Allergy
From Wikipedia, the free encyclopedia
An allergy is a hypersensitivity disorder
of the immune system.[1]
Allergic reactions occur when a person's immune system reacts to normally
harmless substances in the environment. A substance that causes a reaction is called an allergen. These
reactions are acquired, predictable, and rapid. Allergy is one of four forms of hypersensitivity
and is formally called type I (or immediate) hypersensitivity. Allergic reactions
are distinctive because of excessive activation of certain white blood cells
called mast cells
and basophils by a type of antibody called Immunoglobulin E
(IgE). This reaction results in an inflammatory
response which can range from uncomfortable to dangerous.
Mild allergies like hay fever
are very common in the human population
and cause symptoms such as red eyes, itchiness, and runny nose,
eczema, hives, or an asthma attack. Allergies can play a major role in conditions such
as asthma. In some
people, severe allergies to environmental or dietary allergens or to medication
may result in life-threatening reactions called anaphylaxis.
Food allergies,
and reactions to the venom of stinging insects such as wasps and bees are often associated with these severe reactions.[2]
A variety of tests exist to diagnose
allergic conditions. If done they should be ordered and interpreted in light of
a person's history of exposure as many positive test results do not mean a
clinically significant allergy.[3]
Tests include placing possible allergens on the skin and looking for a reaction
such as swelling and blood tests to look for an allergen-specific IgE.
Treatments for allergies include
avoiding known allergens, steroids that
modify the immune system in general, and medications such as antihistamines and decongestants
which reduce symptoms. Many of these medications are taken by mouth, although epinephrine,
which is used to treat anaphylactic reactions, is injected. Immunotherapy uses injected allergens to desensitize the body's response.
Signs
and symptoms
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Common symptoms
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|
|
Affected organ
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Symptom
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Sneezing, coughing, bronchoconstriction,
wheezing
and dyspnea,
sometimes outright attacks of asthma,
in severe cases the airway constricts due to swelling known as laryngeal
edema
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|
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feeling of fullness, possibly pain, and impaired hearing
due to the lack of eustachian
tube drainage.
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Many allergens such as dust or
pollen are airborne particles. In these cases, symptoms arise in areas in
contact with air, such as eyes, nose, and lungs. For instance, allergic rhinitis,
also known as hay fever, causes irritation of the nose, sneezing, itching, and
redness of the eyes.[4]
Inhaled allergens can also lead to asthmatic
symptoms, caused by narrowing of the airways (bronchoconstriction) and increased production of mucus in the lungs, shortness of breath (dyspnea),
coughing and wheezing.[5]
Aside from these ambient allergens,
allergic reactions can result from foods, insect stings, and reactions to medications
like aspirin and antibiotics
such as penicillin. Symptoms of food allergy include abdominal pain,
bloating,
vomiting, diarrhea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory
(asthmatic) reactions, or rhinitis.[6]
Insect stings, antibiotics, and certain medicines produce a systemic allergic
response that is also called anaphylaxis;
multiple organ systems can be affected, including the digestive system,
the respiratory system, and the circulatory system.[7][8][9]
Depending on the rate of severity, it can cause cutaneous
reactions, bronchoconstriction, edema, hypotension, coma, and even death. This type of reaction can be triggered suddenly, or the
onset can be delayed. The severity of this type of allergic response often
requires injections of epinephrine, sometimes through a device known as the EpiPen or Twinject auto-injector. The nature of anaphylaxis
is such that the reaction can seem to be subsiding, but may recur throughout a
prolonged period of time.[9]
Substances that come into contact
with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema.[10]
Skin allergies frequently cause rashes, or swelling and inflammation within the
skin, in what is known as a "wheal and
flare" reaction characteristic of hives and angioedema.[11]
Cause
Risk factors for allergy can be
placed in two general categories, namely host and environmental factors.[12]
Host factors include heredity, gender, race, and age, with heredity being by far the most significant.
