Allergy

An allergy is an exaggerated immune response where the body mistakenly identifies an ordinarily harmless allergen as a threat.[1][2][3][4] Allergic reactions give rise to allergic diseases such as hay fever, allergic conjunctivitis, allergic asthma, atopic dermatitis, food allergies, and anaphylaxis.[5] Symptoms of allergic diseases may include red eyes, an itchy rash, sneezing, coughing, a runny nose, shortness of breath, or swelling.[6][7][8]

Common allergens include pollen, certain foods, metals, insect stings, medications, and materials, such as latex.[1][9] The development of allergies is due to genetic and environmental factors.[9] The mechanism of allergic reactions involves immunoglobulin E antibodies (IgE) binding to an allergen and then to a receptor on mast cells or basophils, where they trigger the release of inflammatory chemicals such as histamine.[10] Diagnosis is typically based on a person's medical history.[7] Further testing of the skin or blood may be useful in certain cases.[7] Positive tests, however, may not necessarily mean there is a significant allergy to the substance in question.[11]

Early exposure of children to potential allergens may be protective.[12] Treatments for allergies include avoidance of known allergens and the use of medications such as steroids and antihistamines.[13] In severe reactions, injectable adrenaline (epinephrine) is recommended.[14] Allergen immunotherapy, which gradually exposes people to larger and larger amounts of allergen, is useful for some types of allergies such as hay fever and reactions to insect bites.[13] Its use in food allergies is unclear.[13]

Allergies are common.[15] In the developed world, about 20% of people are affected by allergic rhinitis,[16] food allergy affects 10% of adults and 8% of children,[17] and about 20% have or have had atopic dermatitis at some point in time.[18] Depending on the country, about 1–18% of people have asthma.[19][20] Anaphylaxis occurs in between 0.05–2% of people.[21] Rates of many allergic diseases appear to be increasing.[14][22][23] The word "allergy" was first used by Clemens von Pirquet in 1906.[9]

## Contents

* 1 Signs and symptoms
* 1.1 Skin
* 2 Cause
* 2.1 Dust mites
* 2.2 Foods
* 2.3 Latex
* 2.4 Medications
* 2.5 Insect stings
* 2.6 Toxins interacting with proteins
* 2.7 Genetics
* 2.8 Hygiene hypothesis
* 2.9 Stress
* 2.10 Other environmental factors
* 3 Pathophysiology
* 3.1 Acute response
* 3.2 Late-phase response
* 3.3 Allergic contact dermatitis
* 4 Diagnosis
* 4.1 Skin prick testing
* 4.2 Patch testing
* 4.3 Blood testing
* 4.4 Other testing
* 4.5 Differential diagnosis
* 5 Prevention
* 6 Management
* 6.1 Medication
* 6.2 Immunotherapy
* 6.3 Alternative medicine
* 7 Epidemiology
* 7.1 Changing frequency
* 8 History
* 8.1 Diagnosis
* 9 Medical specialty
* 10 Research
* 11 See also
* 12 References
* 13 External links

## Signs and symptoms

Affected organ | Common signs and symptoms

|

Nose | Swelling of the nasal mucosa (allergic rhinitis) runny nose, sneezing
Sinuses | Allergic sinusitis
Eyes | Redness and itching of the conjunctiva (allergic conjunctivitis, watery)
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 exposed to air, such as the eyes, nose, and lungs.[24] For instance, allergic rhinitis, also known as hay fever, irritates the nose, sneezing, itching, and redness of the eyes.[25] Inhaled allergens can also lead to increased production of mucus in the lungs, shortness of breath, coughing, and wheezing.[26] Allergic rhinitis can simultaneously occur with other allergic responses such as asthma.[27]

Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin.[24][28] Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhea, itchy skin, and hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis.[29]

Insect stings, food, antibiotics, and certain medicines may 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.[30][31][32] Depending on the severity, anaphylaxis can include skin reactions, bronchoconstriction, swelling, low blood pressure, coma, and death. This type of reaction can be triggered suddenly or have a delayed onset. The anaphylactic reaction may seem to subside, but may recur over time.[32]

Allergic conjunctivitis (left), and chronic allergic otitis in a dog (right).

### Skin

Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema.[33] 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.[34]

A 21-year-old male arms during an allergy skin test. A visible raised, red wheal indicates a positive allergic reaction. The positive control (H) shows a strong reaction, while the negative control (C) shows no visible response.

With insect stings, a large local reaction may occur as an area of skin redness greater than 10 cm in size that can last one to two days.[35] This reaction may also occur after immunotherapy.[36]

The skin forms an effective barrier to the entry of most allergens, but this barrier cannot withstand everything. For example, an insect sting can breach the barrier and inject allergen into the affected spot.[37] When an allergen enters the epidermis or dermis, it triggers a localized allergic reaction which activates the mast cells in the skin resulting in an immediate increase in permeability of blood vessels, leading to fluid leakage and swelling in the affected area.[38] Mast-cell activation also stimulates a skin lesion called the wheal-and-flare reaction.[39] Then the release of chemicals from local nerve endings by a nerve axon reflex causes the widening of surrounding cutaneous blood vessels, which causes redness of the surrounding skin.[39]

As part of the allergic response, the body has developed a secondary response that, in some individuals, causes a more widespread and sustained skin swelling.[38] This usually occurs about 8 hours after the allergen originally comes in contact with the skin. When an allergen is ingested, a dispersed form of wheal-and-flare reaction, known as urticaria or hives, will appear when the allergen enters the bloodstream and eventually reaches the skin.[38][40] The way the skin reacts to different allergens and allows to test for exiting allergies by injecting a very small amount of an allergen into the skin, which cause skin reaction in the site of injection.[38] Even though these injections are very small and local, they still pose the risk of causing systemic anaphylaxis.[38]

## Cause

Risk factors for allergies can be placed in two broad categories: host and environmental factors.[41] Host factors include heredity, sex, race, and age, with heredity being by far the most significant. However, there has been a recent increase 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.[42]

### Dust mites

House dust mites (Dermatophagoides pteronyssinus)

Dust mite allergy, also known as house dust allergy, is a sensitization and allergic reaction to the droppings of house dust mites. The allergy is common[43] and can trigger allergic reactions such as asthma, eczema, or itching.[44]

The mite's gut contains potent digestive enzymes (notably peptidase 1) that persist in their faeces and are major inducers of allergic reactions such as wheezing. The mite's exoskeleton can also contribute to allergic reactions.[45] Unlike scabies mites or skin follicle mites, house dust mites do not burrow under the skin and are not parasitic.[46]

Dust mite-proof encasements to mattress, pillow, and duvet prevent chronic contact with allergens.[47]

### Foods

Main article: Medicine:Food allergy

In many countries restaurants are required to display possible food allergens list on the menu.

A wide variety of foods can cause allergic reactions, but 90% of allergic responses to foods are caused by cow's milk, soy, eggs, wheat, peanuts, tree nuts, fish, and shellfish.[48] Other food allergies, affecting less than 1 person per 10,000 population, may be considered "rare".[49] The most common food allergy in the US population is a sensitivity to crustacea.[49] Although peanut allergies are notorious for their severity, peanut allergies are not the most common food allergy in adults or children. Other allergens may trigger severe or life-threatening reactions and are more common when combined with asthma.[48]

Rates of allergies differ between adults and children. Children can sometimes outgrow peanut allergies. Egg allergies affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5.[50] The sensitivity is usually to proteins in the white, rather than the yolk.[51]

Milk-protein allergies—distinct from lactose intolerance—are most common in children.[52] Approximately 60% of milk-protein reactions are immunoglobulin E–mediated, with the remaining usually attributable to inflammation of the colon.[53] Some people are unable to tolerate milk from goats or sheep as well as from cows, and many are also unable to tolerate dairy products such as cheese. Roughly 10% of children with a milk allergy will have a reaction to beef.[54] Lactose intolerance, a common reaction to milk, is not a form of allergy at all, but due to the absence of an enzyme in the digestive tract.[55]

Those with tree nut allergies may be allergic to one or many tree nuts, including pecans, pistachios, and walnuts.[51] In addition, seeds, including sesame seeds and poppy seeds, contain oils in which protein is present, which may elicit an allergic reaction.[51]

Allergens can be transferred from one food to another through genetic engineering; however, genetic modification can also remove allergens. Little research has been done on the natural variation of allergen concentrations in unmodified crops.[56][57]

### Latex

Latex masks is one of the latex-containing products that can cause allergy.

