allergy

Allergies Health videos on seasonal allergies, including allergy treatment options.

(ăl'ər-jē)

1. An abnormally high sensitivity to certain substances, such as pollens, foods, or microorganisms. Common indications of allergy may include sneezing, itching, and skin rashes.
2. Informal. An adverse sentiment; antipathy: an allergy to cocktail parties.

[German Allergie : Greek allos, other; see allo- + Greek ergon, action.]

View more Health videos

Before the Diet of Sugar he was using razor blades And excited soon after with an allergy to maidenheads—For Time Being, 1944.

For more information on allergy, visit Britannica.com.

Altered reactivity in humans and animals to allergens (substances foreign to the body that cause allergy) induced by exposure through injection, inhalation, ingestion, or skin contact. The most common clinical manifestations of allergy are hay fever, asthma, hives, atopic (endogenous) eczema, and eczematous skin lesions caused by direct contact with allergens such as poison ivy or certain chemicals.

A large variety of substances may cause allergies: pollens, animal proteins, molds, foods, insect venoms, foreign serum proteins, industrial chemicals, and drugs. Most natural allergens are proteins or polysaccharides of moderate molecular size (molecular weights of 10,000 to 200,000). Chemicals or drugs of lower molecular weight (haptens) have first to bind to the body's own proteins (carriers) in order to become fully effective allergens.

For the development of the hypersensitivity state underlying clinical allergies, repeated contact with the allergen is required. Duration of the sensitization period is usually dependent upon the sensitizing strength of the allergen and the intensity of exposure. Some allergens (for example, saliva, urine, and hair proteins of domestic animals) are more sensitizing than others. In most instances, repeated contact with minute amounts of allergen is required; several annual seasonal exposures to grass pollens or ragweed pollen usually occur before an overt manifestation of hay fever. On the other hand, allergy to cow milk proteins in infants can develop within a few weeks. When previous contacts with allergens have not been apparent (for example, antibiotics in food), an allergy may become clinically manifest even upon the first conscious encounter with the offending substance.

Besides the intrinsic sensitizing properties of allergens, individual predisposition of the allergic person to become sensitized also plays an important role. Clinical manifestations, such as hay fever, allergic asthma, and atopic (endogenous) dermatitis, occur more frequently in some families. In other clinical forms of allergy, genetic predisposition, though possibly present as well, is not as evident.

Exposure to sensitizing allergens may induce several types of immune response, and the diversity of immunological mechanisms involved is responsible for the various clinical forms of allergic reactions which are encountered in practice. Three principal types of immune responses are encountered: the production of IgE antibodies, IgG or IgM antibodies, and sensitized lymphocytes. See also Antibody; Immunoglobulin.

Diagnosis of allergic diseases encompasses several facets. Since many clinical manifestations of allergy are mimicked by nonallergic mechanisms, it is usually necessary to use additional diagnostic procedures to ascertain whether the person has developed an immune response toward the incriminated allergen. Such procedures primarily consist of skin tests, in which a small amount of allergen is applied on or injected into the skin. If the individual is sensitized, a local immediate reaction ensues, taking the form of a wheal (for IgE-mediated reactions), or swelling and redness occurs after several hours (for delayed hypersensitivity reactions). The blood may also be analyzed for IgE and IgG antibodies by serological assays, and sensitized lymphocytes are investigated by culturing them with the allergen.

Since the discovery of the responsible allergens markedly influences therapy and facilitates prediction of the allergy's outcome, it is important to achieve as precise a diagnosis as possible. Most tests indicate whether the individual is sensitized to a given allergen, but not whether the allergen is in fact still causing the disease. Since in most cases the hypersensitive state persists for many years, it may well happen that sensitization is detected for an allergen to which the individual is no longer exposed and which therefore no longer causes symptoms. In such cases, exposition tests, consisting of close observation of the individual after deliberate exposure to the putative allergen, may yield useful information.

The most efficient treatment, following identification of the offending allergen, remains elimination of allergen from the person's environment and avoidance of further exposure. This form of treatment is essential for allergies caused by most household and workplace allergens. See also Antigen; Hypersensitivity.

Adverse reaction to foods caused by the production of antibodies.

The word ‘allergy’ was first used in 1906 by a Viennese paediatrician, Baron Clemens von Pirquet, to mean ‘altered reactivity’. It was applied to any abnormal response to a substance. This wide meaning has been retained by some people, but in Britain many doctors limit the term to responses which involve an over-reaction by the body's immune system. Such responses include the classic allergic disorders of asthma, eczema, hay fever, non-seasonal rhinitis (runny nose) and urticaria (nettle rash). These disorders may be triggered by pollen, house dust, fungi, drugs, air pollutants, and some food constituents. The specific allergy-causing substance (allergen) provokes an immunological reaction in skin-prick tests. In the 1960s, scientists discovered that such reactions involve the production of a specific antibody called immunoglobulin E. This binds to the surface of special large cells (mast cells), stimulating them to secrete histamine, serotonin, and prostaglandins. These are the chemicals that produce the allergic reactions such as inflammation of the nasal membranes in hay fever or the contraction of the tubes leading to the lungs which causes asthma.

True food allergies involve the release of immunoglobulin E when a problem food is eaten. Allergens occur in cow's milk, eggs, nuts, fish, and shellfish, causing allergic reactions that show up in skin and blood tests. They also produce symptoms such as urticaria and a tight chest that makes breathing difficult. Most reactions are short-lived and relatively harmless, but severe allergic reactions leading to anaphylactic shock and death are not uncommon. These reactions may occur in food allergies (nuts are an especial problem) and in response to bee stings in sensitive people. Very few people (probably less than 1 per cent) suffer a true food allergy but between 20 and 30 per cent may have an adverse reaction to food which is not revealed by skin or blood tests (see food intolerance).

Every spring and summer, many people suffer from hay fever, a very common form of allergy. The symptoms include itchy eyes, sneezing, and congested nostrils. Most of these symptoms can be controlled by antihistamine or steroid nasal spray. Unfortunately, in some forms of allergy, violent reactions may take place leading to serious or even fatal consequences — anaphylactic shock — as seen in allergies to seafood, nuts, or certain drugs such as penicillin.

In the realm of immunology, substances that cause immune responses or allergic reactions are known as antigens. Specific antigens that provoke an allergic reaction are called allergens. Typical allergens include pollens, house-dust mites, animal dander, bacteria, foods, drugs, and chemicals. At present, we do not know why, in similar amounts and circumstances, these substances are harmless to most people but can cause health hazards in others. Avoidance of known allergens is the best protection against such reactions.

In the immune system several mechanisms have been evolved to protect the body against antigens. Prominent among these are the lymphocytes, white blood cells that are specialized to react to specific antigens. There are two kinds of lymphocytes — B cells and T cells. B cells produce antibodies, which are proteins that bind to and destroy or neutralize antigens. T cells do not produce antibodies; instead, they produce cytokines — soluble molecules mediating interaction between cells. T cells also bind directly to an antigen and initiate an attack on it by ‘presenting’ parts of it to B cells, to stimulate antibody production.

Allergic reactions

Depending on whether the antigen triggers a response by B cells or T cells, allergic (hypersensitivity) reactions can have immediate or delayed effects. They are classified as Type I, II, III, and IV. Type I, II, and III allergic reactions are the products of B cell stimulation, and, as a result of antibody-antigen responses, these reactions take immediate effect. Different types of reaction may occur together — for example, in asthma, bronchial reactions to allergens show both an immediate and a late-phase response.

Type I reactions; which include hay fever and insect venom allergy, involve the class of antibodies known as immunoglobulin E (IgE). IgE molecules are bound to mast cells, which are found in connective tissue. When enough antigen has bound with the IgE antibodies, the mast cells release granules of histamine and heparin and produce other substances that cause inflammation. These potent chemicals dilate blood vessels and constrict bronchial air passages. Histamine is responsible for the visible symptoms of an allergic attack, such as running nose, wheezing, and tissue swelling. Antihistamines or steroid nasal spray are often used to give temporary relief. An alternative treatment is desensitization, in which increasing amounts of the antigen are injected over a period of time until the sufferer no longer experiences an allergic response.

In severe allergic reactions, ‘complement’ fragments (anaphylatoxins) — proteins circulating in the blood — stimulate a more massive release of substances from mast cells which dilate blood vessels and constrict bronchioles. This sequence of events results in the collapse of the circulatory system, together with respiratory symptoms, leading to a potentially fatal reaction — anaphylactic shock.

Drug allergy is a hypersensitivity reaction to therapeutic agents. It occurs occasionally on second exposure to a drug against which an individual has already produced antibodies. It remains to be established why some drugs rarely cause allergic reactions (e.g. tetracyclines, digitalis), while others frequently provoke them (e.g. penicillin, phenytoin).

The mechanisms of immune activation in drug allergy are similar to antibody responses to foreign molecules, especially proteins, that enter the body. Although drug molecules are too small to be antigenic by themselves, they can conjugate to body proteins and elicit an immune response. Symptoms vary with the drug and the sensitivity of the affected person, but include, as separate reactions, hives (urticaria), serum sickness, and, sometimes, anaphylaxis. Several drugs can successfully counteract these allergic symptoms (antihistamines, cromolyn, and corticosteroids) — but at present, the best way to combat drug allergy is to identify the offending drug and to observe a lifelong avoidance of that particular compound and its derivatives.

Type II reactions involve different immunoglobulins, known as IgG or IgM, which are antibodies against antigens on the surface of certain ‘target’ cells or in their immediate environment. These antigens may be natural components of healthy cells, or they may be extrinsic components induced by drugs or infectious microbes. The resulting antigen-antibody complex activates the complement system: a series of potent enzymes that destroy the target cell. An example of Type II reactions is autoimmune haemolytic anaemia. In patients with this condition, antibodies destroy their own red blood cells, leading to anaemia.

Type III reactions result when the antigen- antibody complexes (immune complexes) become deposited on the walls of the small blood vessels. Normally, phagocytes remove immune complexes effectively. However, if this mechanism is overloaded, the immune complexes persist and are eventually deposited in a range of tissues and organs. These complexes then trigger the complement system, resulting in damage to blood vessels and inflammation; an example is glomerulonephritis, when the ‘filtering’ components of the kidneys are affected.

Type IV allergic reactions are the only ones that involve delayed hypersensitivity. These reactions are caused by the actions of T cells. Here the antigens are trapped inside macrophages and cannot be cleared. T cells are then activated to produce cytokines, which mediate a range of inflammatory responses. In contrast to the rapid responses mediated by B-cell antibodies, T cells take longer to accumulate at the site where the antigen is present. Thus the allergic responses are delayed and appear 12 to 24 hours or more after exposure to an appropriate antigen. Contact dermatitis is one example, in which the skin responds to allergens such as nickel and rubber accelerators. These substances penetrate the skin and become linked to a carrier protein, capable of producing allergic reactions.

Hypersensitivity involving T-cell-mediated immunity occurs also in some chronic diseases due to infectious agents such as the mycobacteria that cause leprosy and tuberculosis, and parasitic worms such as schistosomiasis.