However, there have been recent increases in the incidence of allergic
disorders that cannot be explained by genetic factors alone. Four major
environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution,
allergen levels, and dietary changes.[13]
Foods
A wide variety of foods can cause
allergic reactions, but 90% of allergic responses to foods are caused by cow's milk, soy, eggs, wheat, peanuts, tree nuts, fish and shellfish.[14]
Other food allergies, affecting less than 1 person per 10,000 population, may be
considered "rare".[15]
The most common food allergy,
at least in the US population, is a sensitivity to crustacea.[15]
Although peanut allergies are notorious for their severity, peanut allergies
are not the most common food allergy in adults or children. Severe or life-threatening
reactions may be triggered by other allergens and are more common when combined
with asthma.[14]
Rates of allergies differ between
adults and children. Peanut allergies can sometimes be outgrown by children. Egg
allergies affect one to two percent of children but are outgrown by about
two-thirds of children by the age of 5.[16]
The sensitivity is usually to proteins in the white rather than the yolk.[17]
Milk allergies are the most
prevalent in children.[18]
Some sufferers are unable to tolerate milk from cows, goats, or sheep, and many
sufferers are also unable to tolerate dairy products such as cheese. Lactose intolerance, a common reaction to milk, is not a form of allergy, but
rather due to the absence of an enzyme in the digestive tract. A small portion
of children with a milk allergy, roughly ten percent, will have a reaction to beef. Beef contains a small amount of protein that is present in
cow's milk.[19]
Sufferers of tree nut allergies may be allergic to one or many tree nuts,
including pecans, pistachios, pine nuts, and walnuts.[17]
Also seeds,
including sesame seeds and poppy seeds,
contain oils where protein is present, which may elicit an allergic reaction.[17]
Non-food
proteins
Latex can
trigger an IgE-mediated cutaneous, respiratory, and systemic reaction. The
prevalence of latex allergy in the general population is believed to be less
than one percent. In a hospital study, one in 800 surgical patients (0.125
percent) report latex sensitivity, although the sensitivity among healthcare
workers is higher, between seven and ten percent. Researchers attribute this
higher level to the exposure of healthcare workers to areas with significant
airborne latex allergens, such as operating rooms, intensive-care units, and
dental suites. These latex-rich environments may sensitize healthcare workers
who regularly inhale allergenic proteins.[20]
The most prevalent response to latex
is an allergic contact dermatitis, a delayed hypersensitive reaction appearing
as dry, crusted lesions. This reaction usually lasts 48 to 96 hours. Sweating
or rubbing the area under the glove aggravates the lesions, possibly leading to
ulcerations.[20]
Anaphylactic reactions occur most often in sensitive patients, who have been
exposed to the surgeon's latex gloves during abdominal surgery, but other mucosal
exposures, such as dental procedures, can also produce systemic reactions.[20]
Latex and banana sensitivity may
cross-react; furthermore,those with latex allergy may also have sensitivities
to avocado, kiwifruit, and chestnut.[21]
These patients often have perioral itching and local urticaria.
Only occasionally have these food-induced allergies induced systemic responses.
Researchers suspect that the cross-reactivity of latex with banana, avocado,
kiwifruit, and chestnut occurs because latex proteins are structurally homologous with some plant proteins.[20]
Toxins
interacting with proteins
Another non-food protein reaction, urushiol-induced
contact dermatitis, originates after contact with poison ivy,
eastern poison oak, western
poison oak, or poison sumac.
Urushiol, which is
not itself a protein, acts as a hapten and chemically reacts with, binds to, and changes the shape
of integral
membrane proteins on exposed skin cells. The immune
system does not recognize the affected cells as normal parts of the body,
causing a T-cell-mediated immune response.[22]
Of these poisonous plants, sumac is the most virulent.[23]
The resulting dermatological response to the reaction between urushiol and
membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking.[24]
Estimates vary on the percentage of
the population that will have an immune system response. Approximately 25
percent of the population will have a strong allergic response to urushiol. In
general, approximately 80 percent to 90 percent of adults will develop a rash
if they are exposed to .0050 milligrams (7.7×10−5 gr) of
purified urushiol, but some people are so sensitive that it takes only a
molecular trace on the skin to initiate an allergic reaction.[25]
Genetic
basis
Allergic diseases are strongly familial: identical twins
are likely to have the same allergic diseases about 70% of the time; the same
allergy occurs about 40% of the time in non-identical twins.[26]
Allergic parents are more likely to have allergic children,[27]
and those children's allergies are likely to be more severe than those in
children of non-allergic parents. Some allergies, however, are not consistent
along genealogies;
parents who are allergic to peanuts may have children who are allergic to ragweed. It seems
that the likelihood of developing allergies is inherited
and related to an irregularity in the immune system, but the specific allergen is not.[27]
The risk of allergic sensitization and the development of allergies varies with age, with