Latex can trigger an IgE-mediated cutaneous, respiratory, and systemic reaction.[58] The prevalence of latex allergy in the general population is believed to be less than one percent. In a hospital study, 1 in 800 surgical patients (0.125 percent) reported latex sensitivity, although the sensitivity among healthcare workers is higher, between seven and ten percent.[59] 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.[60]

The most prevalent response to latex is allergic contact dermatitis, a delayed hypersensitivity reaction that manifests as dry, crusted lesions. This reaction usually lasts 48–96 hours. Sweating or rubbing the area under the glove aggravates the lesions, possibly leading to ulcerations.[60] Anaphylactic reactions occur most often in sensitive patients who have been exposed to a surgeon's latex gloves during abdominal surgery, but other mucosal exposures, such as dental procedures, can also produce systemic reactions.[60]

Latex and banana sensitivity may cross-react. Furthermore, those with latex allergy may also have sensitivities to avocado, kiwifruit, and chestnut.[61] These people 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 other plant proteins.[60]

### Medications

Main article: Medicine:Drug allergy

See also: Medicine:Adverse drug reaction and Drug eruption

About 10% of people report that they are allergic to penicillin; however, of that 10%, 90% turn out not to be.[62] Serious allergies only occur in about 0.03%.[62]

During a sting mosquito injects saliva proteins into the human bloodstream, which can cause allergy.

### Insect stings

One of the main sources of human allergies is insects. Insect bites, stings, ingestion, and inhalation can trigger an insect allergy.[63]

### 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.[64]

Of these poisonous plants, sumac is the most virulent.[65][66] The resulting dermatological response to the reaction between urushiol and membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking.[67]

Estimates vary on the fraction of the population that will have an immune system response. Approximately 25% of the population will have a strong allergic response to urushiol. In general, approximately 80–90% of adults will develop a rash if they are exposed to 0.0050 mg (7.7×10−5 gr) of purified urushiol. Some people are so sensitive that a molecular trace on the skin can initiate an allergic reaction.[68]

### Genetics

Identical twins are similar not only visually but in many reactions to the diseases including allergic reactions.

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.[69] Allergic parents are more likely to have allergic children[70] and those children's allergies are likely to be more severe than those in children of non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. The likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.[70]

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.[71] Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.[71] The peak prevalence of hay fever is highest in children and young adults, and the incidence of asthma is highest in children under 10.[72]

Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration.[70] It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.[73]

Researchers have worked to characterize genes involved in inflammation and the maintenance of mucosal integrity. The identified genes associated with allergic disease severity, progression, and development primarily function in four areas: regulating inflammatory responses (IFN-α, TLR-1, IL-13, IL-4, IL-5, HLA-G, iNOS), maintaining vascular endothelium and mucosal lining (FLG, PLAUR, CTNNA3, PDCH1, COL29A1), mediating immune cell function (PHF11, H1R, HDC, TSLP, STAT6, RERE, PPP2R3C), and influencing susceptibility to allergic sensitization (e.g., ORMDL3, CHI3L1).[74]

Multiple studies have investigated the genetic profiles of individuals with predispositions to and experiences of allergic diseases, revealing a complex polygenic architecture. Specific genetic loci, such as MIIP, CXCR4, SCML4, CYP1B1, ICOS, and LINC00824, have been directly associated with allergic disorders.[74] Additionally, some loci show pleiotropic effects, linking them to both autoimmune and allergic conditions, including PRDM2, G3BP1, HBS1L, and POU2AF1.[74] These genes engage in shared inflammatory pathways across various epithelial tissues—such as the skin, esophagus, vagina, and lung—highlighting common genetic factors that contribute to the pathogenesis of asthma and other allergic diseases.[74]

In atopic patients, transcriptome studies have identified IL-13-related pathways as key for eosinophilic airway inflammation and remodeling. That causes the body to experience the type of airflow restriction of allergic asthma.[74] Expression of genes was quite variable: genes associated with inflammation were found almost exclusively in superficial airways, while genes related to airway remodeling were mainly present in endobronchial biopsy specimens.[74] This enhanced gene profile was similar across multiple sample sizes – nasal brushing, sputum, endobronchial brushing – demonstrating the importance of eosinophilic inflammation, mast cell degranulation and group 3 innate lymphoid cells in severe adult-onset asthma.[74] IL-13 is an immunoregulatory cytokine that is made mostly by activated T-helper 2 (Th2) cells.[75] It is an important cytokine for many steps in B-cell maturation and differentiation, since it increases CD23 and MHC class II molecules, and aids in B-cell isotype switching to IgE.[74][75] IL-13 also suppresses macrophage function by reducing the release of pro-inflammatory cytokines and chemokines.[75][76] The more striking thing is that IL-13 is the prime mover in allergen-induced asthma via pathways that are independent of IgE and eosinophils.[75]

### Hygiene hypothesis

Main article: Unsolved:Hygiene hypothesis

Greek goddess of cleanliness Hygieia by Gustav Klimt (1900 - 1907)

Allergic diseases are caused by inappropriate immunological responses to harmless antigens driven by a TH2-mediated immune response. Many bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses. The first proposed mechanism of action of the hygiene hypothesis was that insufficient stimulation of the TH1 arm of the immune system leads to an overactive TH2 arm, which in turn leads to allergic disease.[77] In other words, individuals living in too sterile an environment are not exposed to enough pathogens to keep the immune system busy. Since our bodies evolved to deal with a certain level of such pathogens, when they are not exposed to this level, the immune system will attack harmless antigens. Thus, normally benign microbial objects—like pollen—will trigger an immune response.[78]

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.[79] 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.[80] 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.[81]

Epidemiological data support the hygiene hypothesis. Studies have shown that various immunological and autoimmune diseases are much less common in the developing world than in 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.[82] Longitudinal studies in the third world demonstrate an increase in immunological disorders as a country grows more affluent and, it is presumed, cleaner.[83] The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases.[84] The use of antibacterial cleaning products has also been associated with a higher incidence of asthma, as has birth by caesarean section rather than vaginal birth.[85][86]

### Stress

Chronic stress can aggravate allergic conditions. This has been attributed to a T helper 2 (TH2)-predominant response driven by suppression of interleukin 12 by both the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. Stress management in highly susceptible individuals may improve symptoms.[87]

### Other environmental factors

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.[88] Historically, the trees planted in urban areas were predominantly male to prevent litter from seeds and fruits, but the high ratio of male trees causes high pollen counts, a phenomenon that horticulturist Tom Ogren has called "botanical sexism".[89]

Alterations in exposure to microorganisms is another plausible explanation, at present, for the increase in atopic allergy.[42] 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.[90] 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.[91]

Hookworm life cycle. The adults spend all their life in the gut of infected humans, challenging their immune system.