Organ transplantation (of kidney, heart, or lungs, respectively) is increasingly used to save patients with renal failure, cardiac failure, or cystic fibrosis. Unfortunately, T cells of the recipients can recognize and respond to foreign antigens of the grafts, leading to their eventual destruction. Immunosuppressive drugs such as steroids and cyclosporin are successful in preventing rejection. However, these drugs do not work specifically against the particular unwanted functions of macrophages or T-cells, and may reduce the patients' resistance to infections.

— Tai-Ping Fan

See also autoimmune disease; phagocytes; thymus.

Definition: aversion
Antonyms: affinity, liking

Definition

Allergies are abnormal reactions of the immune system that occur in response to otherwise harmless substances.

Description

Allergies are among the most common of medical disorders. It is estimated that 60 million Americans, or more than one in every five people, suffer from some form of allergy, with similar proportions throughout much of the rest of the world. Allergy is the single largest reason for school absence and is a major source of lost productivity in the workplace.

Allergies are a type of immune reaction. Normally, the immune system responds to foreign microorganisms, or particles, like pollen or dust, by producing specific proteins, called antibodies, that are capable of binding to identifying molecules, or antigens, on the foreign particle. This reaction between antibody and antigen sets off a series of reactions designed to protect the body from infection. When this same series of reactions is triggered by harmless, everyday substances, it is called an allergy. The substance that causes the allergy is called an allergen.

All allergic reactions involve a special set of cells in the immune system known as mast cells. Mast cells, found in the lining of the nasal passages and eyelids, display a special type of antibody, called immunoglobulin type E (IgE), on their surface. Inside, mast cells store reactive chemicals in small packets, called granules. When the antibodies encounter allergens, they trigger release of the granules, which spill out their chemicals onto neighboring cells, including blood vessels and nerve cells. One of these chemicals, histamine, binds to the surfaces of these other cells, through special proteins called histamine receptors. Interaction of histamine with receptors on blood vessels causes neighboring cells to become leaky, leading to the fluid collection in the body's tissues, swelling, and increased redness characteristic of a runny nose and red, irritated eyes. Histamine also stimulates pain receptors, causing the itchy nose, eyes, and throat common in allergic rhinitis. In the gastrointestinal tract, these reactions lead to swelling and irritation of the intestinal lining, which causes the cramping and diarrhea typical of food allergy. Allergens that enter the circulation may cause hives, angioedema, anaphylaxis, or atopic dermatitis. Allergens on the skin usually cause a delayed hypersensitivity reaction. This type of allergic response may develop over several days following contact with the allergen, and symptoms may persist for a week or more.

Demographics

According to the National Institute of Allergy and Infectious Diseases, annually, more than 50 million Americans suffer from allergic diseases, with approximately 36 million suffering from allergic rhinitis. Upto 6 percent of the general population suffers from an allergy to latex, and children with spina bifida who have had multiple surgical procedures are at higher risk for allergic reactions to latex. Atopic dermatitis is one of the most common skin conditions and occurs commonly in infants and children. Prevalence in the United States is about 10 percent. Food allergies occur in 8 percent of children aged six years and younger. Peanut or other nut allergies affect about 3 million Americans and produce the most severe reactions. Acute allergic hives affect from 10 percent to 20 percent of Americans at some time during their lifetime, and half of those affected have symptoms for more than six months. Allergies to stinging insects occur in about 3.5 percent of Americans. According to the American Academy of Allergy, Asthma, and Immunology, if one parent has an allergic disease, a child has a 48 percent risk of developing allergies. If both parents have allergies, risk increases to 70 percent.

Causes and Symptoms

Allergens enter the body through four main routes: the airways, the skin, the gastrointestinal tract, and the circulatory system.

Airborne allergens cause the sneezing, runny nose, and itchy, bloodshot eyes of allergic rhinitis (hay fever). Airborne allergens can also affect the lining of the lungs, causing asthma, or the conjunctiva of the eyes, causing allergic conjunctivitis. The most common airborne allergens are the following:

• plant pollens
• animal fur and dander
• body parts and excrement from dust mites (microscopic creatures found in all houses)
• excrement from cockroaches
• house dust
• mold spores
• cigarette smoke
• solvents
• cleaners

Allergens in food can cause itching and swelling of the lips and throat, cramps, and diarrhea. When absorbed into the bloodstream, they may cause hives (urticaria) or more severe reactions involving recurrent, non-inflammatory swelling of the skin, mucous membranes, organs, and brain (angioedema). Some food allergens may cause anaphylaxis, a potentially life-threatening condition marked by tissue swelling, airway constriction, and drop in blood pressure. Common food allergens include the following:

• nuts, especially peanuts, walnuts, and brazil nuts
• fish, mollusks, and shellfish
• eggs
• wheat
• milk
• food additives and preservatives

In contact with the skin, allergens can cause reddening, itching, and blistering, called contact dermatitis. Skin reactions can also occur from allergens introduced through the airways or gastrointestinal tract. This type of reaction is known as atopic dermatitis. Dermatitis may arise from an allergic response (such as from poison ivy) or exposure to an irritant causing nonimmune damage to skin cells (such as soap, cold, and chemical agents). Injection of allergens, from insect bites and stings or drug administration, can introduce allergens directly into the circulation, where they may cause system-wide responses (including anaphylaxis), as well as the local ones of swelling and irritation at the injection site.

Common causes of contact dermatitis include the following:

• poison ivy, oak, and sumac
• nickel or nickel alloys
• latex

Insects and other arthropods whose bites or stings typically cause allergy include the following:

• bees, wasps, and hornets
• mosquitoes
• fleas

The following types of drugs commonly cause allergic reactions:

• penicillin or other antibiotics
• flu vaccines
• tetanus toxoid vaccine
• gamma globulin

Children and adolescents with allergies are not equally sensitive to all allergens. Some may have severe allergic rhinitis but no food allergies, for instance, or be extremely sensitive to nuts but not to any other food. Allergies may get worse over time. For example, childhood ragweed allergy may progress to year-round dust and pollen allergy. On the other hand, a child may outgrow allergic sensitivity. Infant or childhood atopic dermatitis disappears in almost all people. More commonly, what seems to be loss of sensitivity is instead a reduced exposure to allergens or an increased tolerance for the same level of symptoms.

Symptoms depend on the specific type of allergic reaction. Allergic rhinitis is characterized by an itchy, runny nose, sneezing, and often a scratchy or irritated throat due to postnasal drip. Inflammation of the thin membrane covering the eye (allergic conjunctivitis) causes redness, irritation, and increased tearing in the eyes. Asthma causes wheezing, coughing, and shortness of breath. Symptoms of food allergies depend on the tissues most sensitive to the allergen and whether the allergen spread systemically by the circulatory system. Gastrointestinal symptoms may include swelling and tingling in the lips, tongue, palate or throat; nausea; cramping; diarrhea; and gas. Contact dermatitis is marked by red, itchy, weepy skin blisters, and an eczema that is slow to heal. It sometimes has a characteristic pattern from the object containing the allergen, such as a glove allergy with clear demarcation on the hands, wrist, and arms where the gloves are worn, or on the earlobes by wearing earrings.

Whole-body or systemic reactions may occur from any type of allergen but are more common following ingestion or injection of an allergen. Skin reactions include the raised, red, and itchy patches called hives that characteristically blanch with pressure and resolve within 24 hours. A deeper and more extensive skin reaction, involving more extensive fluid collection and pain, is called angioedema. This response usually occurs on the extremities, fingers, toes, and parts of the head, neck, and face. Anaphylaxis is marked by airway constriction, blood pressure drop, widespread tissue swelling, heart rhythm abnormalities, and in some cases, loss of consciousness. Other symptoms may include dizziness, weakness, seizures, coughing, flushing, or cramping. The symptoms may begin within five minutes after exposure to the allergen up to one hour or more later. Commonly, this is associated with allergies to medications, foods, and insect venoms. In some individuals, anaphylaxis can occur with exercise, plasma exchange, hemodialysis, reaction to insulin, radiocontrast media used in certain types of medical tests, and on rare occasions during the administration of local anesthetics.

When to Call the Doctor

Parents should consult a physician when a child has repeated and prolonged symptoms. Allergic rhinitis may be mistaken for a cold or other upper respiratory infection. Usually, a fever indicates an infection. Food allergies and allergies to insect stings or medications can be especially dangerous, causing anaphylactic reactions that require emergency treatment.

Diagnosis

Allergies can often be diagnosed by a careful medical history, matching the onset of symptoms to the exposure to possible allergens. Allergy is suspected if the symptoms presented are characteristic of an allergic reaction, and this occurs repeatedly upon exposure to the suspected allergen. Allergy tests can also be conducted to determine allergens.

Skin Tests

Skin tests are performed by administering a tiny dose of the suspected allergen by pricking, scratching, puncturing, or injecting the skin. The allergen is applied to the skin as an aqueous extract, usually on the back, forearms, or top of the thighs. Once in the skin, the allergen may produce a classic immune wheal and flare response (a skin lesion with a raised, white, compressible area surrounded by a red flare). The tests usually begin with prick tests or patch tests that expose the skin to small amounts of allergen to observe the response. A positive reaction occurs on the skin even if the allergen is at levels normally encountered in food or in the airways. Reactions are usually evaluated approximately 15 minutes after exposure. Intradermal skin tests involve injection of the allergen into the dermis of the skin. These tests are more sensitive and are used for allergies associated with risk of death, such as allergies to antibiotics. Skin testing may be painful for children.

Provocation Tests

These tests involve the administration of allergen to elicit an immune response. Provocation tests, most commonly done with airborne allergens, present the allergen directly through the route normally involved. Delayed

allergic contact dermatitis diagnosis involves similar methods by application of a skin patch with allergen to induce an allergic skin reaction. Food allergen provocation tests require abstinence from the suspect allergen for two weeks or more, followed by ingestion of a measured amount of the test substance administered as an opaque capsule along with a placebo control. Provocation tests are not used if anaphylaxis is a concern given the patient's medical history.

Treatment

Avoiding allergens is the first line of defense to reduce the possibility of an allergic attack. However, complete environmental control is often difficult to accomplish; hence, therapeutic interventions are usually necessary. A large number of prescription and over-the-counter drugs are available for treatment of immediate hypersensitivity reactions. Most of these products work by decreasing the ability of histamine to provoke symptoms. Other drugs counteract the effects of histamine by stimulating other systems or reducing immune responses in general.

Antihistamines

Antihistamines are drugs used to treat the symptoms of allergic rhinitis by blocking the action of histamine, a chemical released by the immune system in allergic reactions. Antihistamines are available as prescription and over-the-counter tablets, topical gels or creams, nasal sprays, and eye drops.

Commonly used antihistamines include the following:

• diphenhydramine (Benadryl)
• loratadine (Claritin)
• cetirizine (Zyrtec)
• fexofenadine (Allegra)
• clemastine fumarate (Tavist)
• chlorpheniramine (Chlor Trimeton)
• brompheniramine (Dimetapp)

Decongestants

Decongestants dry up nasal passage tissues and reduce swollen nasal membranes so as to relieve congestion. Decongestants are available as nasal sprays or drops, oral tablets, or syrups. Decongestants are stimulants and may cause increased heart rate and blood pressure, headaches, and agitation. Use of nasal spray decongestants for longer than four to five days can cause loss of effectiveness and rebound congestion, in which nasal passages become more severely swollen than before treatment. Saline nasal sprays, which do not contain decongestants, may be used for longer periods of time to help congestion and nasal passage irritation.

