with generalized
urticaria, rhino-conjunctivitis, orolaryngeal and gastrointestinal symptoms, asthma, and, at worst,
anaphylaxis.[57] Additionally, adult-onset asthma has been associated with periocular
xanthogranulomas.[58]
[edit] Environmental
Many environmental risk factors have been associated with asthma development and morbidity
in children. Recent studies show a relationship between exposure to air pollutants (e.g. from
traffic) and childhood asthma.[59] This research finds that both the occurrence of the disease and
exacerbation of childhood asthma are affected by outdoor air pollutants. High levels of endotoxin
exposure may contribute to asthma risk.[60]
Viral respiratory infections are not only one of the leading triggers of an exacerbation but may
increase one's risk of developing asthma especially in young children.[15][38]
Respiratory infections such as rhinovirus, Chlamydia pneumoniae and Bordetella pertussis are
correlated with asthma exacerbations.[61]
Psychological stress has long been suspected of being an asthma trigger, but only in recent
decades has convincing scientific evidence substantiated this hypothesis. Rather than stress
directly causing the asthma symptoms, it is thought that stress modulates the immune system to
increase the magnitude of the airway inflammatory response to allergens and irritants.[62][63]
Beta blocker medications such as metoprolol may trigger asthma in those who are susceptible.[64]
[edit] Tobacco
Maternal tobacco smoking during pregnancy and after delivery is associated with a greater risk
of asthma-like symptoms, wheezing, and respiratory infections during childhood.[65] Low air
quality, from traffic pollution or high ozone levels,[66] has been repeatedly associated with
increased asthma morbidity and has a suggested association with asthma development that needs
further research.[62][67]
[edit] Hygiene hypothesis
Antibiotic use early in life has been linked to development of asthma[68] in several examples; it is
thought that antibiotics make children who are predisposed to atopic immune responses
susceptible to development of asthma because they modify gut flora, and thus the immune
system (as described by the hygiene hypothesis).[69] The hygiene hypothesis (see below) is a
hypothesis about the cause of asthma and other allergic disease, and is supported by
epidemiologic data for asthma.[70] All of these things may negatively affect exposure to beneficial
bacteria and other immune system modulators that are important during development, and thus
may cause an increased risk for asthma and allergy.
Caesarean sections have been associated with asthma, possibly because of modifications to the
immune system (as described by the hygiene hypothesis).[71]
[edit] Volatile organic compounds
Observational studies have found that indoor exposure to volatile organic compounds (VOCs)
may be one of the triggers of asthma, however experimental studies have not confirmed these
observations.[72] Even VOC exposure at low levels has been associated with an increase in the
risk of pediatric asthma. Because there are so many VOCs in the air, measuring total VOC
concentrations in the indoor environment may not represent the exposure of individual
compounds.[73][74] Exposure to VOCs is associated with an increase in the IL-4 producing Th2
cells and a reduction in IFN- producing Th1 cells. Thus the mechanism of action of VOC
exposure may be allergic sensitization mediated by a Th2 cell phenotype.[75] Different individual
variations in discomfort, from no response to excessive response, were seen in one of the studies.