Parasitic worms 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.[92] 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.[93] This gives rise to a new slant on the hygiene hypothesis theory—that co-evolution of humans 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.[94]

In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants.[95] 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.[88] Clinical trials have been initiated to test the effectiveness of helminthic therapy with certain worms in treating some allergies.[96] It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.[96]

## Pathophysiology

A summary diagram that explains how allergy develops Tissues affected in allergic inflammation

### Acute response

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

In the initial stages of allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional antigen-presenting cell causes a response in a type of immune cell called a TH2 lymphocyte, a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These TH2 cells interact with other lymphocytes called B cells, whose role is the 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. At this stage, the IgE-coated cells are sensitized to the allergen.[42]

If later exposure to the same allergen occurs, the allergen can bind to 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 specific body systems. Asthma is localized to the respiratory system, and eczema is localized to the dermis.[42]

### 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.[97] Cytokines from mast cells may play a role in the persistence of long-term effects. Late-phase responses in asthma differ slightly from those seen in other allergic responses. They are still caused by the release of mediators from eosinophils and remain dependent on TH2 cell activity.[98]

### Allergic contact dermatitis

Although allergic contact dermatitis is termed an "allergic" reaction (which usually refers to type I hypersensitivity), its pathophysiology involves a reaction that more correctly corresponds to a type IV hypersensitivity reaction.[99] In type IV hypersensitivity, there is activation of certain types of T cells (CD8+) that destroy target cells on contact, as well as activated macrophages that produce hydrolytic enzymes.[100]

## Diagnosis

An allergy testing machine being operated in a diagnostic immunology lab

Effective management of allergic diseases relies on the ability to make an accurate diagnosis.[101] Allergy testing can help confirm or rule out allergies.[102][103] Correct diagnosis, counseling, and avoidance advice based on valid allergy test results reduce the incidence of symptoms and need for medications, and improve quality of life.[102] To assess the presence of allergen-specific IgE antibodies, two different methods can be used: a skin prick test or an allergy blood test. Both methods are recommended, and they have similar diagnostic value.[103][104]

Skin prick tests and blood tests are equally cost-effective, and health economic evidence shows that both tests are cost-effective compared with no test.[102] Early and more accurate diagnoses save costs due to reduced consultations, referrals to secondary care, misdiagnosis, and emergency admissions.[105]

Allergy undergoes dynamic changes over time. Regular allergy testing of relevant allergens provides information on if and how patient management can be changed 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 2–3 years for allergy to peanut, tree nuts, fish, and crustacean shellfish.[103] 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.[106]

### Skin prick testing

Skin testing on arm Skin testing on back

Skin testing is also known as "puncture testing" and "prick testing" since it involves a series of tiny punctures or pricks being placed into the patient's skin. Tiny amounts of suspected allergens and/or their extracts (e.g., pollen, grass, mite proteins, peanut extract) 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 negative and positive control are also included for comparison (e.g., negative is saline or glycerin; positive is histamine). A small plastic or metal device is used to puncture or prick the skin. Sometimes, allergens are injected "intradermally" into the patient's skin, with a needle and syringe. Common areas for testing include the inside of the 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 ranges 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 usually done by allergists on a scale of severity, with +/− meaning borderline reactivity, and 4+ representing 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.[107]

In general, a positive response is interpreted when the wheal of an antigen is ≥3mm larger than the wheal of the negative control (e.g., saline or glycerin).[108] Some patients may believe they have determined their own allergic sensitivity from observation. A skin test is much better than patient observation for allergy detection.[109]

If a serious life-threatening anaphylactic reaction has brought a patient in for evaluation, some allergists will prefer an initial blood test before performing the skin prick test. Skin tests may not be an option if the patient has widespread skin disease or has taken antihistamines in the last several days.

### Patch testing

Patch test

Patch testing is a method used to determine whether a specific substance causes allergic skin inflammation. It tests for delayed reactions. It is used to help ascertain the cause of skin contact allergy or contact dermatitis. Adhesive patches, usually treated with several common allergic chemicals or skin sensitizers, are applied to the back. The skin is then examined for possible local reactions at least twice, usually at 48 hours after patch application, and again two or three days later.

### 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) or general practitioner. 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 get an allergy blood test. For babies and very young children, a single needle stick for allergy blood testing is often gentler than several skin pricks.

An allergy blood test is available through most laboratories. A sample of the patient's blood is sent to a laboratory for analysis, and the results are sent back a few days later. Multiple allergens can be detected with a single blood sample. Allergy blood tests are very safe since the person is not exposed to any allergens during the testing procedure. After the onset of anaphylaxis or a severe allergic reaction, guidelines recommend that emergency departments obtain a time-sensitive blood test to determine blood tryptase levels and assess for mast cell activation.[110]

The test measures the concentration of specific IgE antibodies in the blood. Quantitative IgE test results increase the possibility of ranking how different substances may affect symptoms. A 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 cannot 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.[111][112]

A low total IgE level is not adequate to rule out sensitization to commonly inhaled allergens.[113] 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 high total IgE have a high probability of allergic sensitization, but further investigation with allergy tests for specific IgE antibodies for a carefully chosen set of allergens is often warranted.

Laboratory methods to measure specific IgE antibodies for allergy testing include enzyme-linked immunosorbent assay,[114] radioallergosorbent test,[114] fluorescent enzyme immunoassay,[115] and chemiluminescence immunoassay.[116][117]

### Other testing

An applied kinesiologist demonstrating a manual muscle test (MMT), which is ineffective in cases of allergies.

Challenge testing: Challenge testing is when tiny amounts of a suspected allergen are introduced to the body orally, through inhalation, or via other routes. Except for testing food and medication allergies, challenges are rarely performed. When this type of testing is chosen, it must be closely supervised by an allergist.

Elimination/challenge tests: This testing method is used most often with foods or medicines. A patient with a suspected allergen is instructed to avoid that allergen entirely for a set time. If the patient experiences significant improvement, he may then be "challenged" by reintroducing the allergen to see whether symptoms recur.

Unreliable tests: There are other types of allergy testing methods that are unreliable, including applied kinesiology (allergy testing through muscle relaxation), cytotoxicity testing, urine autoinjection, skin titration (Rinkel method), and provocative and neutralization (subcutaneous) testing or sublingual provocation.[118]

### Differential diagnosis

Before a diagnosis of allergic disease can be confirmed, other plausible causes of the presenting symptoms must be considered.[119] Vasomotor rhinitis, for example, is one of many illnesses that share symptoms with allergic rhinitis, underscoring the need for professional differential diagnosis.[120] 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.

## Prevention

Researchers designed the Learning Early About Peanut Allergy (LEAP) study after noting that Israeli children, who start eating peanut foods early, have lower peanut allergy rates than similar children in the UK; infants in the study were fed a peanut snack pictured in the image.[121]

Giving peanut products early in childhood may decrease the risk of allergies, and only breastfeeding during at least the first few months of life may decrease the risk of allergic dermatitis.[122][123] There is little evidence that a mother's diet during pregnancy or breastfeeding affects the risk of allergies,[122] although there has been some research to show that irregular cow's milk exposure might increase the risk of cow's milk allergy.[124] There is some evidence that delayed introduction of certain foods is useful,[122] and that early exposure to potential allergens may actually be protective.[12]

According to recent studies from pediatric professionals in the U.K. and North Carolina, they suggest that early exposure to peanut products has greatly reduced peanut allergies among young children in the U.S. Following milestone research from a decade ago, the studies found that pediatric guidelines from 2015 and 2017 were revised to encourage introducing peanuts to high risk infants from the early ages of 4 to 6 months. Researchers who examined the collected data found a 43% drop in the frequency of peanut allergies. This prevented an estimated 40,000 cases and resulted in a noticeable decline in overall food allergy cases. While this is notable, some pediatric experts want to ensure that caution is still provided to the public about the real-world implementation of guidelines since there are potential inconsistencies and limitations. These findings focus on the benefits and risks of early allergen introductions to hopefully slow the rise of food allergies.[125]

Fish oil supplementation during pregnancy is associated with a lower risk of food sensitivities.[123] Probiotic supplements during pregnancy or infancy may help to prevent atopic dermatitis.[126][127]

## Management

Management of allergies typically involves avoiding the allergy trigger and taking medications to relieve symptoms.[13] Allergen immunotherapy may be useful for some types of allergies.[13]

### Medication

Several medications may be used to block the actions of allergic mediators, prevent cell activation, and degranulation processes. These include antihistamines, glucocorticoids, epinephrine (adrenaline), mast cell stabilizers, and antileukotriene agents are common treatments of allergic diseases.[128] Anticholinergics, decongestants, and other compounds thought to impair eosinophil chemotaxis are also commonly used. Although rare, the severity of anaphylaxis often requires epinephrine injection, and where medical care is unavailable, a device known as an epinephrine autoinjector may be used.[32]

### Immunotherapy

Anti-allergy immunotherapy

Allergen immunotherapy is useful for environmental allergies, allergies to insect bites, and asthma.[13][129] Its benefit for food allergies is unclear and thus not recommended.[13] Immunotherapy involves exposing people to larger and larger amounts of allergen in an effort to change the immune system's response.[13]

Meta-analyses have found that injections of allergens under the skin is effective in the treatment in allergic rhinitis in children[130][131] and in asthma.[129] The benefits may last for years after treatment is stopped.[132] It is generally safe and effective for allergic rhinitis and conjunctivitis, allergic forms of asthma, and stinging insects.[133]