Commonly used decongestants include the following:

• oxymetazoline (Afrin)
• pseudoephedrine (Sudafed)
• phenylephrine (Neo Synephrine)

Corticosteroids

Corticosteroids reduce mucous membrane inflammation and are available by prescription and taken as a series of oral tablets. Corticosteroids are also available as nasal sprays. Allergies tend to become worse as the season progresses because the immune system becomes sensitized to particular antigens and can produce a faster, stronger response. Corticosteroids are especially effective at reducing this seasonal sensitization because they work more slowly and last longer than most other medication types. Side effects may include headaches, nosebleeds, and unpleasant taste sensations. Long-term use of oral corticosteroids may cause more serious side effects, such as weight gain, cataracts, weakening bones, high blood pressure, elevated blood sugar, and easy bruising.

Mast Cell Stabilizers

Cromolyn sodium prevents the release of mast cell granules, thereby preventing release of histamine and the other chemicals contained in them. Cromolyn sodium is available in nasal sprays or via an inhaler. It is most frequently prescribed when allergic rhinitis is accompanied by asthma.

Immunotherapy

Immunotherapy, also known as desensitization therapy or allergy shots, alters the balance of antibody types in the body, thereby reducing the ability of IgE to cause allergic reactions. Immunotherapy is preceded by allergy testing to determine the precise allergens responsible. Injections involve very small but gradually increasing amounts of allergen, over several weeks or months, with periodic boosters. Full benefits may take up to several years to achieve and are not seen at all in about one in five patients. Individuals receiving all shots are monitored closely following each shot because of the small risk of anaphylaxis, a condition that can result in difficulty breathing and a sharp drop in blood pressure.

Treatment of Contact Dermatitis

An individual suffering from contact dermatitis should initially take steps to avoid possible sources of exposure to the offending agent. Calamine lotion applied to affected skin can reduce irritation somewhat, as can cold-water compresses. Topical antihistamine and corticosteroid sprays, gels, and creams are available to reduce itching. Side effects of topical agents may include overdrying of the skin. In the case of acute contact dermatitis, short-term oral corticosteroid therapy may be appropriate. Moderately strong corticosteroids can also be applied as a wrap for 24 hours. Healthcare workers are especially at risk for hand eruptions due to latex glove use.

Treatment of Anaphylaxis

The emergency condition of anaphylaxis is treated with injection of adrenaline, also known as epinephrine. Children and adolescents who are prone to anaphylaxis because of food or insect allergies often carry an Epipen containing adrenaline in a hypodermic needle. Other medications may be given to aid the action of the Epipen. Prompt injection can prevent a more serious reaction from developing. Particular care should be taken to assess the affected child's airway status, and he or she should be placed in a recumbent pose and vital signs determined. Emergency treatment may be required for severe reactions.

Nutritional Concerns

For children and adolescents with food allergies, all foods must be monitored to make sure that the allergen is not an ingredient or was not used during preparation. In individuals with severe food allergies to peanuts, peanut oil used to fry foods, or even the fumes produced during cooking with peanut oil have been known to cause anaphylactic shock.

Parents whose children have allergies to foods, like milk and gluten, which are common ingredients in many other foods, can purchase gluten-free foods and lactose-free foods in most grocery stores. Cookbooks dealing with allergies to these foods are also available.

Prognosis

Allergies can improve over time, although they often worsen. While anaphylaxis and severe asthma are life threatening, other allergic reactions are not. Learning to recognize and avoid allergy-provoking situations allows most children and adolescents with allergies to lead normal lives.

Prevention

Avoiding allergens is the best means of limiting allergic reactions. For food allergies, there is no effective treatment except avoidance. By determining the allergens that are causing reactions most people can learn to avoid allergic reactions from food, drugs, and contact allergens such as poison ivy or latex. Airborne allergens are more difficult to avoid. Preventive measures for airborne allergens include the following:

• staying indoors with windows closed during the morning hours, when pollen levels are highest
• keeping car windows up while driving
• using a surgical face mask when outside
• avoiding uncut fields
• learning which trees are producing pollen in which seasons and avoiding forests at the height of pollen season
• washing clothes and hair after being outside
• regularly cleaning air conditioner filters in the home
• using electrostatic filters for central air conditioning

For mold spores, the following steps will help:

• keeping the house dry through ventilation and use of dehumidifiers
• using a disinfectant such as diluted bleach to clean surfaces such as bathroom floors and walls
• having air ducts cleaned and disinfected
• cleaning and disinfecting air conditioners and coolers
• throwing out moldy or mildewed books, shoes, pillows, or furniture

For house dust, the following steps will help:

• vacuuming frequently and changing the bag regularly; using a bag with small pores to catch extra-fine particles
• cleaning floors and walls with a damp mop
• installing electrostatic filters in heating and cooling ducts and changing all filters regularly

For animal dander, the following steps will help:

• avoiding contact if possible
• washing hands after contact
• vacuuming frequently
• keeping pets out of the bedroom and off furniture, rugs, and other dander-catching surfaces
• bathing and grooming pets frequently

Parents may find it helpful to keep an allergy journal for their child to track occurrence of allergic responses. For seasonal allergic rhinitis, they may use a calendar to note when symptoms begin and end. Documenting the level of seasonal allergens at the time can help determine when seasonal allergies tend to occur and what allergens affect the child. Local weather reports on television and on Web sites provide detailed allergen maps of pollen and mold/mildew spores. Antihistamines can then be taken as a preventive measure before symptoms begin each season. For children with allergies to foods, keeping a journal of foods eaten can help identify specific food allergens.

Parental Concerns

For children who resist taking pills, many antihistamines are available as flavored chewable tablets, tablets that easily dissolve on the tongue, or flavored syrups. Because many over-the-counter allergy medicines contain multiple drugs, parents should be sure to read the prescribing and dosage information for any antihistamine their children are taking to ensure safe use.

Parents of children and adolescents with severe food and insect sting allergies that might result in sudden anaphylactic reactions should make sure that their children and any other family members and caregivers fully understand the severity of the allergic response and the need for immediate administration of epinephrine. Parents should consider having children with these severe allergies wear a medical alert bracelet.

Children with severe food allergies to whole food groups, such as milk or wheat, may require dietary management by a dietitian or nutritionist to ensure they receive the proper nutrients and a well-balanced diet. Breastfeeding mothers of highly allergic infants may need to eliminate suspected food allergens from their diets, because food proteins ingested by a mother can be transferred to the infant via breast milk. Special formulas are available for infants sensitive to breast milk, cow's milk, and soy milk.

Resources

Books

Borrel, Marie. 60 Tips: Allergies. London: Hachette Illustrated, 2004.

Cross, Linda. How to Manage Your Child's Life-Threatening Food Allergies. Lake Forest, CA: Plumtree Press, 2004.

Dadamo, Peter J. Eat Right for Your Type Allergies. East Rutherford, NJ: Penguin Group, 2005.

Ford, Jean. Breathe Easy: A Teen's Guide to Allergies and Asthma. Broomall, PA: Mason Crest Publishers, 2005.

Taylor, R., et al. Allergy Relief and Prevention, 3rd. ed. Vancouver: Hartley and Marks, 2000.

Periodicals

Ansel, K. "Working with the Food-Allergic Child. Today's Dietitian. 4 (November 2002): 36–39.

Organizations

Allergy and Asthma Network. 3554 Chain Bridge Road, Suite 200. Web site: www.aanma.org.

American Academy of Allergy, Asthma, and Immunology. 611 East Wells St, Milwaukee, WI 53202. Web site: www.aaaai.org.

Asthma and Allergy Foundation of America. 1125 15th Street NW, Suite 502, Washington, DC 20005. Web site: www.aafa.org/.

Web Sites

"All About Allergies." Nemours Foundation. Available online at www.kidshealth.org/parent/medical/allergies/allergy.html (accessed October 26, 2004).

[Article by: Jennifer E. Sisk, MA]

An abnormal condition of the skin or mucous membranes resulting from an overzealous immune response and heightened sensitivity to a substance that is, in normal amounts, harmless to the majority of people. Causes include house dust, fungi, and drugs. Of particular interest in sport is the hypersensitivity of some athletes to adhesive tape (see allergic contact dermatitis) and antibiotics.

A Bee Gathers Nectar and Pollen

From our Archives: Today's Highlights, March 29, 2005

Treatment of allergies became a part of psychosomatics, and subsequently psychoanalysis, following the work of the Chicago School, especially Franz Alexander and Thomas M. French in 1941. Alexander and French focused primarily on asthma rather than cutaneous allergic reactions, but later authors approached these initial studies quite differently. Distancing themselves from the idea of hysterical conversion, they established a link between psychic conflict and analogous somatic conflict. With respect to allergy, they looked for the conflicting elements they considered characteristic. For asthma, these conflicts were primarily conflicts between infants' dependence on their mothers and instinctual demands that threatened this dependence. The crisis itself was associated with an inhibition of emotional expression, especially tears.

Because these factors were not specific, other authors returned to classical methods of analysis. Phyllis Greenacre (1945) insisted that oral sadism can be masked by streams of crocodile tears; here emotional expression assumes renewed importance in an interpretive framework. Jacob Arlow (1955) considered an allergic attack to be a manifestation of transference essentially associated with sadistic fantasies of incorporation. Melitta Sperling (1963) also demonstrated the links between allergies and pregenital factors. Philip C. Wilson (1968) hypothesized that transferential acting may be involved. In the end, the dimension of conversion returned to the foreground. Michel de M'Uzan (1968) insisted on the need to clarify the formation of somatic symptoms, and he turned to the notion of psychosomatic structure.

Pierre Marty reinvigorated the concept of allergies through his description of the allergic character (1976), which followed his account of the allergic object relation fifteen years earlier. He gave the allergic character the following traits: absence or avoidance of aggressiveness, a capacity for identification, absence or avoidance of conflict, considerable merging with the other, and projection as a mode of identification. To describe these traits in turn, absence or avoidance of aggressiveness gives subjects a socially agreeable cast, but is based on a weak capacity for negation, which in turn indicates a weak superego. The capacity for identification was already included in the allergic object relation. Merging with the other (absence of anxiety in the face of the foreign) is also characteristic of certain forms of primary epilepsy and allergic epilepsy, described by Marie-Thérèse Neyraut-Sutterman. Projection, described in 1957, becomes a mode of identification. As a consequence, subjects are unable to project bad objects or to distinguish good from bad.

Only when the allergic child is able, through stranger anxiety, to be afraid do allergic mechanisms begin to diminish. The features above can be found together in a character neurosis (which Pierre Marty referred to as a common allergy bundle), or they can appear as simple, relatively invasive traits that form a more or less split-off component of the personality, manifested only during regression (Pierre Marty referred to these as lateral lines) or deep splitting (parallel lines).

An allergic crisis can be triggered by the overriding of identificatory possibilities, as when the child is presented with two equally invested objects where the identifications have been kept separate. For Pierre Marty, a somatic manifestation is seen as a way station within a regressive movement and not, as in the psychogenetic approach, as the somatic expression of a traumatic situation. For Michel Fain, the unconscious of the typical allergic is the seat of the mother's desire to have the child regress to a primary narcissistic stage of feelings of unity with her, a desire that keeps an entire portion of the ego of the allergic patient in an embryonic state.

