Drug-induced urticaria and angioedema

Urticaria and angioedema are the most common manifestations of drug hypersensitivity and are caused by drugs that differ in chemical nature and mechanisms of action. The pathogenesis of drug-induced urticaria and angioedema can be based on immunological and non-immunological reactions. Immunological (allergic) urticaria and associated angioedema most often develop due to immunoglobulin E-mediated reactions. Non-immunological hypersensitivity is caused by the direct action of an agonist drug on target cells, followed by the release of a wide range of inflammatory mediators and cytokines, or the effect of drugs on the metabolism of several biologically active substances that stimulate inflammatory cells. Isolated angioedema (not accompanied by urticaria) may be a sign of drug allergy but is more often due to heterogeneous non-immunological reactions that activate mastocytes and basophils in various ways. Another common variant of drug-induced isolated angioedema is not associated with target cell degranulation but develops according to different mechanisms, leading to excessive bradykinin accumulation. Finally, some drugs may exacerbate the pathology of the complement system in patients with hereditary or acquired angioedema.

Here, the etiology, pathogenesis, clinical picture, diagnosis, principles of therapy, and prevention of heterogeneous variants of drug-induced urticaria and angioedema are considered from modern positions.