To a lesser extent, the evidence also supports the use of sublingual immunotherapy for rhinitis and asthma.[132] For seasonal allergies the benefit is small.[134] In this form the allergen is given under the tongue and people often prefer it to injections.[132] Immunotherapy is not recommended as a stand-alone treatment for asthma.[132]

Flower of a butterbur

### Alternative medicine

An experimental treatment, enzyme potentiated desensitization (EPD), has been tried for decades but is not generally accepted as effective.[135] EPD uses dilutions of allergen and an enzyme, beta-glucuronidase, to which T-regulatory lymphocytes are supposed to respond by favoring desensitization, or down-regulation, rather than sensitization. EPD has also been tried for the treatment of autoimmune diseases, but evidence does not show effectiveness.[135]

A review found 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 adolescent ailments, there is no convincing evidence that supports the use of homeopathic treatments.[136]

According to the National Center for Complementary and Integrative Health, U.S., the evidence is relatively strong that saline nasal irrigation and butterbur are effective, when compared to other alternative medicine treatments, for which the scientific evidence is weak, negative, or nonexistent, such as honey, acupuncture, omega 3's, probiotics, astragalus, capsaicin, grape seed extract, Pycnogenol, quercetin, spirulina, stinging nettle, tinospora, or guduchi. [137][138]

## Epidemiology

The allergic diseases—hay fever and asthma—have increased in the Western world over the past 2–3 decades.[139] 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,[140] although some suggest that a steady rise in sensitization has been occurring since the 1920s.[141] The number of new cases per year of atopy in developing countries has, in general, remained much lower.[140]

Allergic conditions: Statistics and epidemiology  Allergy type | United States | United Kingdom[142]

|
|

Allergic rhinitis | 35.9 million[143] (about 11% of the population[144]) | 3.3 million (about 5.5% of the population[145])
Asthma | 10 million have allergic asthma (about 3% of the population). The prevalence of asthma increased 75% from 1980 to 1994. Asthma prevalence is 39% higher in African Americans than in Europeans.[146] | 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, the prevalence increased from 3% to 10% in children.[147] | 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.[148] An estimated 150 people die annually from anaphylaxis due to food allergy.[149] | 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.[150] | Unknown
Drug allergies | Anaphylactic reactions to penicillin cause 400 deaths per year. | Unknown
Food allergies | 7.6% of children and 10.8% of adults.[151] Peanut and/or tree nut (e.g., walnut) allergy affects about three million Americans, or 1.1% of the population.[149] | 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.[152]

### Changing frequency

The "F-diagram" (feces, fingers, flies, fields, fluids, food), showing pathways of fecal–oral disease transmission. The vertical blue lines show barriers: toilets, safe water, hygiene and handwashing.

Although genetic factors govern susceptibility to atopic disease, increases in atopy have occurred within too short a period to be explained by a genetic change in the population, thus pointing to environmental or lifestyle changes.[140] Several hypotheses have been identified to explain this increased rate. Increased exposure to perennial allergens may be due to housing changes and increased time spent indoors, and changes in cleanliness may decrease activation of a common immune control mechanism.s[153] or hygiene, and exacerbated by dietary changes, obesity, and decline in physical exercise.[139] The hygiene hypothesis maintains[154] that high living standards and hygienic conditions expose children to fewer infections. It is thought that reduced bacterial and viral infections early in life direct the maturing immune system away from TH1 type responses, leading to unrestrained TH2 responses that allow for an increase in allergy.[94][155]

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%,[156] and an increased rate of parasitic infections has been associated with a decreased prevalence of asthma.[157] It is speculated that these infections exert their effect by critically altering TH1/TH2 regulation.[158] Important elements of newer hygiene hypotheses also include exposure to endotoxins, exposure to pets and growing up on a farm.[158]

## History

The Great Cameo of France, a cameo five layers sardonyx, Rome, c. AD 23, depicting the emperor Tiberius seated with his mother Livia and in front of his designated heir Germanicus, with the latter's wife Agrippina the Elder; above them float the deceased members of their house: Augustus, Drusus Julius Caesar, and Nero Claudius Drusus

Some symptoms attributable to allergic diseases are mentioned in ancient sources.[159] Particularly, three members of the Roman Julio-Claudian dynasty (Augustus, Claudius and Britannicus) are suspected to have a family history of atopy.[159][160] The concept of "allergy" was originally introduced in 1906 by the Viennese pediatrician Clemens von Pirquet, after he noticed that patients who had received injections of horse serum or smallpox vaccine usually had quicker, more severe reactions to second injections.[161] Pirquet called this phenomenon "allergy" from the Ancient Greek words ἄλλος allos meaning "other" and ἔργον ergon meaning "work".[162]

All forms of hypersensitivity were previously classified as allergies, and all were thought to be caused by an improper activation of the immune system. Later, it became clear that several disease mechanisms were implicated, with a common link to disordered immune system activation. 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.[163]

With this new classification, the word allergy, sometimes clarified as a true allergy, was restricted to type I hypersensitivities (also called immediate hypersensitivity), which are characterized as rapidly developing reactions involving IgE antibodies.[164]

A breakthrough in understanding the mechanisms of allergy was the discovery of the antibody class labeled immunoglobulin E (IgE). IgE was simultaneously discovered in 1966–67 by two independent groups:[165] Ishizaka's team at the Children's Asthma Research Institute and Hospital in Denver, USA,[166] and by Gunnar Johansson and Hans Bennich in Uppsala, Sweden.[167] Their joint paper was published in April 1969.[168]

### Diagnosis

Radiometric assays include the radioallergosorbent test (RAST test) method, which uses IgE-binding (anti-IgE) antibodies labeled with radioactive isotopes for quantifying the levels of IgE antibody in the blood.[169]

The 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.[170]

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 as well, yet they are all called RASTs, making it difficult to distinguish between them. For these reasons, it is now recommended that the use of RAST as a generic descriptor of these tests be abandoned.[11]

The updated version, the ImmunoCAP Specific IgE blood test, is the only specific IgE assay the Food and Drug Administration has approved to quantitatively report to its detection limit of 0.1kU/L.[170]

## Medical specialty

Allergist/ImmunologistOccupation

Names|

* Physician

Occupation type

| Specialty

Activity sectors

| Medicine
Description

Education required

* Doctor of Medicine (M.D.)
* Doctor of Osteopathic medicine (D.O.)
* Bachelor of Medicine, Bachelor of Surgery (M.B.B.S.)
* Bachelor of Medicine, Bachelor of Surgery (MBChB)

Fields of
employment

| Hospitals, Clinics

The medical speciality that studies, diagnoses, and treats diseases caused by allergies is called allergology.[171] An allergist is a physician specially trained to manage and treat allergies, asthma, and other allergic diseases. In the United States, physicians holding certification by the American Board of Allergy and Immunology (ABAI) have completed an accredited educational program and evaluation process, including a proctored examination to demonstrate knowledge, skills, and experience in patient care in allergy and immunology.[172] 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 undergo three years of training in internal medicine (to become an internist) or pediatrics (to become a pediatrician). Once physicians have finished training in one of these specialties, they must pass the exam of either the American Board of Pediatrics (ABP), the American Osteopathic Board of Pediatrics (AOBP), the American Board of Internal Medicine (ABIM), or the American Osteopathic Board of Internal Medicine (AOBIM). Internists or pediatricians wishing to focus on the sub-specialty of allergy-immunology then complete at least an additional two years of study, called a fellowship, in an allergy/immunology training program. Allergists/immunologists listed as ABAI-certified have successfully passed the certifying ABAI examination following their fellowship.[173]

In the United Kingdom, allergy is a subspecialty of general medicine or pediatrics. After obtaining postgraduate exams (MRCP or MRCPCH), 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.[174]

In 2006, the House of Lords convened a subcommittee. It concluded likewise in 2007 that allergy services were insufficient to deal with what the Lords referred to as an "allergy epidemic" and its social cost; it made several recommendations.[175]

## Research

Low-allergen foods are being developed, as are improvements in skin prick test predictions; evaluation of the atopy patch test, wasp sting outcomes predictions, a rapidly disintegrating epinephrine tablet, and anti-IL-5 for eosinophilic diseases.[176]