For Marty, these properties and variations result in distinct therapeutic indications. In typical cases, the allergic individual is very adaptable, also in the allergic's relation to the analyst and to analysis. The down side of this is that there is a risk of an outbreak of somatic manifestations at the end of treatment. He therefore recommends psychotherapy as a prophylactic, which can help the patient to recognize unconscious factors and become aware of the danger of certain object relations. Marty believes that medical treatment is indicated for somatic disorders, and that analysis and psychotherapy should not be recommended for allergic manifestations.

This conception of an allergic quasi-structure has led to more recent work by Léon Kreisler (1982), Michel Fain (1969), and Gérard Szwec (1993), who have addressed these problems in children.

Bibliography

Alexander, Franz, and French, Thomas M. (1941). Psychogenic factors in bronchial asthma. Washington, DC: National Research Council.

Arlow, Jacob. (1955). Notes on oral symbolism. Psychoanalytic Quarterly, 24, 63-74.

Fain, Michel. (1969). Réflexions sur la structure allergique. Revue française de psychanalyse, 33 (2).

Greenacre, Phyllis. (1945). Pathological weeping. Psychoanalytic Quarterly, 14 62-75.

Kreisler, Léon. (1982). L'économie psychosomatique de l'enfant asthmatique:à propos d'un cas d'asthme grave chez un préadolescent Psychothérapies, 2 (1), 15-24.

Marty, Pierre. (1976). Les mouvements individuels de vie et de mort. Vol. 1: Essai d'économie psychosomatique. Paris: Payot.

M'Uzan, Michel de. (1968). Comment on "Psychosomatic Asthma and Acting Out," by Ph. Wilson. International Journal of Psycho-Analysis, 49 (2-3), 333-335.

Sperling, Melitta. (1963). Fetishism in children. Psychoanalytic Quarterly, 32, 374-392.

Szwec, Gérard. (1993). La psychosomatique de l'enfant asthmatique. Paris: Presses Universitaires de France.

Wilson, C. Philip. (1968). Psychosomatic asthma and acting out: A case of bronchial asthma that developed de novo in the terminal phase. International Journal of Psycho-Analysis, 49 (2-3), 330-333.

—ROBERT ASSÉO

Food allergy has been recognized since the time of Hippocrates. People with adverse reactions to food can be difficult to evaluate because overlap exists between true food allergy and toxic and other reactions to chemicals or other food ingredients. The incidence of food allergy is increasing in the industrialized world, raising questions about the interactive effects between environmental and genetic factors. There is a considerable burden on society in terms of cost of treatment, death from anaphylactic reactions, and the anxiety produced by real or perceived food allergy. Avoidance of the food is the current treatment, but new strategies are being developed.

Definitions

Adverse reactions to the ingestion of food that can be reproduced is termed intolerance or hypersensitivity. Since this does not imply an underlying cause, it may encompass immune or nonimmune mechanisms. For example, chemicals such as caffeine may cause reproducible symptoms, but this is not mediated by the immune system. True food allergy or food hypersensitivity is defined as a reproducible adverse reaction to food caused by the immune system creating antibodies or cellular inflammation.

Type I IgE-mediated food allergy. The classic example is immediate anaphylactic reaction to food. In susceptible individuals after exposure to the food, the immune system creates specific IgE antibodies to that food. IgE is produced by the immune system's B-lymphocytes, and is bound to receptors on the surface of mast cells. Mast cells reside in tissues at body surfaces such as the skin, eyes, nose, throat, lung, and gastrointestinal tract. Mast cells are made up of granules containing chemicals including histamine. When the food protein contacts and binds to adjacent specific IgE molecules at the mast cell surface, a cascade of events occurs leading to degranulation of mast cells and release of chemicals that cause the allergic reaction. This may include skin hives, airway swelling, wheezing, abdominal pain, vomiting and/or diarrhea. This may progress to anaphylaxis, shock, and even death. This reactivity to food can be demonstrated by skin-prick tests, which have been used to diagnose allergy since the 1870s. Food protein is placed on the skin, the skin is scratched or pricked, and a hive will develop in the presence of skin mast cells with IgE directed against the food. In the 1920s Prausnitz and Kustner showed that a substance circulating in the blood of the allergic individual was responsible for a positive skin test, because blood serum could be transferred to the skin of a nonallergic individual resulting in a positive skin test. IgE is that substance, and food-specific IgE can be measured directly in the blood, by means of the IgE RAST (radioallergosorbent) test. Diagnosis of this immediate type of food allergy rests on the history of rapid onset of symptoms, demonstration of positive skin-prick test or specific IgE RAST. Challenging an individual with the food is the ultimate way to prove a food allergy.

Non-IgE-mediated food allergy. Other immune mechanisms can be responsible for allergic reactions to foods. The classic example is celiac disease (celiac sprue or gluten-induced enteropathy). This is an immune system reaction to wheat (gluten). Patients do not have IgE antibody directed against wheat, but exposure to gluten over a period of time causes inflammation of the intestine and a characteristic atrophy or flattening of the normal intestinal villous folds. The diagnosis rests on the characteristic biopsy of the small intestine coupled with another type of antibody (IgA) against wheat protein. Any food may also cause similar intestinal inflammation, leading to varying symptoms and signs depending on the area of the intestine affected. Unlike IgE-mediated allergy or celiac disease, there are no readily available confirmatory tests for these other food allergies.

Prevalence

Food allergy is perceived as being common; however, large studies support the idea that true food allergy is less common than people think. A study of 480 infants from birth to age three revealed 28 percent were suspected by their parents as having food allergy; however, this was confirmed in only 8 percent of this group. The prevalence then decreases with age. Twenty percent of adults suspect food allergy, though allergy is confirmed in only 1 to 2 percent of adults. Although food allergies in adults tend to persist with age, many infants and children out-grow them with time.

Recently, interest has grown over the apparent increase in the prevalence and severity of food allergy. This has paralleled an increase in other atopic disorders such as asthma in industrialized nations compared with children of similar genetic background in developing countries (atopic refers to a tendency to develop allergic conditions such as hay fever, asthma, or food allergies). The "hygiene hypothesis" contends that through evolution, the human immune system has developed with a specific microbial environment, and reduced exposure to microbes in the developed world may lead to increased allergic response. Further study is needed.

Type I Immediate (Ige-Mediated) Hypersensitivity Reactions to Food

Immediate hypersensitivity reactions to foods are most common in young children, with 50 percent of these reactions occurring in the first year of life. The majority is from cow's milk and soy protein from infant formulas. Other foods begin to predominate in older children, including eggs, fish, peanuts, and wheat, and along with milk and soy account for over 90 percent of food allergy in children. Peanut, tree nut, and shellfish allergy predominate in adults. Exposures may occur inadvertently due to improper labeling, changes in product composition with time, and contamination of foods during processing. Symptoms from multiple organ systems may occur, beginning within minutes. Unfortunately, fatal anaphylactic reactions (shock) to food occur despite strict dietary avoidance and treatment of reactions. Families, caregivers, and individuals with a history of anaphylaxis to food require education in diet and in the use of self-administered epinephrine. Individuals should be observed in a hospital setting after a significant reaction. Exercise-induced anaphylaxis to food occurs when the combination of ingesting the food followed by exercise leads to anaphylaxis. Oral allergy syndrome describes symptoms of itching of the mouth and throat often attributable to eating fruits, and typically does not progress. Chronic hives or urticaria can be caused by foods, but it is a common misconception that these conditions are usually food-related; only in 1 to 2 percent of cases is urticaria or chronic hives a reaction to food. Atopic dermatitis (AD) or eczema is a chronic skin condition found in atopic individuals. Patients with AD have a 30 to 40 percent prevalence of food allergy.

Investigation and treatment of type I immediate reactions to food. The rapid onset of symptoms after ingestion correlates highly with positive skin-prick or IgE RAST tests to the offending food, making confirmation of immediate hypersensitivity straightforward. Consultation with an allergist and dietitian is recommended. Groups such as the Food Allergy and Anaphylaxis Network can provide support and educational materials.

Non-Ige-Mediated Food Allergy

The spectrum of non-IgE food allergy is quite varied, and the symptoms often parallel the area of inflammation in the gastrointestinal tract (see sidebar). Avoidance of the food will resolve symptoms and intestinal inflammation; rechallenge with the food will reproduce the injury. However, unlike IgE food allergy, symptoms may take days or weeks to resolve or reappear with elimination or exposure respectively, making evaluation even more difficult.

Celiac disease or gluten-induced enteropathy (see sidebar) is a chronic intestinal condition caused by non-IgE mediated allergy to gluten, a protein in wheat and other grains. Chronic exposure to gluten causes inflammation and atrophy of small intestinal folds, leading to symptoms of malabsorption of food. Typically, patients have diarrhea, weight loss, and abdominal bloating. There is a genetic predisposition to celiac disease, but onset may occur at any age, suggesting an environmental factor such as infection may be needed in some individuals to trigger the inflammatory process. The disease has a higher prevalence (up to 1 in 400–500) in individuals of eastern European descent. Celiac disease is associated with a skin condition (dermatitis herpetiformis), thyroid disease, diabetes, and Down syndrome.

Allergic or eosinophilic colitis in infants is a common manifestation of non-IgE food protein allergy. It is characterized by diarrhea with blood and mucus. It is caused by milk or soy formula and may occur in breast-fed infants from dietary antigens transmitted through breast milk. Colon biopsy shows allergic inflammation.

Food protein-induced enterocolitis is a severe reaction to food, often delayed four to six hours, without evidence of IgE. Patients present with lethargy, vomiting, and diarrhea. Recovery is within six to eight hours after fluid resuscitation. A careful history usually reveals the offending food, although this may not be appreciated unless multiple episodes occur.

Chronic enteropathy from food allergy can also lead to inflammation with villous atrophy similar to celiac disease. Most patients have diarrhea, in addition to weight loss, anemia, and low albumin from protein loss from the intestine.

Allergic gastritis is inflammation of the stomach with pain and vomiting. As with other non-IgE food allergy, biopsies of the stomach demonstrate allergic (eosinophilic) inflammation.

Allergic esophagitis is characterized by intense eosinophilia of the esophagus on biopsy. Patients complain of pain and problems with swallowing, even to the point of having food impactions in the esophagus. Treatment with hypoallergenic formula has been shown to improve esophagitis in infants; however, older children and adults may require corticosteroid medication.

Infantile colic and excessive irritability can be symptoms related to allergy in a subgroup of infants. By definition, colic is a condition with increased crying behavior in infants, for which no cause can be found. However, since allergy can potentially lead to inflammation and pain, formula allergy is often considered.

Attempts have been made to associate a variety of other problems with food allergy including joint disease, migraine, and behavioral and developmental disorders such as autism. Causal relationship between food allergy and these disorders remains unproven.

