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Immediate hypersensitivity reactions commonly involve IgE antibodies, which bind to Fc epsilon RI receptors on mast cells and basophils. Within minutes of exposure, the allergen crosslinks cell-bound IgE molecules, activating mast cells or basophils to degranulate. Clinical manifestations of immediate hypersensitivity result from the action of released mediators within tissues. Both preformed and newly generated mediators from released granules cause vasodilation, visceral smooth muscle contraction, mucous secretory gland stimulation, vascular permeability, and tissue inflammation. Arachidonic acid metabolites, cytokines, and other mediators (eg, chemoattractants) can induce a late-phase inflammatory response that appears several hours later as a delayed biphasic reaction or when allergen exposure is continuous (eg, pollen).


Immediate hypersensitivity IgE-mediated allergic reactions to foods commonly occur within 2 hours of ingestion and are much less common in adults as a de novo food allergy than in children. Typical reactions include a combination of emesis, diarrhea, urticaria with or without angioedema, bronchial hypersensitivity, and hypotension. A serum tryptase may be elevated during anaphylactic reactions within a few hours after the exposure (see Anaphylaxis, Laboratory Findings below). The most common systemic food allergies are caused by milk, egg, wheat, soy, fish, shellfish, peanuts, and tree nut allergens. Shellfish, peanuts, and tree nuts are the most common causes of food anaphylaxis in adults; milk and egg allergies are more common in children but often resolve by adulthood. Diagnosis of food allergy is based on a correlative history, skin tests, and serum specific IgE tests. There is no role for specific IgG or IgA testing for evaluating food immediate hypersensitivity. Because of frequent false-positive IgE tests especially among atopic patients (eg, eczema) the use of indiscriminate screening of IgE panels to foods is not recommended; oral food challenge with a reproducible immediate hypersensitivity reaction remains the gold standard for diagnosis. Food challenge, however, should only be conducted by an experienced provider in a setting equipped to treat anaphylaxis. Management of food allergy involves strict avoidance of the food and guaranteed access to epinephrine autoinjectors. The use of oral immunotherapy to treat food allergy in children and adolescents, should only be performed by an experienced allergist immunologist.

Other IgE-mediated food reactions include oral allergy syndrome and hypersensitivity to alpha-gal (galactose-alpha-1,3-galactose). Oral allergy syndrome and pollen-associated food allergy syndrome result from cross-reactivity between certain food and pollen proteins. Affected individuals have known seasonal pollen allergies (most commonly tree pollens) and experience itching of the oral mucosa upon ingestion of cross-reactive raw fruits and vegetables. In contrast to systemic food allergy, symptoms are mostly limited to the oropharynx.

Alpha-galglycosylates proteins in mammals and is found in mammal derived meats, which are beef, pork, lamb, and mutton. Sensitization to this carbohydrate is epidemiologically linked to Lone Star (Amblyomma americanum) tick bites, but the pathogenesis is not entirely clear. In contrast to conventional immediate hypersensitivity IgE-mediated food allergy to proteins, the alpha gal IgE-mediated reaction typically occurs ...

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