## See also

* Allergic shiner
* GWAS in allergy
* Histamine intolerance
* List of allergens
* Oral allergy syndrome

## References

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2. ↑ "Allergy Defined | AAAAI". https://www.aaaai.org/tools-for-the-public/allergy,-asthma-immunology-glossary/allergy-defined.
3. ↑ "Allergy | British Society for Immunology". https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy.
4. ↑ Resch, Klaus; Martin, Michael U. (2008) (in en), Allergy, Springer, Berlin, Heidelberg, pp. 58–64, doi:10.1007/978-3-540-38918-7_231, ISBN 978-3-540-38918-7, https://link.springer.com/rwe/10.1007/978-3-540-38918-7_231, retrieved 2025-07-04
5. ↑ "Types of Allergic Diseases". 29 May 2015. https://www.niaid.nih.gov/topics/allergicdiseases/Pages/allergic-diseases-types.aspx.
6. ↑ "Environmental Allergies: Symptoms". 22 April 2015. https://www.niaid.nih.gov/topics/environmental-allergies/Pages/symptoms.aspx.
7. ↑ 7.0 7.1 7.2 "Food Allergy An Overview". July 2012. https://www.niaid.nih.gov/topics/foodAllergy/Documents/foodallergy.pdf.
8. ↑ "Cow's milk allergy versus cow milk intolerance". Annals of Allergy, Asthma & Immunology 89 (6 Suppl 1): 56–60. December 2002. doi:10.1016/S1081-1206(10)62124-2. PMID 12487206.
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52. ↑ Maleki, Burks & Helm 2006, pp. 41
53. ↑ "World Allergy Organization". http://www.worldallergy.org/professional/allergic_diseases_center/foodallergy/.
54. ↑ Sicherer 64
55. ↑ Cleveland Clinic medical professional (2023-03-03). "Lactose Intolerance". https://my.clevelandclinic.org/health/diseases/7317-lactose-intolerance.
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61. ↑ "Sensitization from chestnuts and bananas in patients with urticaria and anaphylaxis from contact with latex". Annals of Allergy 70 (1): 35–39. January 1993. PMID 7678724.
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67. ↑ DermAtlas -1892628434
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70. ↑ 70.0 70.1 70.2 "Risk factors for allergy". European Journal of Pediatrics 158 (2): 89–94. February 1999. doi:10.1007/s004310051024. PMID 10048601.
71. ↑ 71.0 71.1 "Prediction and detection of allergy development: influence of genetic and environmental factors". The Journal of Pediatrics 121 (5 Pt 2): S58–63. November 1992. doi:10.1016/S0022-3476(05)81408-8. PMID 1447635.
72. ↑ "Epidemiology of atopy and atopic disease". Allergy and allergic diseases. 2. London: Blackwell Science. 1997. pp. 1208–24.
73. ↑ "African Americans with asthma: genetic insights". Proceedings of the American Thoracic Society 4 (1): 58–68. January 2007. doi:10.1513/pats.200607-146JG. PMID 17202293.
74. ↑ 74.0 74.1 74.2 74.3 74.4 74.5 74.6 74.7 Falcon, Robbi Miguel G.; Caoili, Salvador Eugenio C. (2023). "Immunologic, genetic, and ecological interplay of factors involved in allergic diseases". Frontiers in Allergy (Frontiers) 4. doi:10.3389/falgy.2023.1215616. PMID 37601647.
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76. ↑ Zhu, Chunhua; Zhang, Aihua; Songming, Huang; Ding, Guixia; Pan, Xiaoqin; Chen, Ronghua (2010). "Interleukin-13 inhibits cytokines synthesis by blocking nuclear factor-ΚB and c-jun N-terminal kinase in human mesangial cells". Journal of Biomedical Research (U.S. National Library of Medicine) 24 (4): 308–316. doi:10.1016/S1674-8301(10)60043-7. PMID 23554645.
77. ↑ "Do common childhood infections 'teach' the immune system not to be allergic?". Immunology Today 21 (3): 118–20. March 2000. doi:10.1016/S0167-5699(00)01582-6. PMID 10777250.
78. ↑ "The Hygiene Hypothesis". Edward Willett. 30 January 2013. http://edwardwillett.com/2000/05/the-hygiene-hypothesis/.
79. ↑ Perkin, Michael R; Strachan, David P (2022-11-24). "The hygiene hypothesis for allergy – conception and evolution". Frontiers in Allergy (Frontiers Media SA) 3. doi:10.3389/falgy.2022.1051368. ISSN 2673-6101. PMID 36506644.
80. ↑ Bonis, Peter A. L. (2009). "Putting the Puzzle Together: Epidemiological and Clinical Clues in the Etiology of Eosinophilic Esophagitis". Immunology and Allergy Clinics of North America (Elsevier BV) 29 (1): 41–52. doi:10.1016/j.iac.2008.09.005. ISSN 0889-8561. PMID 19141340.
81. ↑ Stiemsma, Leah; Reynolds, Lisa; Turvey, Stuart; Finlay, Brett (2015). "The hygiene hypothesis: current perspectives and future therapies". ImmunoTargets and Therapy (Informa UK Limited) 4: 143–157. doi:10.2147/itt.s61528. ISSN 2253-1556. PMID 27471720.
82. ↑ "Migration to a western country increases asthma symptoms but not eosinophilic airway inflammation". Pediatric Pulmonology 36 (3): 209–15. September 2003. doi:10.1002/ppul.10323. PMID 12910582. . Retrieved 6 July 2008.
83. ↑ "Exercise-induced bronchospasm and atopy in Ghana: two surveys ten years apart". PLOS Medicine 4 (2). February 2007. doi:10.1371/journal.pmed.0040070. PMID 17326711.
84. ↑ "Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis". Chest 129 (3): 610–18. March 2006. doi:10.1378/chest.129.3.610. PMID 16537858.
85. ↑ "A meta-analysis of the association between Caesarean section and childhood asthma". Clinical and Experimental Allergy 38 (4): 629–33. April 2008. doi:10.1111/j.1365-2222.2007.02780.x. PMID 18352976.
86. ↑ "The use of household cleaning sprays and adult asthma: an international longitudinal study". American Journal of Respiratory and Critical Care Medicine 176 (8): 735–41. October 2007. doi:10.1164/rccm.200612-1793OC. PMID 17585104.
87. ↑ "Stress and allergic diseases". Immunology and Allergy Clinics of North America 31 (1): 55–68. February 2011. doi:10.1016/j.iac.2010.09.009. PMID 21094923.
88. ↑ 88.0 88.1 "Intestinal worms and human allergy". Parasite Immunology 26 (11–12): 455–67. 2004. doi:10.1111/j.0141-9838.2004.00728.x. PMID 15771681.
89. ↑ "Botanical Sexism Cultivates Home-Grown Allergies". 29 April 2015. https://blogs.scientificamerican.com/guest-blog/botanical-sexism-cultivates-home-grown-allergies/.
90. ↑ "Environmental exposure to endotoxin and its relation to asthma in school-age children". The New England Journal of Medicine 347 (12): 869–77. September 2002. doi:10.1056/NEJMoa020057. PMID 12239255.
91. ↑ "Epidemiological and immunological evidence for the hygiene hypothesis". Immunobiology 212 (6): 441–52. 2007. doi:10.1016/j.imbio.2007.03.006. PMID 17544829.
92. ↑ "Parasitic food-borne and water-borne zoonoses". Revue Scientifique et Technique 19 (1): 240–58. April 2000. doi:10.20506/rst.19.1.1218. PMID 11189719.
93. ↑ "Worms and allergy". Parasite Immunology 28 (10): 525–34. October 2006. doi:10.1111/j.1365-3024.2006.00894.x. PMID 16965288.
94. ↑ 94.0 94.1 "Allergy, parasites, and the hygiene hypothesis". Science 296 (5567): 490–94. April 2002. doi:10.1126/science.296.5567.490. PMID 11964470. Bibcode: 2002Sci...296..490Y.
95. ↑ "Allergens as eukaryotic proteins lacking bacterial homologues". Molecular Immunology 44 (12): 3256–60. May 2007. doi:10.1016/j.molimm.2007.01.019. PMID 17382394.
96. ↑ 96.0 96.1 "Parasite role reversal: worms on trial". Trends in Parasitology 21 (4): 157–60. April 2005. doi:10.1016/j.pt.2005.02.002. PMID 15780835.
97. ↑ "Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses". Current Opinion in Immunology 18 (6): 751–60. December 2006. doi:10.1016/j.coi.2006.09.011. PMID 17011762.