young children most at risk.[28]
Several studies have shown that IgE levels are highest in childhood and fall
rapidly between the ages of 10 and 30 years.[28]
The peak prevalence of hay fever is highest in children and young adults and
the incidence of asthma is highest in children under 10.[29]
Overall, boys have a higher risk of developing allergies than girls,[27]
although for some diseases, namely asthma in young adults, females are more
likely to be affected.[30]
Sex differences tend to decrease in adulthood.[27]
Ethnicity
may play a role in some allergies; however, racial factors have been difficult
to separate from environmental influences and changes due to migration.[27]
It has been suggested that different genetic loci
are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.[31]
Hygiene
hypothesis
Allergic diseases are caused by
inappropriate immunological responses to harmless antigens driven by
a TH2-mediated immune response. Many bacteria and viruses elicit a TH1-mediated
immune response, which down-regulates TH2 responses. The first proposed
mechanism of action of the hygiene hypothesis was that insufficient stimulation
of the TH1 arm of the immune system leads to an overactive TH2 arm, which in
turn leads to allergic disease.[32]
In other words, individuals living in too sterile an environment are not
exposed to enough pathogens to keep the immune system busy. Since our bodies
evolved to deal with a certain level of such pathogens, when they are not
exposed to this level, the immune system will attack harmless antigens and thus
normally benign microbial objects — like pollen — will trigger an immune
response.[33]
The hygiene hypothesis was developed
to explain the observation that hay fever
and eczema, both
allergic diseases, were less common in children from larger families, which
were, it is presumed, exposed to more infectious agents through their siblings,
than in children from families with only one child. The hygiene hypothesis has
been extensively investigated by immunologists
and epidemiologists and has become an important theoretical framework for the
study of allergic disorders. It is used to explain the increase in allergic
diseases that have been seen since industrialization,
and the higher incidence of allergic diseases in more developed countries. The
hygiene hypothesis has now expanded to include exposure to symbiotic bacteria
and parasites as important modulators of immune system development, along with
infectious agents.
Epidemiological data support the
hygiene hypothesis. Studies have shown that various immunological and
autoimmune diseases are much less common in the developing world than the
industrialized world and that immigrants to the industrialized world from the
developing world increasingly develop immunological disorders in relation to
the length of time since arrival in the industrialized world.[34]
Longitudinal studies in the third world demonstrate an increase in
immunological disorders as a country grows more affluent and, it is presumed, cleaner.[35]
The use of antibiotics in the first year of life has been linked to asthma and
other allergic diseases.[36]
The use of antibacterial cleaning products has also been associated with higher
incidence of asthma, as has
birth by Caesarean section rather than vaginal birth.[37][38]
Other
environmental factors
International differences have been
associated with the number of individuals within a population that suffer from
allergy. Allergic diseases are more common in industrialized
countries than in countries that are more traditional or agricultural,
and there is a higher rate of allergic disease in urban
populations versus rural populations, although these differences are becoming less
defined.[39]
Exposure to allergens, especially in
early life, is an important risk factor
for allergy. Alterations in exposure to microorganisms
is another plausible explanation, at present, for the increase in atopic
allergy.[13]
Endotoxin exposure reduces release of inflammatory cytokines
such as TNF-α, IFNγ, interleukin-10,
and interleukin-12 from white blood cells (leukocytes)
that circulate in the blood.[40]
Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought
to be involved in these processes.[41]
Gutworms and similar parasites are
present in untreated drinking water in developing countries, and were present
in the water of developed countries until the routine chlorination and purification of drinking water supplies.[42]
Recent research has shown that some common parasites,
such as intestinal worms (e.g., hookworms),
secrete chemicals into the gut wall (and, hence, the bloodstream) that suppress the
immune system and prevent the body from attacking the parasite.[43]
This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution
of man and parasites has led to an immune system that functions correctly only
in the presence of the parasites. Without them, the immune system becomes
unbalanced and oversensitive.[44]
In particular, research suggests that allergies may coincide with the delayed
establishment of gut flora in infants.[45]
However, the research to support this theory is conflicting, with some studies
performed in China and Ethiopia showing
an increase in allergy in people infected with intestinal worms.[39]
Clinical trials have been initiated to test the effectiveness of certain worms
in treating some allergies.[46]
It may be that the term 'parasite' could turn out to be inappropriate, and in
fact a hitherto unsuspected symbiosis
is at work.[46]
For more information on this topic, see Helminthic therapy.
