Smoking and rheumatoid arthritis.

Smoking and rheumatoid arthritis.
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DOI:
10.3390/ijms151222279
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发表时间:
2014-12-03
影响因子:
5.6
通讯作者:
Shin JI
Shin JI
中科院分区:
生物学2区
文献类型:
--
作者:
Chang K;Yang SM;Kim SH;Han KH;Park SJ;Shin JI

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类风湿性关节炎(RA)是一种由遗传和环境因素共同引起的慢性炎症性疾病。吸烟已被认为是其发展和严重程度的最重要的外在危险因素之一。最近的发展揭示了吸烟者RA的病理生理学,包括氧化应激,炎症,自身抗体形成和表观遗传变化。吸烟和类风湿关节炎的发展之间的关系已经通过流行病学研究以及类风湿关节炎的体内和动物模型得到证实。随着越来越多地使用生物制剂,除了标准的疾病修饰抗风湿药物(DMARD),有兴趣在吸烟如何影响药物反应在RA治疗。最近的证据表明,在重度吸烟者中,抗肿瘤坏死因子(抗TNF)治疗的反应和药物存活率较差,本文介绍了这种效应的可能免疫学机制。
Rheumatoid arthritis (RA) is a chronic inflammatory disease caused by both genetic and environmental factors. Smoking has been implicated as one of the most important extrinsic risk factors for its development and severity. Recent developments have shed light on the pathophysiology of RA in smokers, including oxidative stress, inflammation, autoantibody formation and epigenetic changes. The association of smoking and the development of RA have been demonstrated through epidemiologic studies, as well as through in vivo and animal models of RA. With increased use of biological agents in addition to standard disease-modifying antirheumatic drugs (DMARDs), there has been interest in how smoking affects drug response in RA treatment. Recent evidence suggests the response and drug survival in people treated with anti-tumour necrosis factor (anti-TNF) therapy is poorer in heavy smokers, and possible immunological mechanisms for this effect are presented in the current paper.
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