98. ↑ "Th2 cytokines in the asthma late-phase response". Lancet 370 (9596): 1396–98. October 2007. doi:10.1016/S0140-6736(07)61587-6. PMID 17950849.
99. ↑ "Early inflammatory markers in elicitation of allergic contact dermatitis". BMC Dermatology 2. August 2002. doi:10.1186/1471-5945-2-9. PMID 12167174.
100. ↑ Hou, Wanzhu; Xu, Guangpi; Wang, Hanjie (2011). "Basic immunology and immune system disorders". Treating Autoimmune Disease with Chinese Medicine. Elsevier. pp. 1–12. doi:10.1016/b978-0-443-06974-1.00001-4. ISBN 978-0-443-06974-1.
101. ↑ Portnoy JM (2006). "Evidence-based Allergy Diagnostic Tests". Current Allergy and Asthma Reports 6 (6): 455–61. doi:10.1007/s11882-006-0021-8. PMID 17026871.
102. ↑ 102.0 102.1 102.2 NICE Diagnosis and assessment of food allergy in children and young people in primary care and community settings, 2011
103. ↑ 103.0 103.1 103.2 "Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel". The Journal of Allergy and Clinical Immunology 126 (6 Suppl): S1–58. December 2010. doi:10.1016/j.jaci.2010.10.007. PMID 21134576.
104. ↑ "Overview of Serological-Specific IgE Antibody Testing in Children". Pediatric Allergy and Immunology 11 (6): 447–53. 2011. doi:10.1007/s11882-011-0226-3. PMID 21947715.
105. ↑ "CG116 Food allergy in children and young people: costing report". 23 February 2011. http://guidance.nice.org.uk/CG116/CostingReport/pdf/English.
106. ↑ "Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAID-Sponsored Expert Panel Report". NIH. 2010. https://www.foodallergy.org/sites/default/files/migrated-files/file/niaid-clinician-summary.pdf.
107. ↑ "The predictive value of the skin prick test weal size for the outcome of oral food challenges". Clinical and Experimental Allergy 35 (9): 1220–26. September 2005. doi:10.1111/j.1365-2222.2005.2324.x. PMID 16164451.
108. ↑ "Appropriate use of allergy testing in primary care - Best Tests December 2011". https://bpac.org.nz/BT/2011/December/allergy-testing.aspx#:~:text=If the diameter of the,the age of the individual..
109. ↑ "Accuracy of patient prediction of allergy skin test results". Annals of Allergy, Asthma & Immunology 85 (5): 382–84. November 2000. doi:10.1016/S1081-1206(10)62550-1. PMID 11101180.
110. ↑ Reinhold, Lauren (February 2023). "An Update on Test use Evaluation of Serum Tryptase Levels". The Journal of Allergy and Clinical Immunology 151 (2): AB10. doi:10.1016/j.jaci.2022.12.038. https://www.jacionline.org/article/S0091-6749(22)01692-X/fulltext.
111. ↑ "Quantitative IgE antibody assays in allergic diseases". Journal of Allergy and Clinical Immunology 105 (6): 1077–84. June 2000. doi:10.1067/mai.2000.107041. PMID 10856139.
112. ↑ "Utility of food-specific IgE concentrations in predicting symptomatic food allergy". The Journal of Allergy and Clinical Immunology 107 (5): 891–96. May 2001. doi:10.1067/mai.2001.114708. PMID 11344358.
113. ↑ "Role and interpretation of total serum IgE measurements in the diagnosis of allergic airway disease in adults". Allergy 58 (9): 905–11. September 2003. doi:10.1034/j.1398-9995.2003.00230.x. PMID 12911420.
114. ↑ 114.0 114.1 "Blood Testing for Allergies". http://www.webmd.com/allergies/guide/blood-test.
115. ↑ "Basophil activation test compared to skin prick test and fluorescence enzyme immunoassay for aeroallergen-specific Immunoglobulin-E". Allergy, Asthma, and Clinical Immunology 8 (1). January 2012. doi:10.1186/1710-1492-8-1. PMID 22264407.
116. ↑ Casas ML, Esteban Á, González-Muñoz M, Labrador-Horrillo M, Pascal M, & Teniente-Serra A (2020). VALIDA project: Validation of allergy in vitro diagnostics assays (Tools and recommendations for the assessment of in vitro tests in the diagnosis of allergy). In Advances in Laboratory Medicine (Vol. 1, Issue 4). Walter de Gruyter GmbH. https://doi.org/10.1515/almed-2020-0051
117. ↑ Bulat Lokas S, Plavec D, Rikić Pišković J, Živković J, Nogalo B, & Turkalj M (2017). Allergen-Specific IgE Measurement: Intermethod Comparison of Two Assay Systems in Diagnosing Clinical Allergy. Journal of Clinical Laboratory Analysis, 31(3), e22047. https://doi.org/10.1002/jcla.22047
118. ↑ "Allergy Diagnosis". http://www.theonlineallergist.com/index.php/article/allergy_diagnosis/. The Online Allergist. Retrieved 25 October 2010.
119. ↑ Allergic and Environmental Asthma at eMedicine – Includes discussion of differentials
120. ↑ "Vasomotor rhinitis". American Family Physician 72 (6): 1057–62. September 2005. PMID 16190503. http://www.aafp.org/afp/20050915/1057.html.
121. ↑ Chappell, Bill (2025-10-21). "Reversing peanut advice prevented tens of thousands of allergy cases, researchers say" (in en). NPR. https://www.npr.org/2025/10/21/nx-s1-5580211/peanut-allergy-study.
122. ↑ 122.0 122.1 122.2 "The Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Hydrolyzed Formulas, and Timing of Introduction of Allergenic Complementary Foods". Pediatrics 143 (4). April 2019. doi:10.1542/peds.2019-0281. PMID 30886111.
123. ↑ 123.0 123.1 "Diet during pregnancy and infancy and risk of allergic or autoimmune disease: A systematic review and meta-analysis". PLOS Medicine 15 (2). February 2018. doi:10.1371/journal.pmed.1002507. PMID 29489823.
124. ↑ Abrams, Elissa (May 2023). "Prevention of food allergy in infancy: the role of maternal interventions and exposures during pregnancy and lactation". The Lancet Child & Adolescent Health 7 (5): 358–366. doi:10.1016/S2352-4642(22)00349-2. PMID 36871575. https://www.sciencedirect.com/science/article/abs/pii/S2352464222003492?fr=RR-2&ref=pdf_download&rr=9055b0bd8ab67380.
125. ↑ Chappell, Bill (2025-10-21). "Reversing peanut advice prevented tens of thousands of allergy cases, researchers say" (in en). https://www.kpbs.org/news/science-technology/2025/10/21/reversing-peanut-advice-prevented-tens-of-thousands-of-allergy-cases-researchers-say.
126. ↑ "Probiotics supplementation during pregnancy or infancy for the prevention of atopic dermatitis: a meta-analysis". Epidemiology 23 (3): 402–14. May 2012. doi:10.1097/EDE.0b013e31824d5da2. PMID 22441545.
127. ↑ "Prebiotics in infants for prevention of allergy". The Cochrane Database of Systematic Reviews (3). March 2013. doi:10.1002/14651858.CD006474. PMID 23543544.
128. ↑ "Mast Cell Activation Syndrome". Clinical Reviews in Allergy & Immunology 54 (3): 353–65. June 2018. doi:10.1007/s12016-015-8487-6. PMID 25944644.
129. ↑ 129.0 129.1 "Injection allergen immunotherapy for asthma". The Cochrane Database of Systematic Reviews (8). August 2010. doi:10.1002/14651858.CD001186.pub2. PMID 20687065.
130. ↑ "Efficacy of sublingual immunotherapy in the treatment of allergic rhinitis in pediatric patients 3 to 18 years of age: a meta-analysis of randomized, placebo-controlled, double-blind trials". Annals of Allergy, Asthma & Immunology 97 (2): 141–48. August 2006. doi:10.1016/S1081-1206(10)60004-X. PMID 16937742.
131. ↑ "Allergen injection immunotherapy for seasonal allergic rhinitis". The Cochrane Database of Systematic Reviews 2007 (1). January 2007. doi:10.1002/14651858.CD001936.pub2. PMID 17253469.
132. ↑ 132.0 132.1 132.2 132.3 "Sub-lingual immunotherapy: World Allergy Organization Position Paper 2009". Allergy 64 (Suppl 91): 1–59. December 2009. doi:10.1111/j.1398-9995.2009.02309.x. PMID 20041860. http://www.worldallergy.org/publications/slit-wao-pp_final.pdf.
133. ↑ "Allergen immunotherapy". Mayo Clinic Proceedings 82 (9): 1119–23. September 2007. doi:10.4065/82.9.1119. PMID 17803880.
