Daman L, Lieberman P, Ganier M, Hashimoto K
J Allergy Clin Immunol. 1978 Apr;61(4):273-8. doi: 10.1016/0091-6749(78)90203-8.
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.
通过对一名局限性热荨麻疹患者进行热激发试验,研究了该病的病理生理学。热激发试验后,总溶血补体、C3和B因子的血清水平下降,而C4和C5的水平未下降。血浆组胺水平保持不变。对受影响组织的电子显微镜研究显示,受影响区域存在内皮细胞损伤和嗜中性粒细胞脱颗粒。肥大细胞保持完整。这些数据表明,替代补体途径的激活参与了局限性热荨麻疹的发病机制,并且肥大细胞组胺释放在此病中不发挥重要作用。