Classification and Descriptions of Allergic Reactions to Drugs

Abstract

Four types of hypersensitivities may be distinguished. Type I, or immediate hypersensitivity, occurs within about 30 min, 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 infl ammatory 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 anaphy-laxis but, unlike the latter reactions, anaphylactoid reactions are not immune-mediated. Clinical manifestations of anaphylaxis include ery-thema, 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 angio-edema. 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, throm-bocytopenia, and granulocytopenia. A serum sickness-like reaction is the prototype type III drug hypersensitivity. Type IV drug hypersensitivities are mediated by antigen-specifi c 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, psoriasis, FDE, AGEP, DRESS, SJS, and TEN.