Acute
response
In the early stages of allergy, a
type I hypersensitivity reaction against an allergen encountered for the first
time and presented by a professional Antigen-Presenting Cell causes a response in a type of immune cell called a TH2 lymphocyte,
which belongs to a subset of T cells that
produce a cytokine called interleukin-4
(IL-4). These TH2 cells interact with other lymphocytes
called B cells, whose
role is production of antibodies. Coupled with signals provided by IL-4, this
interaction stimulates the B cell to begin production of a large amount of a
particular type of antibody known as IgE. Secreted IgE circulates in the blood
and binds to an IgE-specific receptor (a kind of Fc receptor
called FcεRI) on the
surface of other kinds of immune cells called mast cells
and basophils,
which are both involved in the acute inflammatory response. The IgE-coated
cells, at this stage, are sensitized to the allergen.[13]
If later exposure to the same
allergen occurs, the allergen can bind to the IgE molecules held on the surface
of the mast cells or basophils. Cross-linking of the IgE and Fc receptors
occurs when more than one IgE-receptor complex interacts with the same
allergenic molecule, and activates the sensitized cell. Activated mast cells
and basophils undergo a process called degranulation,
during which they release histamine
and other inflammatory chemical mediators (cytokines,
interleukins,
leukotrienes,
and prostaglandins) from their granules into the surrounding tissue causing several systemic
effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle
contraction. This results in rhinorrhea,
itchiness, dyspnea, and anaphylaxis.
Depending on the individual, allergen, and mode of introduction, the symptoms
can be system-wide (classical anaphylaxis), or localized to particular body
systems; asthma is localized to the respiratory system and eczema is localized
to the dermis.[13]
Late-phase
response
After the chemical mediators of the
acute response subside, late-phase responses can often occur. This is due to
the migration of other leukocytes such as neutrophils,
lymphocytes,
eosinophils
and macrophages
to the initial site. The reaction is usually seen 2–24 hours after the original
reaction.[47]
Cytokines from mast cells may play a role in the persistence of long-term
effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic
responses, although they are still caused by release of mediators from
eosinophils and are still dependent on activity of TH2 cells.[48]
Diagnosis
Effective management of allergic
diseases relies on the ability to make an accurate diagnosis.[49]
Allergy testing can help confirm or rule out allergies.[50][51]
Correct diagnosis, counseling and avoidance advice based on valid allergy test
results will help reduce the incidence of symptoms, medications and improve
quality of life.[50]
For assessing the presence of allergen-specific IgE antibodies, two different
methods can be used: a skin prick test or an allergy blood test. Both methods
are recommended and have similar diagnostic value.[51][52]
Skin prick tests and blood tests are
equally cost-effective and health economic evidence show that both the IgE
antibody test and the skin prick test were cost effective compared with no
test.[50]
Also, earlier and more accurate diagnoses save cost due to reduced
consultations, referrals to secondary care, misdiagnosis and emergency
admissions.[53]
Allergy undergoes dynamic changes
over time. Regular allergy testing of relevant allergens provides information
on if and how patient management can be changed, in order to improve health and
quality of life. Annual testing is often the practice for determining whether
allergy to milk, egg, soy, and wheat have been outgrown and the testing
interval is extended to 2 to 3 years for allergy to peanut, tree nuts, fish,
and crustacean shellfish.[51]
Results of follow-up testing can guide decision-making regarding whether and
when it is safe to introduce or re-introduce allergenic food into the diet.[54]
Skin testing is also known as "puncture testing" and
"prick testing" due to the series of tiny puncture or pricks made
into the patient's skin. Small amounts of suspected allergens and/or their
extracts (pollen, grass, mite proteins, peanut extract, etc.) are introduced to
sites on the skin marked with pen or dye (the ink/dye should be carefully
selected, lest it cause an allergic response itself). A small plastic or metal
device is used to puncture or prick the skin. Sometimes, the allergens are
injected "intradermally" into the patient's skin, with a needle and
syringe. Common areas for testing include the inside forearm and the back. If
the patient is allergic to the substance, then a visible inflammatory reaction
will usually occur within 30 minutes. This response will range from slight
reddening of the skin to a full-blown hive (called
"wheal and flare") in more sensitive patients similar to a mosquito bite.