Investigation and treatment of non-IgE-mediated food allergy. The diagnosis rests on the resolution of symptoms and/or biopsy findings on an elimination diet, with a return of symptoms on rechallenge. Unlike the rapid response characteristic of IgE-mediated disease, a prolonged challenge may identify delayed reactions with predominantly gastrointestinal symptoms up to six days after exposure. Elemental diets can be used to eliminate dietary protein antigens completely, then systematic rechallenge of the patient with suspected offending foods. As with IgE food allergies, avoidance of the specific food remains the mainstay of therapy.

New Frontiers

There are a number of exciting areas of research into the prevention and treatment of food allergies. Recent reports suggest that the allergic response can be altered by promoting beneficial gut flora ("probiotic therapy"). It has also been discovered that only a few sites (epitopes) on food protein molecules interact with the immune system to create an allergic reaction. Genetic engineering of foods makes it possible to alter these epitopes, creating crops that are "nonallergic." More study is needed to ensure that altering food proteins does not lead to other health concerns or different types of allergy. Other studies are under way to assess the effectiveness of promising new drug therapies for patients with food allergy.

Manifestations of Ige Allergy to Food

 Cardiovascular (shock)
 Respiratory (wheeze, cough)
 Gastrointestinal (acute vomiting, pain, diarrhea)
 Skin (hives, atopic dermatitis)
 Eye (itching, swelling)
 Oral (itching, swelling) 

Manifestations of Non-Ige Allergy to Food

 Growth delay
 Protein-losing enteropathy, edema
 Iron-deficiency anemia
 Chronic diarrhea
 Eosinophilic colitis
 Chronic vomiting/feeding intolerance
 Food protein-induced enterocolitis syndrome
 Atopic dermatitis
 Infantile colic 

Manifestations of Celiac Disease (Gluten-Induced Enteropathy)

 Growth delay
 Chronic diarrhea
 Abdominal distension
 Abdominal pain
 Dermatitis herpetiformis
 Associations: Diabetes, thyroid disease, Down syndrome 

Bibliography

Justinich, Christopher J. "Food Allergy and Eosinophilic Gastroenteropathy." In Pediatric Gastroenterology, vol. 2, edited by Jeffrey S. Hyams and Robert Wyllie, pp. 334–347. Philadelphia: W. B. Saunders, 1999.

Metcalfe, Dean D., H. A. Sampson, and R. A. Simon, eds. Food Allergy: Adverse Reactions to Food and Food Additives. 2d ed, Cambridge, Mass.: Blackwell Science, 1997.

Sampson, H. A. "Food Allergy. Part 2: Diagnosis and Management." Journal of Allergy and Clinical Immunology 103 (1999): 981–989.

Sampson, H. A. "Food Allergy. Part 1: Immunopathogenesis and Clinical Disorders." Journal of Allergy and Clinical Immunology 103 (1999): 717–728.

Sampson, H. A., and J. A. Anderson. "Classification of Gastrointestinal Disease of Infants and Children due to Adverse Immunologic Reactions to Foods." Journal of Pediatric Gastroenterology and Nutrition 30 (suppl) (2000): 1–94.

—Christopher J. Justinich

A highly sensitive reaction of the body to certain substances, such as pollen, that are present in amounts that do not affect most people. Common indications of allergy include sneezing, skin rashes, itching, and runny nose.

LearnThatWord.com is a free vocabulary and spelling program where you only pay for results!

1. a state of altered (usually increased) reactivity of the body to foreign material.
2. hypersensitivity.

An altered reactivity following second or subsequent exposure to antigen (allergen). See also hypersensitivity, allergic.

• atopic a. — hereditary predisposition to develop certain allergies. See atopy.
• bacterial a. — a specific hypersensitivity to a particular bacterial antigen, e.g. Mycobacterium tuberculosis; it is dependent on previous infection with the specific organism.
• bronchial a. — asthma.
• cold a. — a condition manifested by local and systemic reactions, mediated by histamine, which is released from mast cells and basophils as a result of exposure to cold.
• delayed a. — see delayed hypersensitivity.
• drug a. — see drug allergy.
• drying-off a. — see milk allergy (below).
• food a. — called also gastrointestinal allergy; see food hypersensitivity.
• gastrointestinal a. — see food allergy (above).
• hereditary a. — an allergy with a hereditary predisposition. The tendency to develop some forms of allergy is inherited, but the specific clinical form is not. IgE, formerly called reagin or reaginic antibody, may be involved. See also atopy.
• induced a. — allergy resulting from the injection of an antigen, contact with an antigen, or infection with a microorganism, as contrasted with hereditary allergy.
• inhaled a. — see atopy.
• milk a. — a hypersensitivity to the milk protein, α-casein. Signs, varying from urticaria to anaphylaxis, have occurred in Jersey cows when milk escapes from the udder into the bloodstream during the drying off period.
• physical a. — a condition in which physical agents, such as heat, cold or light, trigger an allergic response.

A hypersensitive reaction of the body to an allergen; an antigen-antibody reaction is manifested in several forms—anaphylaxis, asthma, hay fever, urticaria, angioedema, dermatitis, and stomatitis.

Manifestations of allergies. (Regezi/Sciubba/Pogrel, 2000)

• Afflictions and Conditions - allergy: hypersensitivity to particular substance or antigen, such as pollens, furs, feathers, mold, dust, drugs, dyes, cosmetics, or foods, causing characteristic symptoms when encountered, ingested, or inhaled
• Disciplines and Specialties - allergy: study and treatment of allergies

Allergy
Classification and external resources
Hives are a common allergic symptom.
ICD-10	T78.4
ICD-9	995.3
DiseasesDB	33481
MedlinePlus	000812
eMedicine	med/1101
MeSH	D006967

This is a summary diagram that explains how allergy develops. A. the allergen enters the body. B. an Antigen-presenting cell takes up the allergen molecule and presents its epitopes, through the MHC II receptor, onto its surface. The activated antigen presenting cell then migrates to the nearest lymph node C. where its activates T cells that recognize the allergen. They then give the decision for the T cell to differentiate to Th2 cell. D. at the same time, B cells recognize the allergen and through the activated Th2 cell E. the B cell would be activated. F. and differentiate into plasma cells, at which point they would actively synthesize antibodies of the IgE isotype. G. the IgE antibody, that now recognizes epitopes of the allergen molecule, circulates around the body through the lymphatic and cardiovascular systems and finally binds to its FcεRI receptor on mast and basophil cells. H. when the allergen re-enters the body at a later time it binds to the IgE, which is on the cell surface, resulting in an aggregation of the receptor causing the cells to release pre-formed mediators. One of these mediators is histamine which causes the 5 symptoms of allergic inflammation: heat, pain, swelling, redness and itchiness. Another mediator is IL-4, which affects more B cells to differentiate into plasma cells and produce more IgE and thus the vicious cycle continues.

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, hay fever, 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. These include placing possible allergens on the skin and looking for a reaction such as swelling. Blood tests can also be done to look for an allergen-specific IgE.

Treatments for allergies include avoiding known allergens, use of medications such as anti-histamines that specifically prevent allergic reactions, steroids that modify the immune system in general, and medications such as decongestants that reduce the symptoms. Many of these medications are taken by mouth, though epinephrine, which is used to treat anaphylactic reactions, is injected. Immunotherapy uses injected allergens to desensitize the body's response.

Contents 1 Signs and symptoms 2 Cause 2.1 Foods 2.2 Non-food proteins 2.3 Toxins interacting with proteins 2.4 Genetic basis 2.5 Hygiene hypothesis 2.6 Other environmental factors 2.7 Acute response 2.8 Late-phase response 3 Diagnosis 3.1 Skin testing 3.2 Blood testing 3.3 Other 4 Treatment 4.1 Pharmacotherapy 4.2 Immunotherapy 4.3 Unproven and ineffective treatments 5 Epidemiology 6 History 7 Medical specialty 8 See also 9 References 10 External links

Signs and symptoms

Common symptoms of allergy

Affected organ	Symptom
Nose	swelling of the nasal mucosa (allergic rhinitis)
Sinuses	allergic sinusitis
Eyes	redness and itching of the conjunctiva (allergic conjunctivitis)
Airways	Sneezing, coughing, bronchoconstriction, wheezing and dyspnea, sometimes outright attacks of asthma, in severe cases the airway constricts due to swelling known as laryngeal edema
Ears	feeling of fullness, possibly pain, and impaired hearing due to the lack of eustachian tube drainage.
Skin	rashes, such as eczema and hives (urticaria)
Gastrointestinal tract	abdominal pain, bloating, vomiting, diarrhea

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.^[3] 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.^[4]

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.^[5] 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.^[6][7][8] 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.^[8]

Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema.^[9] 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.^[10]

Tissues affected in allergic inflammation.

Cause

Risk factors for allergy can be placed in two general categories, namely host and environmental factors.^[11] 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.^[12]

Foods

One of the most common food allergies is a sensitivity to peanuts. Peanut allergies may be extremely severe, but can sometimes be outgrown by children school-age.^[13] Tree nuts, including pecans, pistachios, pine nuts, and walnuts, are another common allergen. Sufferers may be sensitive to one, or many, tree nuts.^[14] Also seeds, including sesame seeds and poppy seeds, contain oils where protein is present, which may elicit an allergic reaction.^[14]

Egg allergies affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5.^[15] The sensitivity is usually to proteins in the white rather than the yolk.^[14]

Milk, from cows, goats, or sheep, is another common allergy-causing food, and many sufferers are also unable to tolerate dairy products such as cheese. Lactose intolerance, a common reaction to milk, is not in fact a form of allergy. 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.^[16]

Other foods containing allergenic proteins include soy, wheat, fish, shellfish, fruits, vegetables, spices, synthetic and natural colors, chicken, and chemical additives.^{[citation needed]}

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.^[17]

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.^[17] 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.^[17]

Latex and banana sensitivity may cross-react; furthermore, patients with latex allergy may also have sensitivities to avocado, kiwifruit, and chestnut.^[18] 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.^[17]

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.^[19] Of these poisonous plants, sumac is the most virulent.^[20] The resulting dermatological response to the reaction between urushiol and membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking.^[21]

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.^[22]

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.^[23] Allergic parents are more likely to have allergic children,^[24] and their allergies are likely to be more severe than those from 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.^[24]

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.^[25] Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.^[25] The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.^[26] Overall, boys have a higher risk of developing allergy than girls,^[24] although for some diseases, namely asthma in young adults, females are more likely to be affected.^[27] Sex differences tend to decrease in adulthood.^[24] Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration.^[24] It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.^[28]

Hygiene hypothesis

Main article: 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 stated that insufficient stimulation of the TH1 arm of the immune system lead to an overactive TH2 arm, which in turn led to allergic disease.^[29] 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 it is 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.^[30]

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.^[31] Longitudinal studies in the third world demonstrate an increase in immunological disorders as a country grows more affluent and, it is presumed, cleaner.^[32] The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases.^[33] 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.^[34][35]

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.^[36]

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.^[12] 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.^[37] 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.^[38]

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.^[39] 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.^[40] 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.^[41] In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants.^[42] 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.^[36] Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.^[43] It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.^[43] For more information on this topic, see Helminthic therapy.