These variations may be due to the development of tolerance during exposure.[76] Another study
has concluded that formaldehyde may cause asthma-like symptoms. Low VOC emitting
materials should be used while doing repairs or renovations which decreases the symptoms
related to asthma caused by VOCs and formaldehyde.[77] In another study "the indoor
concentration of aliphatic compounds (C8-C11), butanols, and 2,2,4-trimethyl 1,3-pentanediol
diisobutyrate (TXIB) was significantly elevated in newly painted dwellings. The total indoor
VOC was about 100 micrograms/m3 higher in dwellings painted in the last year". The author
concluded that some VOCs may cause inflammatory reactions in the airways and may be the
reason for asthmatic symptoms.[78][79]
[edit] Phthalates
There is a significant association between asthma-like symptoms (wheezing) among preschool
children and the concentration of DEHP (phthalates) in indoor environment.[80] DEHP (diethylhexyl phthalate) is a plasticizer that is commonly used in building material. The hydrolysis
product of DEHP (di-ethylhexyl phthalate) is MEHP (Mono-ethylhexyl phthalate) which mimics
the prostaglandins and thromboxanes in the airway leading to symptoms related to asthma. [81]
Another mechanism that has been studied regarding phthalates causation of asthma is that high
phthalates level can "modulate the murine immune response to a coallergen". Asthma can
develop in the adults who come in contact with heated PVC fumes.[82] Two main type of
phthalates, namely n-butyl benzyl phthalate (BBzP) and di(2-ethylhexyl) phthalate (DEHP), have
been associated between the concentration of polyvinyl chloride (PVC) used as flooring and the
dust concentrations. Water leakage were associated more with BBzP, and buildings construction
were associated with high concentrations of DEHP.[83] Asthma has been shown to have a
relationship with plaster wall materials and wall-to wall carpeting. The onset of asthma was also
related to the floorleveling plaster at home. Therefore, it is important to understand the health
aspect of these materials in the indoor surfaces.[84]
[edit] Genetic
Over 100 genes have been associated with asthma in at least one genetic association study.[85]
However, such studies must be repeated to ensure the findings are not due to chance. Through
the end of 2005, 25 genes had been associated with asthma in six or more separate populations:
[85]
GSTM1
LTA
STAT6
IL4
HLA-DQB1
IL10
GRPA
NOS1
IL13
TNF
CTLA-4
NOD1
CCL5
CD14
FCER1B
SPINK5
CC16
TBXA2R
IL4R
LTC4S
GSTP1
TGFB1
ADRB2 (-2
adrenergic
receptor)
ADAM33
HLA-DRB1
Many of these genes are related to the immune system or to modulating inflammation. However,
even among this list of highly replicated genes associated with asthma, the results have not been
consistent among all of the populations that have been tested.[85] This indicates that these genes
are not associated with asthma under every condition, and that researchers need to do further
investigation to figure out the complex interactions that cause asthma. One theory is that asthma
is a collection of several diseases, and that genes might have a role in only subsets of asthma.
[citation needed]
For example, one group of genetic differences (single nucleotide polymorphisms in
17q21) was associated with asthma that develops in childhood.[86]
[edit] Exacerbation
Some individuals will have stable asthma for weeks or months and then suddenly develop an
episode of acute asthma. Different asthmatic individuals react differently to various factors.[88]
However, most individuals can develop severe exacerbation of asthma from several triggering
agents.[88][89]
Home factors that can lead to exacerbation include dust, house mites, animal dander (especially
cat and dog hair), cockroach allergens and molds at any given home.[88] Perfumes are a common
cause of acute attacks in females and children. Both virus and bacterial infections of the upper
respiratory tract infection can worsen asthma.[88]
[edit] Diagnosis
Severity of acute asthma exacerbations[19]
Near-fatal asthma
Measurements
Exhaustion
Arrhythmia
"Normal" PaCO2
Cyanosis
Silent chest
Poor respiratory effort
Any one of:Peak flow 33-50%
Acute severe asthma
Obstruction of the lumen of the bronchiole by mucoid exudate, goblet cell metaplasia, epithelial
basement membrane thickening and severe inflammation of bronchiole in a patient with asthma.
There is currently not a precise physiologic, immunologic, or histologic test for diagnosing
asthma. The diagnosis is usually made based on the pattern of symptoms (airways obstruction
and hyperresponsiveness) and/or response to therapy (partial or complete reversibility) over time.
[10]
The British Thoracic Society determines a diagnosis of asthma using a response to therapy
approach. If the patient responds to treatment, then this is considered to be a confirmation of the
diagnosis of asthma. The response measured is the reversibility of airway obstruction after
treatment. Airflow in the airways is measured with a peak flow meter or spirometer, and the
following diagnostic criteria are used by the British Thoracic Society:[106]
20% difference on at least three days in a week for at least two weeks;
20% improvement of peak flow following treatment, for example:
o
14 days of 30 mg prednisolone.
