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The pathophysiology of localized heat urticaria was studied by performing a heat challenge on a patient with this disease. Serum levels of total hemolytic complement, C3, and factor B decreased following heat challenge, whereas levels of C4 and C5 did not. Plasma histamine levels remained unchanged. Electron microscopic studies of affected tissue revealed endothelial cell damage and neutrophilic degranulation in the affected area. Mast cells remained intact. These data imply that activation of the alternative complement pathway is involved in the pathogenesis of localized heat urticaria and that mast cell histamine release does not play a significant role in this disease.
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