Acute response

Degranulation process in allergy. Second exposure to allergen.1 - antigen; 2 - IgE antibody; 3 - FcεRI receptor; 4 - preformed mediators (histamine, proteases, chemokines, heparine); 5 - granules; 6 - mast cell; 7 - newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)

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 T_H2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These T_H2 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.^[12]

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.^[12]

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.^[44] Cytokines from mast cells may also 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 T_H2 cells.^[45]

Diagnosis

An allergy testing machine being operated in the diagnostic immunology lab at Lackland Air Force Base

Before a diagnosis of allergic disease can be confirmed, the other possible causes of the presenting symptoms should be carefully considered.^[46] Vasomotor rhinitis, for example, is one of many maladies that shares symptoms with allergic rhinitis, underscoring the need for professional differential diagnosis.^[47] 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.

Effective management of allergic diseases relies on the ability to make an accurate diagnosis^[48]. Allergy testing can help confirm/rule out allergies and consequently reduce adverse reactions and limit unnecessary avoidance and medications. ^[49][50] 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.^[51] For assessing the presence of allergen-specific IgE antibodies, you can use two different methods—a skin prick test or an allergy blood test. Both methods are recommended by the NIH guidelines and have similar diagnostic value in terms of sensitivity and specificity^[52][53].

A healthcare provider can use the test results to identify the specific allergic triggers that may be contributing to the symptoms. Using this information, along with a physical examination and case history, the doctor can diagnose the cause of the symptoms and tailor treatments that will help the patient feel better. A negative result can help the doctor rule out allergies in order to consider other possible.

NIH Guidelines state that: “sIgE tests are useful for identifying foods potentially provoking IgE-mediated food-induced allergic reactions, and specified ‘‘cutoff’’ levels, defined as 95% predictive values, may be more predictive than skin prick tests of clinical reactivity in certain populations.” It further states, “sIgE tests are very useful for detecting the presence of sIgE antibodies, which indicates the presence of allergic sensitization. Fluorescence-labeled antibody assays have comparable sensitivity to that of skin prick tests, and the absolute levels of sIgE antibodies may directly correlate with the likelihood of clinical reactivity when compared with oral food challenges for the identification of foods provoking IgE mediated FA.”^[54]

According to NICE Guidelines, 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.^[55] Also, earlier and more accurate diagnoses save cost due to reduced GP consultations, referrals to secondary care, misdiagnosis and emergency admissions.^[56]

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.^[57] 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.^[58]

Skin testing

Skin testing on arm

Skin testing on back

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.^[59] 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.^[60]

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 you are not exposed to any allergens during the testing procedure.

How does the test work?

The test measures the concentration of specific IgE antibodies in the blood. Quantitative IgE test results increases the possibility of ranking how different substances may affect your 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.^[61][62]

A low total IgE level is not adequate to rule out sensitization to commonly inhaled allergens.^[63] 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.

History

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.^[64] 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.”^[65] 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.

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 utilized most often with foods or medicines. A patient with a particular suspected allergen is instructed to modify his/her diet to totally avoid that allergen for determined period of 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 different commonly 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.

Some "screening" test methods are intended to provide qualitative test results, giving a "yes" or "no" answer in patients with suspected allergic sensitization. One such method has a sensitivity of about 70.8% and a positive predictive value of 72.6% according to a large study.^[66]

Unreliable tests: There are other types of allergy testing methods that the American Academy of Allergy, Asthma, and Immunology considers to be unacceptable.

These unreliable allergy testing methods are:

Applied kinesiology (allergy testing through muscle relaxation), Cytotoxicity testing, Urine autoinjection, Skin titration (Rinkel method), and Provocative and neutralization (subcutaneous) testing or sublingual provocation^[67]

Treatment

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.^[68]

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 histimine release in allergic individuals have demonstrated statisitically significant reduction on Total Nasel Symptom Scores.^[69][70]

Pharmacotherapy

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

Anti-allergy immunotherapy

Desensitization or hyposensitization is a treatment in which the patient 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. 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.^[71] Meta-analyses have also confirmed efficacy of the treatment in allergic rhinitis in children and in asthma.^{[citation needed]} 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.^[72] 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.^[73]

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.^{[citation needed]}

Allergy shot treatment is the closest thing to a ‘cure’ for allergic symptoms. This therapy requires a long-term commitment.

Unproven and ineffective treatments

An experimental treatment, enzyme potentiated desensitization (EPD), has been tried for decades but is not generally accepted as effective.^[74] 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.^[74]

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.^[75]

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.^[76] 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,^[77] although some suggest that a steady rise in sensitization has been occurring since the 1920s.^[78] The incidence of atopy in developing countries has, in general, remained much lower.^[77]

Allergic conditions: Statistics and Epidemiology

Allergy type	United States	United Kingdom[79]
Allergic rhinitis	35.9 million[80] (about 11% of the population[81])	3.3 million (about 5.5% of the population[82])
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.[83]	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.[84]	5.8 million (about 1% severe).
Anaphylaxis	At least 40 deaths per year due to insect venom. About 400 deaths due to penicillin anaphylaxis. About 220 cases of anaphylaxis and 3 deaths per year are due to latex allergy.[85] An estimated 150 people die annually from anaphylaxis due to food allergy.[86]	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.[87]	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.[86]	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	2.3 million (about 3.7%), prevalence has increased by 48.9% between 2001 and 2005.[88]

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.^[77] 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.^[76] The hygiene hypothesis maintains^[89] 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 T_H1 type responses, leading to unrestrained T_H2 responses that allow for an increase in allergy.^[41][90]

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%,^[91] and an increased prevalence of parasitic infections has been associated with a decreased prevalence of asthma.^[92] It is speculated that these infections exert their effect by critically altering T_H1/T_H2 regulation.^[93] Important elements of newer hygiene hypotheses also include exposure to endotoxins, exposure to pets and growing up on a farm.^[93]

History

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.^[94] Pirquet called this phenomenon "allergy" from the Ancient Greek words ἄλλος allos meaning "other" and ἔργον ergon meaning "work".^[95] 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.^[96] 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.^[97]

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.^[98] 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) or the American Board of Internal Medicine (ABIM). 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.^[99]

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.^[100] 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.^[101]