Interpretation of the results of the skin prick test is normally done by
allergists on a scale of severity, with +/- meaning borderline reactivity, and
4+ being a large reaction. Increasingly, allergists are measuring and recording
the diameter of the wheal and flare reaction. Interpretation by well-trained
allergists is often guided by relevant literature.[55]
Some patients may believe they have determined their own allergic sensitivity
from observation, but a skin test has been shown to be much better than patient
observation to detect allergy.[56]
If a serious life threatening
anaphylactic reaction has brought a patient in for evaluation, some allergists
will prefer an initial blood test prior to performing the skin prick test. Skin
tests may not be an option if the patient has widespread skin disease or has
taken antihistamines sometime the last several days.
Blood
testing
An allergy blood test is quick and
simple and can be ordered by a licensed health care provider e.g. an allergy
specialist, GP or PED. Unlike skin-prick testing, a blood test can be performed
irrespective of age, skin condition, medication, symptom, disease activity and
pregnancy. Adults and children of any age can take an allergy blood test. For
babies and very young children, a single needle stick for allergy blood testing
is often more gentle than several skin tests.
An allergy blood test is available
through most laboratories, and a sample of the patient’s blood is sent to a
laboratory for analysis and the results are sent back a few days later.
Multiple allergens can be detected with a single blood sample.
Allergy blood tests are very safe,
since the person is not exposed to any allergens during the testing procedure.
The test measures the concentration
of specific IgE antibodies in the blood. Quantitative IgE test results increase
the possibility of ranking how different substances may affect symptoms. A general
rule of thumb is that the higher the IgE antibody value, the greater the
likelihood of symptoms. Allergens found at low levels that today do not result
in symptoms can nevertheless help predict future symptom development. The
quantitative allergy blood result can help determine what a patient is allergic
to, help predict and follow the disease development, estimate the risk of a
severe reaction and explain cross-reactivity.[57][58]
A low total IgE level is not
adequate to rule out sensitization to commonly inhaled allergens.[59]
Statistical methods,
such as ROC curves, predictive value calculations, and likelihood ratios have
been used to examine the relationship of various testing methods to each other.
These methods have shown that patients with a high total IgE have a high
probability of allergic sensitization, but further investigation with allergy
tests for specific IgE antibodies for a carefully chosen of allergens is often
warranted.
Other
Challenge testing: Challenge testing is when small amounts of a suspected
allergen are introduced to the body orally, through inhalation, or other
routes. Except for testing food and medication allergies, challenges are rarely
performed. When this type of testing is chosen, it must be closely supervised
by an allergist.
Elimination/Challenge tests: This testing method is used most often with foods or
medicines. A patient with a suspected allergen is instructed to modify his/her
diet to totally avoid that allergen for determined time. If the patient
experiences significant improvement, he/she may then be “challenged” by
reintroducing the allergen to see if symptoms can be reproduced.
Patch testing: Patch testing is used to help ascertain the cause of skin
contact allergy, or contact dermatitis. Adhesive patches, usually treated with a number of common
allergic chemicals or skin sensitizers, are applied to the back. The skin is
then examined for possible local reactions at least twice, usually at 48 hours
after application of the patch and again two or three days later.
Unreliable tests: There are other types of allergy testing methods that the
that are unreliable including applied kinesiology (allergy testing through
muscle relaxation), cytotoxicity testing, urine autoinjection, skin titration
(Rinkel method), and provocative and neutralization (subcutaneous) testing or
sublingual provocation.[60]
Differential
diagnosis
Before a diagnosis of allergic
disease can be confirmed, other possible causes of the presenting symptoms
should be considered.[61]
Vasomotor rhinitis, for example, is one of many maladies that
shares symptoms with allergic rhinitis, underscoring the need for professional
differential diagnosis.[62]
Once a diagnosis of asthma, rhinitis, anaphylaxis,
or other allergic disease has been made, there are several methods for
discovering the causative agent of that allergy.
Management
In recent times, there have been
enormous improvements in the medical practices used to treat allergic
conditions. With respect to anaphylaxis
and hypersensitivity reactions to foods, drugs, and insects and in allergic
skin diseases, advances have included the identification of food proteins to
which IgE binding is associated with severe reactions and development of
low-allergen foods, improvements in skin prick test predictions; evaluation of
the atopy patch
test; in wasp sting outcomes predictions and a rapidly disintegrating
epinephrine tablet, and anti-IL-5 for eosinophilic diseases.[63]
Traditional treatment and management
of allergies consisted simply of avoiding the allergen in question or otherwise
reducing exposure. For instance, people with cat allergies were encouraged to
avoid them. However, while avoidance of allergens may reduce symptoms and avoid
life-threatening anaphylaxis, it is difficult to achieve for those with pollen
or similar air-borne allergies. Nonetheless, strict avoidance of allergens is
still considered a useful treatment method, and is often used in managing food
allergies.
