Blake D R, Winyard P, Scott D G, Brailsford S, Blann A, Lunec J
Ann Rheum Dis. 1985 Mar;44(3):176-82. doi: 10.1136/ard.44.3.176.
One of the proposed mechanisms of vascular damage in connective tissue disease is the direct action of a cytotoxic serum factor inducing endothelial cell damage. The nature of this serum factor is unclear, but has been suggested to be a lipoprotein. Sera from patients with (1) systemic necrotising arteritis (polyarteritis nodosa, Wegener's granulomatosis, and necrotising arteritis associated with rheumatoid synovitis), (2) systemic or joint restricted rheumatoid disease, and (3) large vessel/giant cell arteritis have been examined for cytotoxicity to human cultured endothelial cells and azide-resistant ferroxidase-like activity (indicative of the oxidised lipoprotein content). Stored sera from patients with necrotising arteritis showed a significantly enhanced tendency to develop oxidised lipoprotein, which correlated closely with human endothelial cell cytotoxicity. Fresh sera also contained this factor, but to a lesser extent. It is argued that the cytotoxic factor detected in previous clinical studies is in part an in-vitro artefact, although its accelerated development in certain patient groups might suggest an excess of pro-oxidants that have developed in vivo.
结缔组织病中血管损伤的一种推测机制是细胞毒性血清因子的直接作用，该因子可诱导内皮细胞损伤。这种血清因子的性质尚不清楚，但有人认为它是一种脂蛋白。对以下患者的血清进行了检测：（1）系统性坏死性动脉炎（结节性多动脉炎、韦格纳肉芽肿病以及与类风湿性滑膜炎相关的坏死性动脉炎）；（2）全身性或关节局限性类风湿病；（3）大血管/巨细胞动脉炎，检测其对人培养内皮细胞的细胞毒性以及叠氮化物抗性亚铁氧化酶样活性（指示氧化脂蛋白含量）。坏死性动脉炎患者的储存血清显示出氧化脂蛋白生成趋势显著增强，这与对人内皮细胞的细胞毒性密切相关。新鲜血清中也含有这种因子，但含量较少。有人认为，先前临床研究中检测到的细胞毒性因子部分是体外假象，尽管其在某些患者群体中加速生成可能表明体内产生了过量的促氧化剂。
