Cecere F A, Yoshinoya S, Pope R M
Arthritis Rheum. 1981 Mar;24(3):550-3. doi: 10.1002/art.1780240316.
An immunologic mechanism, possibly immune complex mediated, has been suggested as the basis for the pathogenesis of thrombotic thrombocytopenic purpura (TTP). The evidence supporting this concept has been the association of TTP with systemic lupus erythematosus and the successful therapy of TTP by plasmapheresis. However, most investigators have failed to demonstrate elevated circulating immune complexes during the course of TTP. This report describes a young woman with systemic lupus who developed TTP as a terminal event. Elevated levels of immune complexes were associated with periods of active lupus but were not detectable at the time she developed TTP.
一种免疫机制，可能是免疫复合物介导的，已被认为是血栓性血小板减少性紫癜（TTP）发病机制的基础。支持这一概念的证据是TTP与系统性红斑狼疮的关联以及血浆置换对TTP的成功治疗。然而，大多数研究者未能在TTP病程中证明循环免疫复合物升高。本报告描述了一名患有系统性红斑狼疮的年轻女性，她在疾病末期发展为TTP。免疫复合物水平升高与狼疮活动期相关，但在她发生TTP时未检测到。