New technology approaches to
decreasing IgE overproduction, and regulating histamine release in allergic
individuals have demonstrated statistically significant reduction on Total
Nasal Symptom Scores.[64][65]
Medication
Several antagonistic drugs are used to block the action of allergic mediators,
or to prevent activation of cells and degranulation processes. These include antihistamines,
glucocorticoids, epinephrine (adrenaline), theophylline
and cromolyn sodium. Anti-leukotrienes, such as Montelukast
(Singulair) or Zafirlukast (Accolate), are FDA approved for treatment of allergic
diseases.[citation
needed] Anti-cholinergics, decongestants,
mast cell stabilizers, and other compounds thought to impair eosinophil chemotaxis,
are also commonly used. These drugs help to alleviate the symptoms of allergy,
and are imperative in the recovery of acute anaphylaxis,
but play little role in chronic treatment of allergic disorders.
Immunotherapy
Desensitization or hyposensitization
is a treatment in which the person is gradually vaccinated
with progressively larger doses of the allergen in question. This can either
reduce the severity or eliminate hypersensitivity altogether. It relies on the
progressive skewing of IgG antibody production, to block excessive IgE production seen
in atopys.[66]
In a sense, the person builds up immunity to increasing amounts of the allergen
in question. Studies have demonstrated the long-term efficacy and the
preventive effect of immunotherapy in reducing the development of new allergy.[67]
Meta-analyses have also confirmed efficacy of the treatment in allergic
rhinitis in children[68]
and in asthma.[69]
A review by the Mayo Clinic in Rochester confirmed the safety and efficacy of
allergen immunotherapy for allergic rhinitis and conjunctivitis, allergic forms
of asthma, and stinging insect based on numerous well-designed scientific
studies.[70]
In addition, national and international guidelines confirm the clinical
efficacy of injection immunotherapy in rhinitis and asthma, as well as the
safety, provided that recommendations are followed.[71]
A second form of immunotherapy
involves the intravenous injection of monoclonal anti-IgE antibodies. These bind to free and B-cell
associated IgE; signalling their destruction. They do not bind to IgE already
bound to the Fc receptor on basophils
and mast cells, as this would stimulate the allergic inflammatory response. The
first agent of this class is Omalizumab.
While this form of immunotherapy is very effective in treating several types of
atopy, it should not be used in treating the majority of people with
food allergies.[citation
needed]
A third type, Sublingual
immunotherapy, is an orally-administered therapy
that takes advantage of oral immune tolerance
to non-pathogenic antigens such as foods and resident bacteria. This therapy
currently accounts for 40 percent of allergy treatment in Europe.[citation
needed] In the United States, sublingual immunotherapy is gaining
support among traditional allergists and is endorsed by doctors treating
allergy.[72]
Allergy shot treatment is the
closest thing to a ‘cure’ for allergic symptoms. This therapy requires a
long-term commitment.[66]
Other
An experimental treatment, enzyme
potentiated desensitization (EPD),
has been tried for decades but is not generally accepted as effective.[73]
EPD uses dilutions of allergen and an enzyme, beta-glucuronidase, to which T-regulatory lymphocytes are supposed to respond
by favouring desensitization, or down-regulation, rather than sensitization.
EPD has also been tried for the treatment of autoimmune diseases but is not approved by the U.S.