See also

• Allergic inflammation
• List of allergies
• Oral allergy syndrome

References

1. ^ "allergy" at Dorland's Medical Dictionary
2. ^ Kay AB (2000). "Overview of 'allergy and allergic diseases: with a view to the future'". Br. Med. Bull. 56 (4): 843–64. doi:10.1258/0007142001903481. PMID 11359624. 
3. ^ Bope, Edward T.; Rakel, Robert E. (2005). Conn's Current Therapy 2005. Philadelphia, PA: W.B. Saunders Company. p. 880. ISBN 0-7216-3864-3. 
4. ^ Holgate ST (1998). "Asthma and allergy—disorders of civilization?". QJM 91 (3): 171–84. doi:10.1093/qjmed/91.3.171. PMID 9604069. 
5. ^ Rusznak C, Davies RJ (1998). "ABC of allergies. Diagnosing allergy". BMJ 316 (7132): 686–9. PMC 1112683. PMID 9522798. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1112683. 
6. ^ Golden DB (2007). "Insect sting anaphylaxis". Immunol Allergy Clin North Am 27 (2): 261–72, vii. doi:10.1016/j.iac.2007.03.008. PMC 1961691. PMID 17493502. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1961691. 
7. ^ Schafer JA, Mateo N, Parlier GL, Rotschafer JC (2007). "Penicillin allergy skin testing: what do we do now?". Pharmacotherapy 27 (4): 542–5. doi:10.1592/phco.27.4.542. PMID 17381381. 
8. ^ ^{a b} Tang AW (2003). "A practical guide to anaphylaxis". Am Fam Physician 68 (7): 1325–32. PMID 14567487. 
9. ^ Brehler R, Kütting B (2001). "Natural rubber latex allergy: a problem of interdisciplinary concern in medicine". Arch. Intern. Med. 161 (8): 1057–64. doi:10.1001/archinte.161.8.1057. PMID 11322839. 
10. ^ Muller BA (2004). "Urticaria and angioedema: a practical approach". Am Fam Physician 69 (5): 1123–8. PMID 15023012. 
11. ^ Grammatikos AP (2008). "The genetic and environmental basis of atopic diseases". Ann. Med. 40 (7): 482–95. doi:10.1080/07853890802082096. PMID 18608118. 
12. ^ ^{a b c d} Janeway, Charles; Paul Travers, Mark Walport, and Mark Shlomchik (2001). Immunobiology; Fifth Edition. New York and London: Garland Science. pp. e-book. ISBN 978-0-8153-4101-7. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=imm.TOC&depth=10. 
13. ^ Sicherer 62
14. ^ ^{a b c} Sicherer 63
15. ^ Järvinen KM, Beyer K, Vila L, Bardina L, Mishoe M, Sampson HA. (July 2007). "Specificity of IgE antibodies to sequential epitopes of hen's egg ovomucoid as a marker for persistence of egg allergy". J. Allergy. 2007 Jul;62(7):758-65. 62 (7): 758–65. doi:10.1111/j.1398-9995.2007.01332.x. PMID 17573723. 
16. ^ Sicherer 64
17. ^ ^{a b c d} Gordon L. Sussman, MD, FRCP; Donald H. Beezhold. "Allergy to Latex Rubber". Annals of Internal Medicine. vol. 122 no. 1 43–46.
18. ^ Fernández de Corres L, Moneo I, Muñoz D, et al. (January 1993). "Sensitization from chestnuts and bananas in patients with urticaria and anaphylaxis from contact with latex". Ann Allergy 70 (1): 35–9. PMID 7678724. 
19. ^ C. Michael Hogan. Western poison-oak: Toxicodendron diversilobum. GlobalTwitcher, ed. Nicklas Stromberg. 2008. Retrieved 30 April 2010.
20. ^ Keeler, Harriet L. (1900). Our Native Trees and How to Identify Them. New York: Charles Scriber's Sons. pp. 94–96; Frankel, Edward, Ph.D. Poison Ivy, Poison Oak, Poison Sumac and Their Relatives; Pistachios, Mangoes and Cashews. The Boxwood Press. Pacific Grove, Calif. 1991. ISBN 978-0-940168-18-3.
21. ^ DermAtlas -1892628434
22. ^ Armstrong W.P., Epstein W.L. (1995). Herbalgram (American Botanical Council) 34: 36–42.  cited in http://waynesword.palomar.edu/ww0802.htm
23. ^ Galli SJ (2000). "Allergy". Curr. Biol. 10 (3): R93–5. doi:10.1016/S0960-9822(00)00322-5. PMID 10679332. 
24. ^ ^{a b c d e} De Swert LF (1999). "Risk factors for allergy". Eur. J. Pediatr. 158 (2): 89–94. doi:10.1007/s004310051024. PMID 10048601. 
25. ^ ^{a b} Croner S (1992). "Prediction and detection of allergy development: influence of genetic and environmental factors". J. Pediatr. 121 (5 Pt 2): S58–63. doi:10.1016/S0022-3476(05)81408-8. PMID 1447635. 
26. ^ Jarvis D, Burney P (1997). "Epidemiology of atopy and atopic disease". In Kay AB. Allergy and allergic diseases. 2. London: Blackwell Science. pp. 1208–24. 
27. ^ Anderson HR, Pottier AC, Strachan DP (1992). "Asthma from birth to age 23: incidence and relation to prior and concurrent atopic disease". Thorax 47 (7): 537–42. doi:10.1136/thx.47.7.537. PMC 463865. PMID 1412098. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=463865. 
28. ^ Barnes KC, Grant AV, Hansel NN, Gao P, Dunston GM (2007). "African Americans with asthma: genetic insights". Proc Am Thorac Soc 4 (1): 58–68. doi:10.1513/pats.200607-146JG. PMC 2647616. PMID 17202293. Archived from the original on 2010-11-16. http://pats.atsjournals.org/cgi/content/full/4/1/58. 
29. ^ Folkerts G, Walzl G, Openshaw PJ (March 2000). "Do common childhood infections 'teach' the immune system not to be allergic?". Immunol. Today 21 (3): 118–20. doi:10.1016/S0167-5699(00)01582-6. PMID 10777250. http://linkinghub.elsevier.com/retrieve/pii/S0167569900015826. 
30. ^ The Hygiene Hypothesis » Edward Willett
31. ^ Gibson PG, Henry RL, Shah S, Powell H, Wang H (September 2003). "Migration to a western country increases asthma symptoms but not eosinophilic airway inflammation". Pediatr. Pulmonol. 36 (3): 209–15. doi:10.1002/ppul.10323. PMID 12910582. 
32. ^ Addo-Yobo EO, Woodcock A, Allotey A, Baffoe-Bonnie B, Strachan D, Custovic A (February 2007). "Exercise-induced bronchospasm and atopy in Ghana: two surveys ten years apart". PLoS Med. 4 (2): e70. doi:10.1371/journal.pmed.0040070. PMC 1808098. PMID 17326711. Archived from the original on 2010-11-16. http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0040070. Retrieved 2008-07-06. 
33. ^ Marra F, Lynd L, Coombes M "et al." (2006). "Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis". Chest 129 (3): 610–8. doi:10.1378/chest.129.3.610. PMID 16537858. 
34. ^ Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell, CR (2007). "A meta-analysis of the association between Caesarean section and childhood asthma". Clin. And Exper. Allergy 38 (4): 629. doi:10.1111/j.1365-2222.2007.02780.x. PMID 18352976. 
35. ^ Zock JP, Plana E, Jarvis D "et al." (2007). "The use of household cleaning sprays and adult asthma: an international longitudinal study". Am J Respir Crit Care Med 176 (8): 735–41. doi:10.1164/rccm.200612-1793OC. PMC 2020829. PMID 17585104. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2020829. 
36. ^ ^{a b} Cooper PJ (2004). "Intestinal worms and human allergy". Parasite Immunol. 26 (11–12): 455–67. doi:10.1111/j.0141-9838.2004.00728.x. PMID 15771681. 
37. ^ Braun-Fahrländer C, Riedler J, Herz U, et al (2002). "Environmental exposure to endotoxin and its relation to asthma in school-age children". N. Engl. J. Med. 347 (12): 869–77. doi:10.1056/NEJMoa020057. PMID 12239255. 
38. ^ Garn H, Renz H (2007). "Epidemiological and immunological evidence for the hygiene hypothesis". Immunobiology 212 (6): 441–52. doi:10.1016/j.imbio.2007.03.006. PMID 17544829. 
39. ^ Macpherson CN, Gottstein B, Geerts S (2000). "Parasitic food-borne and water-borne zoonoses". Rev. - Off. Int. Epizoot. 19 (1): 240–58. PMID 11189719. 
40. ^ Carvalho EM, Bastos LS, Araújo MI (2006). "Worms and allergy". Parasite Immunol. 28 (10): 525–34. doi:10.1111/j.1365-3024.2006.00894.x. PMID 16965288. 
41. ^ ^{a b} Yazdanbakhsh M, Kremsner PG, van Ree R (2002). "Allergy, parasites, and the hygiene hypothesis". Science 296 (5567): 490–4. doi:10.1126/science.296.5567.490. PMID 11964470. 
42. ^ Emanuelsson C, Spangfort MD (2007). "Allergens as eukaryotic proteins lacking bacterial homologues". Mol. Immunol. 44 (12): 3256–60. doi:10.1016/j.molimm.2007.01.019. PMID 17382394. 
43. ^ ^{a b} Falcone FH, Pritchard DI (2005). "Parasite role reversal: worms on trial". Trends Parasitol. 21 (4): 157–60. doi:10.1016/j.pt.2005.02.002. PMID 15780835. 
44. ^ Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ (2006). "Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses". Curr. Opin. Immunol. 18 (6): 751–60. doi:10.1016/j.coi.2006.09.011. PMID 17011762. 
45. ^ Holt PG, Sly PD (2007). "Th2 cytokines in the asthma late-phase response". Lancet 370 (9596): 1396–8. doi:10.1016/S0140-6736(07)61587-6. PMID 17950849. 
46. ^ Allergic and Environmental Asthma at eMedicine - Includes discussion of differentials
47. ^ Wheeler PW, Wheeler SF (2005). "Vasomotor rhinitis". American Family Physician 72 (6): 1057–62. PMID 16190503. http://www.aafp.org/afp/20050915/1057.html. ^{[dead link]}
48. ^ Portnoy, JM, et al. Evidence-based Allergy Diagnostic Tests, Current Allergy and Asthma Reports 2006, 6:455-461
49. ^ NICE Diagnosis and assessment of food allergy in children and young people in primary care and community settings, 2011
50. ^ Boyce J et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Report of NIAID-Sponsored Expert Panel. J Allergy Clin Immunol 2010; 126: S1–S58
51. ^ NICE Diagnosis and assessment of food allergy in children and young people in primary care and community settings, 2011
52. ^ Cox, L. Overview of Serological-Specific IgE Antibody Testing in Children. Pediatric Allergy and Immunology. 2011.
53. ^ Boyce J et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Report of NIAID-Sponsored Expert Panel. J Allergy Clin Immunol 2010; 126: S1–S58
54. ^ NIH Guidelines for the Diagnosis and Management of Food Allergy in the United States. Report of the NIAID- Sponsored Expert Panel, 2010, NIH Publication no. 11-7700.
55. ^ NICE Diagnosis and assessment of food allergy in children and young people in primary care and community settings, 2011
56. ^ Food Allergy in children and young people. Costing report. Implementing NICE guidance, 2011. http://guidance.nice.org.uk/CG116/CostingReport/pdf/English
57. ^ Boyce J et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Report of NIAID-Sponsored Expert Panel. J Allergy Clin Immunol 2010; 126: S1–S58
58. ^ NIH Guidelines for the Diagnosis and Management of Food Allergy in the United States. Report of the NIAID- Sponsored Expert Panel, 2010, NIH Publication no. 11-7700.
59. ^ Verstege A, Mehl A, Rolinck-Werninghaus C, et al (2005). "The predictive value of the skin prick test weal size for the outcome of oral food challenges". Clin. Exp. Allergy 35 (9): 1220–6. doi:10.1111/j.1365-2222.2005.2324.x. PMID 16164451. 
60. ^ Li JT, Andrist D, Bamlet WR, Wolter TD (2000). "Accuracy of patient prediction of allergy skin test results". Ann. Allergy Asthma Immunol. 85 (5): 382–4. doi:10.1016/S1081-1206(10)62550-1. PMID 11101180. 
61. ^ Yunginger J et alQuantitative IgE antibody assays in allergic disease. J Allergy Clin Immunol 2000; 105: 1077–84.
62. ^ Sampson H et al. Utility of food-specific IgE concentrations in predictin symptomatic food allergy. J Allergy Clin Immunol 2001; 107: 891–6.
63. ^ Kerkhof M, Dubois AE, Postma DS, Schouten JP, de Monchy JG (2003). "Role and interpretation of total serum IgE measurements in the diagnosis of allergic airway disease in adults". Allergy 58 (9): 905–11. doi:10.1034/j.1398-9995.2003.00230.x. PMID 12911420. 
64. ^ Ten RM, Klein JS, Frigas E (1995). "Allergy skin testing". Mayo Clin. Proc. 70 (8): 783–4. PMID 7630219. http://www.mayoclinicproceedings.com/inside.asp?AID=3978&UID=. ^{[dead link]}
65. ^ Cox, et al. Pearls and pitfalls of allergy diagnostic testing. Annals of Allergy, Asthma & Immunology. 2008. 101(6): 580-592
66. ^ Vidal C, Gude F, Boquete O, et al (2005). "Evaluation of the phadiatop test in the diagnosis of allergic sensitization in a general adult population". Journal of Investigational Allergology and Clinical Immunology 15 (2): 124–30. PMID 16047713. 
67. ^ "Allergy Diagnosis". Archived from the original on 2010-11-16. http://www.theonlineallergist.com/index.php/article/allergy_diagnosis/. The Online Allergist. Retrieved 2010-10-25.
68. ^ Sicherer SH, Leung DY (2007). "Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects". J. Allergy Clin. Immunol. 119 (6): 1462–9. doi:10.1016/j.jaci.2007.02.013. PMID 17412401. 
69. ^ Funada, U.; Wada, M.; Kawata, T.; Tanaka, N.; Tadokoro, T.; Maekawa, A. (2000). "Effect of Cobalamin on the Allergic Response in Mice". Bioscience, Biotechnology, and Biochemistry 64 (10): 2053. doi:10.1271/bbb.64.2053.  edit
70. ^ Funada, U.; Wada, M.; Kawata, T.; Mori, K.; Tamai, H.; Isshiki, T.; Onoda, J.; Tanaka, N. et al. (2001). "Vitamin B-12-Deficiency Affects Immunoglobulin Production and Cytokine Levels in Mice". International Journal for Vitamin and Nutrition Research 071: 0060. doi:10.1024/0300-9831.71.1.60.  edit
71. ^ Ross RN, Nelson HS, Finegold I (2000). "Effectiveness of specific immunotherapy in the treatment of allergic rhinitis: an analysis of randomized, prospective, single- or double-blind, placebo-controlled studies". Clinical therapeutics 22 (3): 342–50. doi:10.1016/S0149-2918(00)80038-7. PMID 10963288. 
72. ^ Rank MA, Li JT (September 2007). "Allergen immunotherapy". Mayo Clin. Proc. 82 (9): 1119–23. doi:10.4065/82.9.1119. PMID 17803880. 
73. ^ Passalacqua G, Durham SR (2007). "Allergic rhinitis and its impact on asthma update: allergen immunotherapy". J. Allergy Clin. Immunol. 119 (4): 881–91. doi:10.1016/j.jaci.2007.01.045. PMID 17418661. 
74. ^ ^{a b} Terr AI (2004). "Unproven and controversial forms of immunotherapy". Clinical allergy and immunology 18: 703–10. PMID 15042943. 
75. ^ Altunç U, Pittler MH, Ernst E (2007). "Homeopathy for childhood and adolescence ailments: systematic review of randomized clinical trials". Mayo Clin. Proc. 82 (1): 69–75. doi:10.4065/82.1.69. PMID 17285788. 
76. ^ ^{a b} Platts-Mills TA, Erwin E, Heymann P, Woodfolk J (2005). "Is the hygiene hypothesis still a viable explanation for the increased prevalence of asthma?". Allergy 60 Suppl 79: 25–31. doi:10.1111/j.1398-9995.2005.00854.x. PMID 15842230. 
77. ^ ^{a b c} Bloomfield SF, Stanwell-Smith R, Crevel RW, Pickup J (2006). "Too clean, or not too clean: the hygiene hypothesis and home hygiene". Clin. Exp. Allergy 36 (4): 402–25. doi:10.1111/j.1365-2222.2006.02463.x. PMC 1448690. PMID 16630145. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1448690. 
78. ^ Isolauri E, Huurre A, Salminen S, Impivaara O (2004). "The allergy epidemic extends beyond the past few decades". Clin. Exp. Allergy 34 (7): 1007–10. doi:10.1111/j.1365-2222.2004.01999.x. PMID 15248842. 
79. ^ "Chapter 4: The Extent and Burden of Allergy in the United Kingdom". House of Lords - Science and Technology - Sixth Report. 2007-07-24. Archived from the original on 2010-11-16. http://www.publications.parliament.uk/pa/ld200607/ldselect/ldsctech/166/16607.htm. Retrieved 2007-12-03. 
80. ^ "AAAAI - rhinitis, sinusitis, hay fever, stuffy nose, watery eyes, sinus infection". Archived from the original on 2010-11-16. http://www.aaaai.org/patients/gallery/rhinitissinusitis.asp?item=1a. Retrieved 2007-12-03. 
81. ^ Based on an estimated population of 303 million in 2007 U.S. POPClock. U.S. Census Bureau.
82. ^ Based on an estimated population of 60.6 million UK population grows to 60.6 million
83. ^ "AAAAI - asthma, allergy, allergies, prevention of allergies and asthma, treatment for allergies and asthma". Archived from the original on 2010-11-16. http://www.aaaai.org/patients/gallery/prevention.asp?item=1a. Retrieved 2007-12-03. 
84. ^ "AAAAI - skin condition, itchy skin, bumps, red irritated skin, allergic reaction, treating skin condition". Archived from the original on 2010-11-16. http://www.aaaai.org/patients/gallery/skinallergies.asp?item=1a. Retrieved 2007-12-03. 
85. ^ "AAAAI - anaphylaxis, cause of anaphylaxis, prevention, allergist, anaphylaxis statistics". Archived from the original on 2010-11-16. http://www.aaaai.org/patients/gallery/anaphylaxis.asp?item=1a. Retrieved 2007-12-03. 
86. ^ ^{a b} "AAAAI - food allergy, food reactions, anaphylaxis, food allergy prevention". Archived from the original on 2010-11-16. http://www.aaaai.org/patients/gallery/foodallergy.asp?item=1a. Retrieved 2007-12-03. 
87. ^ "AAAAI - stinging insect, allergic reaction to bug bite, treatment for insect bite". Archived from the original on 2010-11-16. http://www.aaaai.org/patients/gallery/insect.asp?item=1a. Retrieved 2007-12-03. 
88. ^ Simpson CR, Newton J, Hippisley-Cox J, Sheikh A (2008). "Incidence and prevalence of multiple allergic disorders recorded in a national primary care database". J Roy Soc Med 101 (11): 558–563. doi:10.1258/jrsm.2008.080196. PMC 2586863. PMID 19029357. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2586863. 
89. ^ Strachan DP (1989). "Hay fever, hygiene, and household size". BMJ 299 (6710): 1259–60. doi:10.1136/bmj.299.6710.1259. PMC 1838109. PMID 2513902. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1838109. 
90. ^ Renz H, Blümer N, Virna S, Sel S, Garn H (2006). "The immunological basis of the hygiene hypothesis". Chem Immunol Allergy. Chemical Immunology and Allergy 91: 30–48. doi:10.1159/000090228. ISBN 3-8055-8000-2. PMID 16354947. 
91. ^ Matricardi PM, Rosmini F, Riondino S, et al (2000). "Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma: epidemiological study". BMJ 320 (7232): 412–7. doi:10.1136/bmj.320.7232.412. PMC 27285. PMID 10669445. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=27285. 
92. ^ Masters S, Barrett-Connor E (1985). "Parasites and asthma—redictive or protective?". Epidemiol Rev 7: 49–58. PMID 4054238. 
93. ^ ^{a b} Sheikh A, Strachan DP (2004). "The hygiene theory: fact or fiction?". Curr Opin Otolaryngol Head Neck Surg 12 (3): 232–6. doi:10.1097/01.moo.0000122311.13359.30. PMID 15167035. 
94. ^ Clemens Peter Pirquet von Cesenatico at Who Named It?
95. ^ Von Pirquet C (1906). "Allergie". Munch Med Wochenschr 53 (5): 1457. PMID 20273584. 
96. ^ Gell PGH, Coombs RRA. (1963). Clinical Aspects of Immunology. London: Blackwell. 
97. ^ Ishizaka K, Ishizaka T, Hornbrook MM (1966). "Physico-chemical properties of human reaginic antibody. IV. Presence of a unique immunoglobulin as a carrier of reaginic activity". J. Immunol. 97 (1): 75–85. PMID 4162440. 
98. ^ "ABAI: American Board of Allergy and Immunology". Archived from the original on 2010-11-16. http://www.abai.org/training.asp. Retrieved 2007-08-05. 
99. ^ "AAAAI - What is an Allergist?". Archived from the original on 2010-11-16. http://www.aaaai.org/media/resources/allergist.asp. Retrieved 2007-08-05. 
100. ^ Royal College of Physicians (2003). Allergy: the unmet need. London, UK: Royal College of Physicians. ISBN 978-1-86016-183-4. PDF versionPDF (1.03 MB)
101. ^ House of Lords - Science and Technology Committee (2007). Allergy - HL 166-I, 6th Report of Session 2006-07 - Volume 1: Report. London, UK: TSO (The Stationery Office). ISBN 978-0-10-401149-2. http://www.publications.parliament.uk/pa/ld200607/ldselect/ldsctech/166/16602.htm. 

