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系统性红斑狼疮中的动脉粥样硬化。

Atherosclerosis in systemic lupus erythematosus.

机构信息

Hospital Management, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.

出版信息

Autoimmunity. 2010 Feb;43(1):98-102. doi: 10.3109/08916930903374527.

DOI:10.3109/08916930903374527
PMID:20014976
Abstract

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease that has a late mortality phase owing mainly to cardiovascular manifestations. Atherosclerosis itself is characterized by inflammatory components, fulfilling the criteria of Witebsky and Rose for an autoimmune disease. SLE patients have increased risk for cardiovascular events, and these are the result of both atherosclerosis and thromboembolic events. Risk factors for atherosclerosis in SLE include "traditional" risk factors (mainly the Framingham risk factors), as well as disease-related factors including disease duration, steroid therapy, and renal disease, and inflammatory mechanisms that specifically contribute to enhanced atherosclerosis in SLE. These include specific antibodies to beta2GPI; anticardiolipin antibodies; anti-oxidized low-density lipoprotein; and antibodies to heat shock proteins, complement activation, impaired ability to activate TGF-beta1, and elevated levels of CRP. These findings stress the importance of surveillance and preventive strategies to control atherosclerosis in SLE.

摘要

系统性红斑狼疮(SLE)是一种自身免疫性风湿病,主要由于心血管表现而导致晚期死亡率。动脉粥样硬化本身的特点是炎症成分,符合 Witebsky 和 Rose 提出的自身免疫性疾病的标准。SLE 患者发生心血管事件的风险增加,这些事件是动脉粥样硬化和血栓栓塞事件的结果。SLE 患者发生动脉粥样硬化的危险因素包括“传统”危险因素(主要是弗莱明汉危险因素),以及与疾病相关的因素,包括疾病持续时间、类固醇治疗和肾脏疾病,以及炎症机制,这些机制特异性地导致 SLE 中动脉粥样硬化的增强。这些机制包括针对β2GPI 的特异性抗体;抗心磷脂抗体;抗氧化低密度脂蛋白;以及针对热休克蛋白、补体激活、TGF-β1 激活能力受损和 CRP 水平升高的抗体。这些发现强调了监测和预防策略对控制 SLE 中动脉粥样硬化的重要性。

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