Food and Drug Administration
or of proven effectiveness.[73]
Systematic literature searches
conducted by the Mayo Clinic through 2006, involving hundreds of articles
studying multiple conditions, including asthma and upper respiratory tract infection,
showed no effectiveness of homeopathic treatments and no difference compared
with placebo. The authors concluded that, based on rigorous clinical trials of
all types of homeopathy for childhood and adolescence ailments, there is no
convincing evidence that supports the use of homeopathic treatments.[74]
Prevention
The consumption of various foods
during pregnancy has been linked to eczema; these include celery, citrus fruit,
raw pepper, margarine, and vegetable oil.[75]
A high intake of antioxidants, zinc, and selenium during pregnancy may help
prevent allergies. This is linked to a reduced risk for childhood-onset asthma,
wheezing, and eczema.[76]
Further research needs to be conducted. After birth, an early introduction of
solid food and high diversity before week 17 could increase a child's risk for
allergies. Studies suggest that introduction of solid food and avoidance of highly
allergenic food such as peanuts during the first year does not help in allergy
prevention.[77]
Epidemiology
Many diseases related to
inflammation such as type 1 diabetes,
rheumatoid arthritis, and allergic diseases — hay fever and asthma — have
increased in the Western world over the past 2-3 decades.[78]
Rapid increases in allergic asthma and other atopic disorders in industrialized
nations, it is estimated, began in the 1960s and 1970s, with further increases
occurring during the 1980s and 1990s,[79]
although some suggest that a steady rise in sensitization has been occurring
since the 1920s.[80]
The incidence of atopy in developing countries has, in general, remained much
lower.[79]
|
Allergic conditions: Statistics
and Epidemiology
|
||
|
Allergy type
|
||
|
Allergic rhinitis
|
||
|
Asthma
|
10 million suffer from allergic asthma (about 3% of the
population). The prevalence of asthma increased 75% from 1980-1994. Asthma
prevalence is 39% higher in African
Americans than in Europeans.[85]
|
5.7 million (about 9.4%). In six and seven year olds
asthma increased from 18.4% to 20.9% over five years, during the same time
the rate decreased from 31% to 24.7% in 13 to 14 year olds.
|
|
Atopic eczema
|
About 9% of the population. Between 1960 and 1990
prevalence has increased from 3% to 10% in children.[86]
|
5.8 million (about 1% severe).
|
|
Anaphylaxis
|
Between 1999 and 2006, 48 deaths occurred in people
ranging from five months to 85 years old.
|
|
|
Insect venom
|
Around 15% of adults have mild, localized allergic
reactions. Systemic reactions occur in 3% of adults and less than 1% of
children.[89]
|
Unknown
|
|
Drug allergies
|
Anaphylactic reactions to penicillin cause 400 deaths per
year.
|
Unknown
|
|
Food allergies
|
About 6% of US children under age 3 and 3.5-4% of the
overall US population.[citation needed]
Peanut and/or tree nut (e.g. walnut)
allergy affects about three million Americans, or 1.1% of the population.[88]
|
5-7% of infants and 1-2% of adults. A 117.3% increase in
peanut allergies was observed from 2001 to 2005, an estimated 25,700 people
in England are affected.
|
|
Multiple allergies (Asthma, eczema and allergic
rhinitis together)
|
Unknown
|
|
Although genetic factors
fundamentally govern susceptibility to atopic disease, increases in atopy have
occurred within too short a time frame to be explained by a genetic change in
the population, thus pointing to environmental or lifestyle changes.[79]
Several hypotheses have been identified to explain this increased prevalence;
increased exposure to perennial allergens due to housing changes and increasing
time spent indoors, and changes in cleanliness or hygiene that have resulted in
the decreased activation of a common immune control mechanism, coupled with
dietary changes, obesity and decline in physical exercise.[78]
The hygiene hypothesis maintains[91]
that high living standards and hygienic conditions exposes children to fewer
infections. It is thought that reduced bacterial and viral infections early in
life direct the maturing immune system away from TH1 type responses,
leading to unrestrained TH2 responses that allow for an increase in
allergy.[44][92]
Changes in rates and types of
infection alone however, have been unable to explain the observed increase in
allergic disease, and recent evidence has focused attention on the importance
of the gastrointestinal microbial environment. Evidence has shown that exposure
to food and fecal-oral pathogens, such as hepatitis A,
Toxoplasma gondii, and Helicobacter pylori (which also tend to be more prevalent in developing
countries), can reduce the overall risk of atopy by more than 60%,[93]
and an increased prevalence of parasitic infections has been associated with a
decreased prevalence of asthma.[94]
It is speculated that these infections exert their effect by critically
altering TH1/TH2 regulation.[95]
Important elements of newer hygiene hypotheses also include exposure to endotoxins,
exposure to pets and
growing up on a farm.[95]
History
Tamil word to describe any abnormal
response to a medicine or an environmental factor is "Azharchi". It
comes from the Siddha medicinal terms that is followed for thousands of year in
South India. The concept of "allergy" was originally introduced in
1906 by the Viennese pediatrician Clemens von Pirquet, after he noted that some of his patients were
hypersensitive to normally innocuous entities such as dust, pollen, or certain foods.[96]
Pirquet called this phenomenon "allergy" from the Ancient Greek words ἄλλος allos meaning "other" and ἔργον ergon meaning "work".[97]
All forms of hypersensitivity used to be classified as allergies, and all were
thought to be caused by an improper activation of the immune system. Later, it
became clear that several different disease
mechanisms were implicated, with the common link to a disordered activation of
the immune system. In 1963, a new classification scheme was designed by Philip
Gell and Robin Coombs
that described four types of hypersensitivity reactions, known as Type I to Type IV hypersensitivity.[98]
With this new classification, the word "allergy" was restricted to
type I hypersensitivities (also called immediate hypersensitivity), which are
characterized as rapidly developing reactions.
