Mathison D A, Arroyave C M, Bhat K N, Hurewitz D S, Marnell D J
Ann Intern Med. 1977 May;86(5):534-8. doi: 10.7326/0003-4819-86-5-534.
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.
在大多数慢性荨麻疹或血管性水肿患者中，未识别出离散的诱发因素或假定的病理生理机制。本文报告了两例病例，其中慢性荨麻疹是免疫性皮肤血管炎的主要表现，该血管炎与补体激活的经典途径和替代途径导致的低补体血症有关。在连续评估的72例慢性荨麻疹患者中，另外10例特发性荨麻疹患者被发现有低补体血症。其中，2例有补体激活经典途径和替代途径的证据，5例仅有经典途径激活的证据，3例主要或仅具有替代途径激活的证据。大多数经典途径激活的患者中发现有循环免疫复合物。低补体血症可能为一些慢性荨麻疹患者的病理生理机制提供线索。