In contrast, the US National Asthma Education and Prevention Program (NAEPP) uses a
symptom patterns approach.[107] Their guidelines for the diagnosis and management of asthma
state that a diagnosis of asthma begins by assessing if any of the following list of indicators is
present.[107][13] While the indicators are not sufficient to support a diagnosis of asthma, the
presence of multiple key indicators increases the probability of a diagnosis of asthma.[107]
Spirometry is needed to establish a diagnosis of asthma.[107]
Recurrent wheeze
Exercise
Viral infection
Mold
Pollen
Changes in weather
Menstrual cycles
The latest guidelines from the U.S. National Asthma Education and Prevention Program
(NAEPP) recommend spirometry at the time of initial diagnosis, after treatment is initiated and
symptoms are stabilized, whenever control of symptoms deteriorates, and every 1 or 2 years on a
regular basis.[108] The NAEPP guidelines do not recommend testing peak expiratory flow as a
regular screening method because it is more variable than spirometry. However, testing peak
flow at rest (or baseline) and after exercise can be helpful, especially in young patients who may
experience only exercise-induced asthma. It may also be useful for daily self-monitoring and for
checking the effects of new medications.[108] Peak flow readings can be charted together with a
record of symptoms or use peak flow charting software. This allows patients to track their peak
flow readings and pass information back to their doctor or respiratory therapist.[109]
Cystic fibrosis
Bronchopulmonary dysplasia
Heart disease
Other causes
Medication induced
Adults
o
Pulmonary embolism
Before diagnosing asthma, alternative possibilities should be considered such as the use of
known bronchoconstrictors (substances that cause narrowing of the airways, e.g. certain antiinflammatory agents or beta-blockers). Among elderly people, the presenting symptom may be
fatigue, cough, or difficulty breathing, all of which may be erroneously attributed to Chronic
obstructive pulmonary disease(COPD), congestive heart failure, or simple aging.[110]
[edit] Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication
of chronic asthma. After the age of 65 most people with obstructive airway disease will have
asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils,
abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this
level of investigation is not performed due to COPD and asthma sharing similar principles of
management: corticosteroids, long acting beta agonists, and smoking cessation.[111] It closely
resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older
age, less symptom reversibility after bronchodilator administration (as measured by spirometry),
and decreased likelihood of family history of atopy.[112][113]
[edit] Others
The term "atopy" was coined to describe this triad of atopic eczema, allergic rhinitis and asthma.
[57]
Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to
acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also
indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a
modified barium swallow test. If the aspiration is indirect (from acid reflux), then treatment is
directed at this is indicated.[citation needed]
[edit] Prevention
The evidence for the effectiveness of measures to prevent the development of asthma is weak.[114]
Ones which show some promise include: limiting smoke exposure both in utero and after
delivery, breastfeeding, increased exposure to respiratory infection per the hygiene hypothesis
(such as in those who attend daycare or are from large families).[114]
[edit] Management
A specific, customized plan for proactively monitoring and managing symptoms should be
created. Someone who has asthma should understand the importance of reducing exposure to
allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment
plan should be written down and adjusted according to changes in symptoms.[115]
The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or
aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, medical treatment
is recommended. Medical treatments used depends on the severity of illness and the frequency of
symptoms. Specific medications for asthma are broadly classified into fast-acting and longacting categories.[116][117]
Bronchodilators are recommended for short-term relief of symptoms. In those with occasional
attacks, no other medication is needed. If mild persistent disease is present (more than two
attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene antagonist
or a mast cell stabilizer is recommended. For those who suffer daily attacks, a higher dose of
inhaled glucocorticoid is used. In a severe asthma exacerbation, oral glucocorticoids are added to
these treatments.[107]
[edit] Medications
Medications used to treat asthma are divided into two general classes: quick-relief medications
used to treat acute symptoms; and long-term control medications used to prevent further
exacerbation.[119]
Fast acting
Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar
efficacy to SABAs.[120] They are however not recommended due to concerns regarding
excessive cardiac stimulation.[121]
Fluticasone propionate metered dose inhaler commonly used for long term control.
