The lp13.3 genomic region -rs599839- is associated with endothelial dysfunction in patients with rheumatoid arthritis

A total of 128 RA patients without history of CV events were genotyped for rs599839 A/G polymorphism. The presence of endothelial dysfunction was assessed by brachial ultrasonography (brachial flow-mediated endothelium-dependent (FMD)).Patients carrying the allele G exhibited more severe endothelial dysfunction (FMD%: 4.61 ± 3.94%) than those carrying the wild allele A (FMD%: 6.01 ± 5.15%) (P = 0.08). Adjustment for gender, age at the time of study, follow-up time and classic CV risk factors disclosed a significant association between the rs599839 polymorphism and FMD (G vs. A: P = 0.0062).Our results confirm an association of the rs599839 polymorphism with endothelial dysfunction in RA.Rheumatoid arthritis (RA) is a complex polygenic autoimmune inflammatory disease with high risk of cardiovascular (CV) complications [1]. This is a consequence of accelerated atherosclerosis [1]. Besides classic CV risk factors and chronic systemic inflammation, recent studies have emphasized the relevance of several genetic polymorphisms, such as HLA-DRB1 and TNF, in the susceptibility to CV disease in RA [2,3].A major issue in the process of accelerated atherosclerosis in RA is the development of endothelial dysfunction, an early step in the development of atherosclerosis. An important step forward might be to identify high-risk RA patients who would benefit from active therapy to prevent clinical disease. Several noninvasive imaging techniques provide the opportunity to study the relationship of surrogate markers to the development of atherosclerosis. Among them, ultrasound techniques based on flow velocity are considered efficient ways to measure subclinical atherosclerosis. Using brachial artery ultrasonography assessment, we and others have disclosed the presence of endothelial dysfunction expressed by abnormal levels of flow-mediated endothelium-dependent vasodilatation (FMD) in patients without clinically evident CV disease who had either long-standing RA [4] or early-onset R