134. ↑ "Efficacy of Grass Pollen Allergen Sublingual Immunotherapy Tablets for Seasonal Allergic Rhinoconjunctivitis: A Systematic Review and Meta-analysis". JAMA Internal Medicine 175 (8): 1301–09. August 2015. doi:10.1001/jamainternmed.2015.2840. PMID 26120825.
135. ↑ 135.0 135.1 "Unproven and controversial forms of immunotherapy". Clinical Allergy and Immunology 18: 703–10. 2004. PMID 15042943.
136. ↑ "Homeopathy for childhood and adolescence ailments: systematic review of randomized clinical trials". Mayo Clinic Proceedings 82 (1): 69–75. January 2007. doi:10.4065/82.1.69. PMID 17285788.
137. ↑ "12 Natural Ways to Defeat Allergies". http://www.webmd.com/allergies/ss/slideshow-natural-relief.
138. ↑ "Seasonal Allergies and Complementary Health Approaches: What the Science Says". 11 April 2013. https://www.nccih.nih.gov/health/providers/digest/allergies-science.
139. ↑ 139.0 139.1 "Is the hygiene hypothesis still a viable explanation for the increased prevalence of asthma?". Allergy 60 (nSuppl 79): 25–31. 2005. doi:10.1111/j.1398-9995.2005.00854.x. PMID 15842230.
140. ↑ 140.0 140.1 140.2 "Too clean, or not too clean: the hygiene hypothesis and home hygiene". Clinical and Experimental Allergy 36 (4): 402–25. April 2006. doi:10.1111/j.1365-2222.2006.02463.x. PMID 16630145.
141. ↑ "The allergy epidemic extends beyond the past few decades". Clinical and Experimental Allergy 34 (7): 1007–10. July 2004. doi:10.1111/j.1365-2222.2004.01999.x. PMID 15248842.
142. ↑ "Chapter 4: The Extent and Burden of Allergy in the United Kingdom". House of Lords – Science and Technology – Sixth Report. 24 July 2007. https://publications.parliament.uk/pa/ld200607/ldselect/ldsctech/166/16607.htm.
143. ↑ "AAAAI – rhinitis, sinusitis, hay fever, stuffy nose, watery eyes, sinus infection". http://www.aaaai.org/patients/gallery/rhinitissinusitis.asp?item=1a.
144. ↑ Based on an estimated population of 303 million in 2007 "U.S. POPClock Projection". U.S. Census Bureau. https://www.census.gov/population/www/popclockus.html.
145. ↑ Based on an estimated population of 60.6 million "UK population grows to 60.6 million". National Statistics. UK Web Archive. http://www.statistics.gov.uk/cci/nugget.asp?id=6.
146. ↑ "AAAAI – asthma, allergy, allergies, prevention of allergies and asthma, treatment for allergies and asthma". http://www.aaaai.org/patients/gallery/prevention.asp?item=1a.
147. ↑ "AAAAI – skin condition, itchy skin, bumps, red irritated skin, allergic reaction, treating skin condition". http://www.aaaai.org/patients/gallery/skinallergies.asp?item=1a.
148. ↑ "AAAAI – anaphylaxis, cause of anaphylaxis, prevention, allergist, anaphylaxis statistics". http://www.aaaai.org/patients/gallery/anaphylaxis.asp?item=1a.
149. ↑ 149.0 149.1 "AAAAI – food allergy, food reactions, anaphylaxis, food allergy prevention". http://www.aaaai.org/patients/gallery/foodallergy.asp?item=1a.
150. ↑ "AAAAI – stinging insect, allergic reaction to bug bite, treatment for insect bite". http://www.aaaai.org/patients/gallery/insect.asp?item=1a.
151. ↑ "Allergy Facts | AAFA.org" (in en). https://www.aafa.org/allergy-facts/.
152. ↑ "Incidence and prevalence of multiple allergic disorders recorded in a national primary care database". Journal of the Royal Society of Medicine 101 (11): 558–63. November 2008. doi:10.1258/jrsm.2008.080196. PMID 19029357.
153. ↑ Dablo, Rose (2022-12-20). "Reduce Allergens By Cleanliness". https://www.cooperclean.com/cooper-clean-blog/how-to-keep-your-house-clean-when-you-have-pets/.
154. ↑ "Hay fever, hygiene, and household size". BMJ 299 (6710): 1259–60. November 1989. doi:10.1136/bmj.299.6710.1259. PMID 2513902.
155. ↑ "The immunological basis of the hygiene hypothesis". Allergy and Asthma in Modern Society: A Scientific Approach. Chemical Immunology and Allergy. 91. 2006. pp. 30–48. doi:10.1159/000090228. ISBN 978-3-8055-8000-7.
156. ↑ "Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma: epidemiological study". BMJ 320 (7232): 412–17. February 2000. doi:10.1136/bmj.320.7232.412. PMID 10669445.
157. ↑ "Parasites and asthma--predictive or protective?". Epidemiologic Reviews 7: 49–58. 1985. doi:10.1093/oxfordjournals.epirev.a036285. PMID 4054238.
158. ↑ 158.0 158.1 "The hygiene theory: fact or fiction?". Current Opinion in Otolaryngology & Head and Neck Surgery 12 (3): 232–36. June 2004. doi:10.1097/01.moo.0000122311.13359.30. PMID 15167035.
159. ↑ 159.0 159.1 Kürşat Epöztürk; Şefik Görkey (2018). "Were Allergic Diseases Prevalent in Antiquity?". Asthma Allergy Immunol. doi:10.21911/aai.406. https://aai.org.tr/index.php/aai/article/download/406/321. Retrieved 22 September 2018.
160. ↑ Ring J. (August 1985). "1st description of an "atopic family anamnesis" in the Julio-Claudian imperial house: Augustus, Claudius, Britannicus". Hautarzt 36 (8): 470–71. PMID 3899999.
161. ↑ Clemens Peter Pirquet von Cesenatico at Who Named It?
162. ↑ Von Pirquet C (1906). "Allergie". Munch Med Wochenschr 53 (5): 388–90. PMID 20273584. Reprinted in "Allergie". Annals of Allergy 4 (5): 388–90. 1946. PMID 20273584.
163. ↑ Clinical Aspects of Immunology. London: Blackwell. 1963.
164. ↑ (in en) The Complement System: Novel Roles in Health and Disease. Springer Science & Business Media. 8 May 2007. p. 361. ISBN 978-1-4020-8056-2. https://books.google.com/books?id=sXagBwAAQBAJ&pg=PA361.
165. ↑ "The discovery of IgE". Allergy 48 (2): 67–71. February 1993. doi:10.1111/j.1398-9995.1993.tb00687.x. PMID 8457034.
166. ↑ "Physico-chemical properties of human reaginic antibody. IV. Presence of a unique immunoglobulin as a carrier of reaginic activity". Journal of Immunology 97 (1): 75–85. July 1966. doi:10.4049/jimmunol.97.1.75. PMID 4162440.
167. ↑ Johansson SG, Bennich H. Immunological studies of an atypical (myeloma) immunoglobulin" Immunology 1967; 13:381–94.
168. ↑ "Histamine release from human leukocytes by anti-gamma E antibodies". Journal of Immunology 102 (4): 884–892. April 1969. doi:10.4049/jimmunol.102.4.884. PMID 4181251.
169. ↑ "Allergy skin testing". Mayo Clinic Proceedings 70 (8): 783–84. August 1995. doi:10.4065/70.8.783. PMID 7630219. http://www.mayoclinicproceedings.org/article/S0025-6196(11)64353-X/abstract.
170. ↑ 170.0 170.1 Mccarty, C. (2018). Immunology: Essential and Fundamental. EDTECH. p. 228. ISBN 978-1-83947-284-8. https://books.google.com/books?id=UePEDwAAQBAJ&pg=PA228. Retrieved 2024-06-29.
171. ↑ "Allergology". https://bellvitgehospital.cat/en/services/allergology.
172. ↑ "ABAI: American Board of Allergy and Immunology". http://www.abai.org/training.asp.
173. ↑ "AAAAI – What is an Allergist?". http://www.aaaai.org/media/resources/allergist.asp.
174. ↑ Allergy: the unmet need. London: Royal College of Physicians. 2003. ISBN 978-1-86016-183-4. http://www.rcplondon.ac.uk/pubs/contents/81e384d6-0328-4653-9cc2-2aa7baa3c56a.pdf. "(1.03 MB)"
175. ↑ House of Lords – Science and Technology Committee (2007). Allergy – HL 166-I, 6th Report of Session 2006–07 – Volume 1: Report. London: TSO (The Stationery Office). ISBN 978-0-10-401149-2. https://publications.parliament.uk/pa/ld200607/ldselect/ldsctech/166/16602.htm.
176. ↑ "Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects". The Journal of Allergy and Clinical Immunology 119 (6): 1462–69. June 2007. doi:10.1016/j.jaci.2007.02.013. PMID 17412401.