External links

• American Academy of Allergy, Asthma & Immunology
• Allergy & Asthma Network Mothers of Asthmatics

ImmunoCAP articles, disease management data, product info from the manufacturer of ImmunoCAP:

• www.isitallergy.com
• www.phadia.com

v d e Health science - Medicine - Allergic conditions Respiratory system Allergic rhinitis · Asthma · Hypersensitivity pneumonitis · Eosinophilic pneumonia · Churg-Strauss syndrome · Allergic bronchopulmonary aspergillosis · Farmer's lung · Laboratory animal allergy Skin Angioedema · Urticaria · Atopic dermatitis · Allergic contact dermatitis · Hypersensitivity vasculitis Blood and immune system Serum sickness Circulatory system Anaphylaxis Digestive system Coeliac disease · Eosinophilic gastroenteritis · Eosinophilic esophagitis · Food allergy · Milk intolerance Nervous system Eosinophilic meningitis Genitourinary system Acute interstitial nephritis Other conditions Drug allergy · Allergic conjunctivitis · Latex allergy M: LMC cell/phys/auag/auab/comp, igrc imdf/ipig/hyps/tumr proc, drug(L3/4)

v d e Consequences of external causes (T66–T78, 990–995) Temperature/radiation elevated temperature: Hyperthermia · Heat syncope reduced temperature: Hypothermia · Immersion foot syndromes (Trench foot • Tropical immersion foot • Warm water immersion foot) · Chilblains · Frostbite · Cold intolerance • Acrocyanosis • Erythrocyanosis crurum radiation: Radiation poisoning · Radiation burn · Chronic radiation keratosis • Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy • Radiation acne • Radiation cancer • Radiation recall reaction • Radiation-induced erythema multiforme • Radiation-induced hypertrophic scar • Radiation-induced keloid • Radiation-induced morphea Air Hypoxia/Asphyxia · Barotrauma (Aerosinusitis, Decompression sickness) · High altitude (Altitude sickness/Chronic mountain sickness, HAPE) Food Starvation Maltreatment Physical abuse · Sexual abuse · Psychological abuse Emesis Motion sickness · Seasickness · Airsickness · Space adaptation syndrome Adverse effect Hypersensitivity (Anaphylaxis, Angioedema, Allergy, Arthus reaction) Adverse drug reaction Other Electric shock · Drowning · Lightning injury Ungrouped skin conditions resulting from physical factors Dermatosis neglecta • Pinch mark • Pseudoverrucous papules and nodules • Sclerosing lymphangiitis • Tropical anhidrotic asthenia  • UV-sensitive syndrome environmental skin conditions: Electrical burn • frictional/traumatic/sports (Black heel and palm • Equestrian perniosis • Jogger's nipple • Pulling boat hands • Runner's rump • Surfer's knots • Tennis toe • Vibration white finger • Weathering nodule of ear • Wrestler's ear • Coral cut  • Painful fat herniation ) • Uranium dermatosis iv use (Skin pop scar • Skin track • Slap mark • Pseudoacanthosis nigricans • Narcotic dermopathy)

v d e Immune disorders: hypersensitivity and autoimmune diseases (279.5–6) Type I/allergy/atopy (IgE) Foreign Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis · Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy Autoimmune none Type II/ADCC (IgM, IgG) Foreign Pernicious anemia · Hemolytic disease of the newborn Autoimmune Cytotoxic Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura  · Bullous pemphigoid  · Pemphigus vulgaris · Rheumatic fever · Goodpasture's syndrome "Type 5"/receptor Graves' disease · Myasthenia gravis Type III (Immune complex) Foreign Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis · Farmer's lung · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction Autoimmune Systemic lupus erythematosus · Subacute bacterial endocarditis · Rheumatoid arthritis Type IV/cell-mediated (T-cells) Foreign Allergic contact dermatitis · Mantoux test Autoimmune Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome  · Multiple sclerosis  · Coeliac disease · Giant-cell arteritis GVHD Transfusion-associated graft versus host disease Unknown/ multiple Foreign Hypersensitivity pneumonitis (Allergic bronchopulmonary aspergillosis) · Transplant rejection · Latex allergy (I+IV) Autoimmune Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease M: LMC cell/phys/auag/auab/comp, igrc imdf/ipig/hyps/tumr proc, drug(L3/4)

This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)

Dansk (Danish)
n. - allergi, overfølsomhed

Nederlands (Dutch)
allergie, afkeer

Français (French)
n. - allergie

Deutsch (German)
n. - Allergie

Ελληνική (Greek)
n. - (παθολ.) αλλεργία, (μτφ.) αποστροφή, απέχθεια

Italiano (Italian)
allergia, insofferenza

Português (Portuguese)
n. - alergia (f) (Med.)

Русский (Russian)
аллергия

Español (Spanish)
n. - alergia

Svenska (Swedish)
n. - allergi

中文（简体）(Chinese (Simplified))
过敏症, 厌恶, 反感

中文（繁體）(Chinese (Traditional))
n. - 過敏症, 厭惡, 反感

한국어 (Korean)
n. - 알레르기, 이상 민감증, 반감

日本語 (Japanese)
n. - アレルギー, 反感, 毛嫌い

العربيه (Arabic)
‏(الاسم) حساسيه الجسم لبعض المواد والأوضاع, نفور‏

עברית (Hebrew)
n. - ‮רגישות מיוחדת, אלרגיה‬

If you are unable to view some languages clearly, click here.

To select your translation preferences click here.