Danning C L, Illei G G, Boumpas D T
Arthritis and Rheumatism Branch, National Institutes of Health, Bethesda, Maryland 20892, USA.
Curr Opin Rheumatol. 1998 Jan;10(1):58-65. doi: 10.1097/00002281-199801000-00009.
Vasculitis is an uncommon but important manifestation of autoimmune rheumatic diseases. Although the blood vessels of any organ can be involved, cutaneous involvement of arterioles and venules is the most common. Autoimmune rheumatic diseases may present as systemic vasculitis, and systemic vasculitis may simulate autoimmune rheumatic diseases. A crucial event in the initiation, localization, and propagation of vascular injury involves activation of the vascular endothelium by a variety of stimuli, including cytokines, complement split products, and cognate interactions between endothelial and T cells. Endothelial cell permissiveness to the deposition of circulating immune complexes or in situ formation of immune complexes in the vessel wall is also important. Vascular injury may be mediated by local or systemic activation of the complement system as well as autoantibody or T-cell-dependent mechanisms. This review focuses on the clinical features and pathogenic mechanisms involved in vasculitis complicating autoimmune rheumatic diseases.
血管炎是自身免疫性风湿性疾病中一种不常见但重要的表现形式。尽管任何器官的血管都可能受累，但小动脉和小静脉的皮肤受累最为常见。自身免疫性风湿性疾病可能表现为系统性血管炎，而系统性血管炎也可能类似自身免疫性风湿性疾病。血管损伤起始、定位和传播过程中的一个关键事件涉及多种刺激物激活血管内皮，这些刺激物包括细胞因子、补体裂解产物以及内皮细胞与T细胞之间的同源相互作用。内皮细胞对循环免疫复合物沉积或血管壁原位免疫复合物形成的易感性也很重要。血管损伤可能由补体系统的局部或全身激活以及自身抗体或T细胞依赖性机制介导。本综述重点关注并发自身免疫性风湿性疾病的血管炎的临床特征和致病机制。