## External links

File:What happens when you are allergic.webm

* Allergy travel guide from Wikivoyage
* "Allergy". MedlinePlus. U.S. National Library of Medicine. https://medlineplus.gov/allergy.html.

Classification|

* ICD-11: Allergic or hypersensitivity conditions
* ICD-10: T78.4
* ICD-9-CM: 995.3
* MeSH: D006967
* DiseasesDB: 33481

|

External resources|

* MedlinePlus: 000812
* eMedicine: med/1101

* v
* t
* e

Allergic conditions

Respiratory system|

* Allergic rhinitis (hay fever)
* Asthma
* Hypersensitivity pneumonitis
* Eosinophilic pneumonia
* Eosinophilic granulomatosis with polyangiitis
* 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
* Egg allergy
* Milk intolerance

Nervous system|

* Eosinophilic meningitis

Genitourinary system|

* Acute interstitial nephritis

Other conditions|

* Drug allergy
* Allergic conjunctivitis
* Latex allergy

* v
* t
* e

Consequences of external causes (T66–T78, 990–995)

Temperature|

| Elevated|

Hyperthermia
Heat syncope

|

Reduced|

Hypothermia
Immersion foot syndromes

Trench foot
Tropical immersion foot
Warm water immersion foot
Chilblains
Frostbite
Aerosol burn
Cold intolerance
Acrocyanosis
Erythrocyanosis crurum

Radiation|

Radiation poisoning
Radiation burn
Chronic radiation keratosis
Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy
Radiation acne
Radiation-induced 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
* Death zone
* HAPE
* HACE

Food|

* Starvation

Maltreatment|

* Physical abuse
* Sexual abuse
* Psychological abuse

Travel|

* Motion sickness
* Seasickness
* Airsickness
* Space adaptation syndrome

Adverse effect|

* Hypersensitivity
* Anaphylaxis
* Angioedema
* Allergy
* Arthus reaction

* Adverse drug reaction

Other|

* Electrical injury
* Drowning
* Lightning injuries

Ungrouped
skin conditions
resulting from
physical factors|

* Dermatosis neglecta
* Pinch mark
* Pseudoverrucous papules and nodules
* Sclerosing lymphangitis
* 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
* t
* e

Hypersensitivity and autoimmune diseases (279.5–6)

Type I/allergy/atopy
(IgE)|

| Foreign|

* Atopic eczema
* Allergic urticaria
* Allergic rhinitis (Hay fever)
* Allergic asthma
* Anaphylaxis
* Food allergy
* common allergies include: Milk
* Egg
* Peanut
* Tree nut
* Seafood
* Soy
* Wheat
* Penicillin allergy

|

Autoimmune|

* Eosinophilic esophagitis

Type II/ADCC

*     * IgM
* IgG

| Foreign|

* Hemolytic disease of the newborn

|

Autoimmune|

| Cytotoxic|

* Autoimmune hemolytic anemia
* Immune thrombocytopenic purpura
* Bullous pemphigoid
* Pemphigus vulgaris
* Rheumatic fever
* Goodpasture syndrome
* Guillain–Barré syndrome

|

"Type V"/receptor|

* Graves' disease
* Myasthenia gravis
* Pernicious anemia

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
* Multiple sclerosis
* Coeliac disease
* Giant-cell arteritis
* Postorgasmic illness syndrome
* Reactive arthritis

GVHD|

* Transfusion-associated graft versus host disease

Unknown/
multiple|

| Foreign|

* Hypersensitivity pneumonitis
* Allergic bronchopulmonary aspergillosis
* Transplant rejection
* Latex allergy (I+IV)

|

Autoimmune|

* Sjögren syndrome
* Autoimmune hepatitis
* Autoimmune polyendocrine syndrome
* APS1
* APS2
* Autoimmune adrenalitis
* Systemic autoimmune disease

* v
* t
* e

Medicine

Specialties
and
subspecialties|

Surgery

* Cardiac surgery
* Cardiothoracic surgery
* Colorectal surgery
* Eye surgery
* General surgery
* Neurosurgery
* Oral and maxillofacial surgery
* [[[Medicine:Orthopedic surgery|Orthopedic surgery]]
* Hand surgery
* Otolaryngology
* ENT
* Pediatric surgery
* Plastic surgery
* Reproductive surgery
* Surgical oncology
* Thoracic surgery
* Transplant surgery
* Trauma surgery
* Urology
* Andrology
* Vascular surgery

Internal medicine

* Allergy / Immunology
* Angiology
* Cardiology
* Endocrinology
* Gastroenterology
* Hepatology
* Geriatrics
* Hematology
* Hospital medicine|
* Infectious disease
* Nephrology
* Oncology
* Pulmonology
* Rheumatology

Obstetrics and gynaecology

* Gynaecology
* Gynecologic oncology
* Maternal–fetal medicine
* Obstetrics
* Reproductive endocrinology and infertility
* Urogynecology

Diagnostic

* Radiology
* Interventional radiology
* Nuclear medicine
* Pathology
* Anatomical
* Clinical pathology
* Clinical chemistry
* Clinical immunology
* Cytopathology
* Medical microbiology
* Transfusion medicine

Other specialties

* Addiction medicine
* Adolescent medicine
* Anesthesiology
* Dermatology
* Disaster medicine
* Diving medicine
* Emergency medicine
* Mass gathering medicine
* Family medicine
* General practice
* Hospital medicine
* Intensive care medicine
* Medical genetics
* Narcology
* Neurology
* Clinical neurophysiology
* Occupational medicine
* Ophthalmology
* Oral medicine
* Pain management
* Palliative care
* Pediatrics
* Neonatology
* Physical medicine and rehabilitation
* PM&R
* Preventive medicine
* Psychiatry
* Addiction psychiatry
* Radiation oncology
* Reproductive medicine
* Sexual medicine
* Sleep medicine
* Sports medicine
* Transplantation medicine
* Tropical medicine
* Travel medicine
* Venereology

Medical education|

* Medical school
* Bachelor of Medicine, Bachelor of Surgery
* Bachelor of Medical Sciences
* Master of Medicine
* Master of Surgery
* Doctor of Medicine
* Doctor of Osteopathic Medicine
* MD–PhD

Related topics|

* Alternative medicine
* Allied health
* Dentistry
* Podiatry
* Physiotherapy
* Molecular oncology
* Nanomedicine
* Personalized medicine
* Public health
* Traditional medicine
* Veterinary medicine
* Physician
* Chief physician
* History of medicine

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Original source: https://en.wikipedia.org/wiki/Allergy. Read more

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