Abstract
Four types of hypersensitivities may be distinguished. Type I, or immediate hypersensitivity, occurs within about 30 min and is IgE antibody-mediated, and the allergic signs and symptoms are triggered by cross-linking of mast cell-bound IgE which leads to mast cell degranulation and release of inflammatory mediators. Drugs well-known to cause type I reactions include β-lactams, neuromuscular blockers, and some NSAIDs. Anaphylactoid reactions may mimic the signs and symptoms of anaphylaxis, but, unlike the latter reactions, anaphylactoid reactions are not immune-mediated. Clinical manifestations of anaphylaxis include erythema, urticaria, angioedema, bronchospasm, and cardiovascular collapse. Urticaria is often associated with angioedema and anaphylaxis. ACE inhibitors are responsible for one in six hospital admissions for angioedema. Types II and III hypersensitivities are known as antibody-dependent cytotoxic and immune complex-mediated hypersensitivities, respectively. Examples of drug-induced type II reactions are hemolytic anemia, thrombocytopenia, and granulocytopenia. A serum sickness-like reaction is the prototype type III drug hypersensitivity. Type IV drug hypersensitivities are mediated by antigen-specific T cells. Reactions occur 48–72 h after antigen exposure and are therefore referred to as delayed. Examples of delayed cutaneous reactions include allergic contact dermatitis (irritant contact dermatitis is not a type IV delayed-type reaction), SDRIFE (baboon syndrome), psoriasis, FDE, AGEP, DRESS, SJS, and TEN. Other cutaneous reactions of unclear pathogenesis include vitiligo and Sweet’s syndrome. Pruritus, which is not a type IV reaction, is provoked by a large number of different drugs.
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Baldo, B.A., Pham, N.H. (2021). Classification and Descriptions of Allergic Reactions to Drugs. In: Drug Allergy. Springer, Cham. https://doi.org/10.1007/978-3-030-51740-3_2
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