DAVID A. MATHISON, M.D., F.A.C.P.; CARLOS M. ARROYAVE, M.D.; K. NARAS BHAT, M.D., F.A.C.P.; DAVID S. HUREWITZ; DANIEL J. MARNELL
A discrete evoking factor or presumed pathophysiologic mechanism is not recognized in the majority of patients with chronic urticaria or angioedema. Two cases are reported in which chronic urticaria was the main manifestation of an immune cutaneous vasculitis associated with hypocomplementemia attributable to classic and alternative mechanisms of complement activation. Among 72 consecutive patients evaluated for chronic urticaria, 10 additional patients with idiopathic urticaria were found to have hypocomplementemia. Of these, two had evidence of classic and alternative mechanisms of complement activation, five had evidence of only classic pathway activation, and three evidence of predominately or exclusively alternative pathway activation. Circulating immune complexes were found in the majority of patients with classic pathway activation. Hypocomplementemia may provide clues to pathophysiologic mechanisms operative in some patients with chronic urticaria.
MATHISON DA, ARROYAVE CM, BHAT KN, et al. Hypocomplementemia in Chronic Idiopathic Urticaria. Ann Intern Med. 1977;86:534–538. doi: 10.7326/0003-4819-86-5-534
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Published: Ann Intern Med. 1977;86(5):534-538.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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