Urticaria. An updated review

• Published in: Archives of dermatology (1960) Vol. 113; no. 1; p. 80
• Main Authors: Monroe, E W, Jones, H E
• Format: Journal Article
• Language: English
• Published: United States 01-01-1977
• Subjects: Bites and Stings - complications; Cold Temperature - adverse effects; Complement System Proteins - physiology; Cyclic AMP - physiology; Drug Hypersensitivity; Food Hypersensitivity; Histamine Release; Hot Temperature - adverse effects; Humans; Hypersensitivity; Immunoglobulin E; Infection - complications; Methods; Pressure - adverse effects; Psychophysiologic Disorders; Ultraviolet Rays - adverse effects; Urticaria - diagnosis; Urticaria - etiology; Urticaria - genetics; Urticaria - immunology; Urticaria - therapy
• ISSN: 0003-987X
• DOI: 10.1001/archderm.1977.01640010082015

Urticaria can result from many different stimuli, and numerous factors, both immunologic and nonimmunologic, are involved in its pathogenesis. Most commonly considered of immunologic mechanisms is the type I hypersensitivity state mediated by IgE. 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, we review 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. Special consideration is given to histamine and the factors that regulate is secretory release from mast cells and basophils, including the modulating role of intracellular levels of cyclic adenosine monophosphate.