Urticaria. An updated review

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Abstract
Urticaria [human] can result from many different stimuli; numerous factors, immunologic and nonimmunologic, are involved in its pathogenesis. Most commonly considered of immunologic mechanisms is the type 1 hypersensitivity state mediated by IgE [immunoglobulin E]. Another immunologic mechanism involves the activation of the complement cascade, which produces anaphylatoxins that can release histamine. Immunologic, nonimmunologic, genetic and modulating factors converge on mast cells and basophils to release mediators capable of producing urticarial lesions. In addition to the clinical and laboratory diagnosis and treatment regimens, such mediators as histamine, kinins, serotonin, slow-reacting substance of anaphylaxis, prostaglandins, acetylcholine, fibrin degradation products and anaphylatoxins that increase vascular permeability and can thereby produce wheals are reviewed. Special consideration is given to histamine and the factors that regulate its secretory release from mast cells and basophils, including the modulating role of intracellular levels of cyclic AMP.

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