A major breakthrough in
understanding the mechanisms of allergy was the discovery of the antibody class
labeled immunoglobulin E (IgE) - Kimishige Ishizaka and co-workers were the first to isolate and describe IgE
in the 1960s.[99]
Diagnosis
Radiometric assays include the radioallergosorbent
test (RAST) test method, which uses IgE-binding
(anti-IgE) antibodies labeled with radioactive isotopes for quantifying the levels of IgE antibody in the blood.[100]
Other newer methods use colorimetric or fluorescence-labeled technology in the
place of radioactive isotopes.
The market-leading RAST methodology
was invented and marketed in 1974 by Pharmacia Diagnostics AB, Uppsala, Sweden,
and the acronym RAST is actually a brand name. In 1989, Pharmacia Diagnostics
AB replaced it with a superior test named the ImmunoCAP Specific IgE blood
test, which uses the newer fluorescence-labeled technology. American College of
Allergy Asthma and Immunology (ACAAI) and the American Academy of Allergy
Asthma and Immunology (AAAAI) issued the Joint Task Force Report “Pearls and
pitfalls of allergy diagnostic testing” in 2008, and is firm in its statement
that the term RAST is now obsolete:
“The term RAST became a
colloquialism for all varieties of (in vitro allergy) tests. This is
unfortunate because it is well recognized that there are well-performing tests
and some that do not perform so well, yet they are all called RASTs, making it
difficult to distinguish which is which. For these reasons, it is now
recommended that use of RAST as a generic descriptor of these tests be
abandoned.”[101]
The new version, the ImmunoCAP Specific IgE blood test, is the only specific
IgE assay to receive FDA approval to quantitatively report to its detection
limit of 0.1kU/l.
Medical
specialty
An allergist is a physician
specially trained to manage and treat allergies,
asthma and the
other allergic diseases. In the United States
physicians holding certification by the American Board of Allergy and
Immunology (ABAI) have successfully completed an accredited educational program
and an evaluation process, including a secure, proctored examination to
demonstrate the knowledge, skills, and experience to the provision of patient
care in allergy and immunology.[102]
Becoming an allergist/immunologist requires completion of at least nine years
of training. After completing medical school and graduating with a medical
degree, a physician will then undergo three years of training in internal medicine
(to become an internist) or pediatrics (to become a pediatrician). Once
physicians have finished training in one of these specialties, they must pass
the exam of either the American Board of Pediatrics (ABP), the American
Osteopathic Board of Pediatrics
(AOBP), the American
Board of Internal Medicine (ABIM) or
the American
Osteopathic Board of Internal Medicine
(AOBIM). Internists or pediatricians wishing to focus on the sub-specialty of
allergy-immunology then complete at least an additional two years of study,
called a fellowship, in an allergy/immunology training program.
Allergist/immunologists listed as ABAI-certified have successfully passed the
certifying examination of the American Board of Allergy and Immunology (ABAI),
following their fellowship.[103]
In the United Kingdom,
allergy is a subspecialty of general medicine
or pediatrics.
After obtaining postgraduate exams (MRCP or MRCPCH
respectively), a doctor works for several years as a specialist registrar before qualifying for the General Medical Council specialist register. Allergy services may also be delivered
by immunologists. A 2003 Royal
College of Physicians report presented a case for
improvement of what were felt to be inadequate allergy services in the UK.[104]
In 2006, the House of Lords convened a subcommittee that reported in 2007. It concluded
likewise that allergy services were insufficient to deal with what the Lords
referred to as an "allergy epidemic" and its social cost; it made
several other recommendations.[105]
The entire wiki link can be found at:
http://en.wikipedia.org/wiki/Allergy
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