Endothelial dysfunction in joint disease

被引:39
作者
Prati, Clement [1 ,2 ]
Demougeot, Celine [2 ]
Guillot, Xavier [1 ]
Godfrin-Valnet, Marie [1 ]
Wendling, Daniel [1 ,3 ]
机构
[1] CHRU Besancon, Serv Rhumatol, F-25000 Besancon, France
[2] Univ Franche Comte, EA 4267 Fonct & Dysfonct Epithel, Franche Comte, France
[3] Univ Franche Comte, EA 4266 Agents Pathogenes & Inflammat, Franche Comte, France
关键词
Endothelial dysfunction; Rheumatoid arthritis; Spondyloarthritis; Lupus; PLASMA ASYMMETRIC DIMETHYLARGININE; RHEUMATOID-ARTHRITIS PATIENTS; FLOW-MEDIATED VASODILATATION; CONVERTING ENZYME-INHIBITION; ADJUVANT-INDUCED ARTHRITIS; SUBCLINICAL ATHEROSCLEROSIS; ANKYLOSING-SPONDYLITIS; CARDIOVASCULAR-DISEASE; VASCULAR FUNCTION; AORTIC STIFFNESS;
D O I
10.1016/j.jbspin.2014.01.014
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Inflammatory joint diseases and autoimmune diseases with joint manifestations are associated with premature and accelerated atherogenesis. Patients with rheumatoid arthritis (RA) have a 5- to 10-year decrease in life expectancy compared to the general population, and those exhibiting extraarticular manifestations have the greatest excess mortality. RA is now established as an independent cardiovascular risk factor. Complex interactions linking conventional cardiovascular risk factors, systemic inflammation, and vascular function may explain the increased cardiovascular risk among RA patients. Endothelial dysfunction is now recognized as both the key step in early atherogenesis and a contributor to atheroma plaque progression at later stages. Endothelial dysfunction is defined as impaired endothelium-dependent bloodvessel dilation in response to a stimulus. The underlying mechanisms remain speculative. Over the last decade, a role for endothelial dysfunction in the cardiovascular complications of inflammatory joint disease has been hypothesized and several maintenance drugs targeting this phenomenon have been tested, with promising results. (C) 2014 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:386 / 391
页数:6
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