Glucocorticoids are the most effective treatment available for long term control.[122]
Inhaled forms are usually used except in the case of severe persistent disease, in which
oral steroids may be needed.[122] Inhaled formulations may be used once or twice daily,
depending on the severity of symptoms.[123]
Long acting beta-adrenoceptor agonists (LABA) have at least a 12-hour effect. They are
however not to be used without a steroid due to an increased risk of severe symptoms.[124]
[125][126]
In December 2008, members of the FDA's drug-safety office recommended
withdrawing approval for these medications in children. Discussion is ongoing about
their use in adults.[127]
Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to
glucocorticoids.[122]
Delivery methods
Medications are typically provided as metered-dose inhalers (MDIs) in combination with an
asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the
medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be
used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms
however insufficient evidence is available to determine whether or not a difference exist in those
severe symptomatology.[128]
Safety and adverse effects
Long-term use of glucocorticoids carries a significant potential for adverse effects. The incidence
of cataracts is increased in people undergoing treatment for asthma with corticosteroids, due to
altered regulation of lens epithelial cells.[129] The incidence of osteoporosis is also increased, due
to changes in bone remodeling.[130][131]
[edit] Other
When asthma is unresponsive to usual medications, other options are available for both
emergency management and prevention of flairs. For emergency management other options
include:
Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive
cases.[134]
Intravenous salbutamol is not supported by available evidence and is thus used only in
extreme cases.[132]
Methylxanthines (such as theophylline) were once widely used, but do not add
significantly to the effects of inhaled beta-agonists.[132]
For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs
bronchial thermoplasty can lead to clinical improvements.[136] It involves the delivery of
controlled thermal energy to the airway wall during a series of bronchoscopies and result in a
prolonged reduction in airway smooth muscle mass.[136]
mite exposure level from high levels to low levels).[144] Washing laundry/rugs in hot water was
also found to improve control of allergens.[15]
A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic
and respiratory therapeutic manoeuvres, found there is insufficient evidence to support their use
in treating.[145] The Buteyko breathing technique for controlling hyperventilation may result in a
reduction in medications use however does not have any effect on lung function.[146] Thus an
expert panel felt that evidence was insufficient to support its use.[140]
[edit] Prognosis
The prognosis for asthma is good, especially for children with mild disease.[13][not in citation given] Of
asthma diagnosed during childhood, 54% of cases will no longer carry the diagnosis after a
decade.[citation needed] The extent of permanent lung damage in people with asthma is unclear. Airway
remodeling is observed, but it is unknown whether these represent harmful or beneficial changes.
[147]
Although conclusions from studies are mixed, most studies show that early treatment with
glucocorticoids prevents or ameliorates decline in lung function as measured by several
parameters.[148] For those who continue to suffer from mild symptoms, corticosteroids can help
most to live their lives with few disabilities. It is more likely to consider immediate medication
of inhaled corticosteroids as soon as asthma attacks occur. According to studies conducted,
patients with relatively mild asthma who have received inhaled corticosteroids within 12 months
of their first asthma symptoms achieved good functional control of asthma after 10 years of
individualized therapy as compared to patients who received this medication after 2 years (or
more) from their first attacks.[citation needed] Though they (delayed) also had good functional control
of asthma, they were observed to exhibit slightly less optimal disease control and more signs of
airway inflammation.[citation needed]
Asthma mortality has decreased over the last few decades due to better recognition and
improvement in care.[149]
[edit] Epidemiology
300350
350400
400450
450500
500550
550600
>600
The prevalence of childhood asthma in the United States has increased since 1980, especially in
younger children.
