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动脉粥样硬化和类风湿关节炎:不仅仅是简单的关联。

Atherosclerosis and rheumatoid arthritis: more than a simple association.

机构信息

Department of Rheumatology, University and IRCCS Foundation Policlinico San Matteo, Viale Golgi 19, 27100 Pavia, Italy.

出版信息

Mediators Inflamm. 2012;2012:147354. doi: 10.1155/2012/147354. Epub 2012 Sep 13.

Abstract

In the last decades a large amount of evidence linked rheumatoid arthritis (RA) to atherosclerosis. In fact, RA patients have an increased risk of cardiovascular events that is not fully explained by other classic cardiovascular risk factors. RA and atherosclerosis may share several common pathomechanisms and inflammation undoubtedly plays a primary role. The proinflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, involved in the pathogenesis of RA, are also independently predictive of subsequent cardiovascular disease (CVD). In RA, inflammation alters HDL constituents and the concentration of LDL and HDL, thus facilitating atherosclerosis and CVD events. On the other hand, also the increase of oxidative processes, frequently observed in RA, induces atherosclerosis. Interestingly, some genetic polymorphisms associated with RA occurrence enhance atherosclerosis, however, other polymorphisms associated with RA susceptibility do not increase CVD risk. Several other mechanisms may influence atherosclerotic processes in RA. Moreover, atherosclerosis may be directly mediated also by underlying autoimmune processes, and indirectly by the occurrence of metabolic syndrome and impaired physical activity. Finally, the effects of RA therapies on cardiovascular system in general and on atherosclerosis in particular are really wide and different. However, the starting point of every RA treatment is that disease control, or better remission, is the best way we have for the reduction of CVD occurrence.

摘要

在过去几十年中,大量证据将类风湿关节炎 (RA) 与动脉粥样硬化联系起来。事实上,RA 患者发生心血管事件的风险增加,而这不能完全用其他经典心血管危险因素来解释。RA 和动脉粥样硬化可能有一些共同的发病机制,炎症无疑起着主要作用。参与 RA 发病机制的促炎细胞因子,如肿瘤坏死因子-α和白细胞介素-6,也可独立预测随后发生的心血管疾病 (CVD)。在 RA 中,炎症改变了 HDL 的成分以及 LDL 和 HDL 的浓度,从而促进了动脉粥样硬化和 CVD 事件的发生。另一方面,在 RA 中经常观察到的氧化过程的增加也会导致动脉粥样硬化。有趣的是,一些与 RA 发生相关的遗传多态性会增强动脉粥样硬化,但与 RA 易感性相关的其他多态性不会增加 CVD 风险。其他一些机制可能会影响 RA 中的动脉粥样硬化过程。此外,动脉粥样硬化也可能直接由潜在的自身免疫过程介导,间接由代谢综合征和身体活动受损引起。最后,RA 治疗对心血管系统的影响,尤其是对动脉粥样硬化的影响非常广泛且不同。然而,RA 治疗的起点是疾病控制,或者更好的缓解,是我们减少 CVD 发生的最佳方法。

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