As of 2009, 300 million people worldwide were affected by asthma leading to approximately
250,000 deaths per year.[12][124][151][152]
It is estimated that asthma has a 7-10% prevalence worldwide.[153] As of 1998, there was a great
disparity in the prevalence of asthma across the world, with a trend toward more developed and
westernized countries having higher rates of asthma[154], with as high as a 20 to 60-fold
difference. Westernization however does not explain the entire difference in asthma prevalence
between countries, and the disparities may also be affected by differences in genetic, social and
environmental risk factors.[62] Mortality however is most common in low to middle income
countries,[155] while symptoms were most prevalent (as much as 20%) in the United Kingdom,
Australia, New Zealand, and Republic of Ireland; they were lowest (as low as 23%) in Eastern
Europe, Indonesia, Greece, Uzbekistan, India, and Ethiopia.[154][dated info]
While asthma is more common in affluent countries, it is by no means a restricted problem; the
WHO estimate that there are between 15 and 20 million people with asthma in India.[citation needed] In
the U.S., urban residents, Hispanics, and African Americans are affected more than the
population as a whole.[citation needed] Striking increases in asthma prevalence have been observed in
populations migrating from a rural environment to an urban one,[156][dated info] or from a third-world
country to Westernized one.[157][dated info]
Asthma affects approximately 7% of the population of the United States[124] and 5% of people in
the United Kingdom.[158] Asthma causes 4,210 deaths per year in the United States.[153][159] In 2005
in the United States asthma affected more than 22 million people including 6 million children.[160]
It accounted for nearly 1/2 million hospitalizations that same year.[160] More boys have asthma
than girls, but more women have it than men.[161] Of all children, African Americans and Latinos
who live in cities are more at risk for developing asthma.[citation needed] African American children in
the U.S. are four times more likely to die of asthma and three times more likely to be
hospitalized, compared to their white counterparts.[citation needed] In some Latino neighborhoods, as
many as one in three children has been found to have asthma.[162]
In England, an estimated 261,400 people were newly diagnosed with asthma in 2005; 5.7 million
people had an asthma diagnosis and were prescribed 32.6 million asthma-related prescriptions.
[163]
The frequency of atopic dermatitis, asthma, urticaria and allergic contact dermatitis has been
found to be lower in psoriatic patients.[57]
[edit] Variability
Asthma prevalence in the US is higher than in most other countries in the world, but varies
drastically between diverse US populations.[62] In the US, asthma prevalence is highest in Puerto
Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in
Mexicans and Koreans.[169][170][171] Mortality rates follow similar trends, and response to
salbutamol is lower in Puerto Ricans than in African Americans or Mexicans.[172][173] As with
worldwide asthma disparities, differences in asthma prevalence, mortality, and drug response in
the US may be explained by differences in genetic, social and environmental risk factors.
Asthma prevalence also differs between populations of the same ethnicity who are born and live
in different places.[174] US-born Mexican populations, for example, have higher asthma rates than
non-US born Mexican populations that are living in the US.[175]
There is no correlation between asthma and gender in children. More adult women are diagnosed
with asthma than adult men, but this does not necessarily mean that more adult women have
asthma.[176]
[edit] History
This section requires expansion.
Asthma was first recognized and named by Hippocrates circa 450 BC. During the 1930s50s,
asthma was considered as being one of the 'holy seven' psychosomatic illnesses. Its aetiology
was considered to be psychological, with treatment often based on psychoanalysis and other
'talking cures'.[177] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed
cry of the child for its mother, so they considered that the treatment of depression was especially
important for individuals with asthma.[177] among the first papers in modern medicine, is one that
was published in 1873 and this paper tried to explain the pathophysiology of the disease.[178] And
one of the first papers discussing treatment of asthma was released in 1872, the author concluded
in his paper that asthma can be cured by rubbing the chest with chloroform liniment.[179] Among
the first times researchers referred to medical treatment was in the year 1880, where Dr. J. B.
Berkart used IV method to administer doses of drug called Pilocarpin.[180][181] In the year 1886,
F.H. Bosworth FH suspected a connection between asthma and hay fever.[182] Epinephrine was
first referred to in the treatment of asthma in 1905,[183] and for acute asthma in 1910.[184]
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