Twenty-five patients who met the American College of Rheumatology 1987 revised diagnostic criteria for RA were randomly selected for this study. The percentage of brachial flow-mediated dilation buy Paclitaxel (%FMD) and maximum carotid intima-media thickness were examined by ultrasonography. The %FMD in the group treated with anti-TNF therapy was significantly higher than that in the group treated with DMARDs (P < 0.001). The %FMD was significantly correlated with anti-TNF therapy (r = 0.684, P < 0.001) and Disease Activity Score C-reactive protein (r = –0.404, P < 0.05).

Multiple regression analysis revealed that anti-TNF therapy was significantly associated with %FMD (β = 0.684, P < 0.001). Anti-TNF therapy may influence endothelial function more than conventional DMARD therapy. Prospective longitudinal studies examining whether anti-TNF therapy was able to improve endothelial function are required. Rheumatoid arthritis RNA Synthesis inhibitor (RA) is a disease associated with increased cardiovascular mortality, resulting from accelerated atherosclerosis.[1, 2] Endothelial dysfunction is an early step in atherogenesis,[3] which may be determined by non-invasive techniques such as brachial ultrasonography (US) which measures flow-mediated endothelium-dependent

vasodilation.[4, 5] Endothelial dysfunction determined by flow-mediated endothelium-dependent vasodilation (FMD) has been observed in both patients with recent onset and low disease activity as well as long-standing RA patients.[6, 7] Hannawi[8] recently reported that carotid

intima-media thickness (IMT) is greater in RA patients with recent disease onset than Farnesyltransferase in age- and sex-matched control individuals. IMT is a useful noninvasive surrogate marker of macrovascular atherosclerosis disease. Gonzalez-Juanatey et al. report the presence of increased IMT in RA patients and a strong correlation between C-reactive protein (CRP) levels and the presence of subclinical atherosclerosis in these patients.[9] Recently, several authors investigated the effects of atherosclerosis on endothelial function or IMT during biologics treatment in patients with RA.[10-14] Patients with RA refractory to conventional disease-modifying anti-rheumatic drugs (DMARDs) exhibited short-term improvement in endothelial dysfunction following anti-tumor necrosis factor (TNF)-alpha therapy.[10, 12] However, the effects of some anti-TNF drugs seem to be transient.[11] Consistent with these findings, other biological therapies such as rituximab have also been reported to improve endothelial dysfunction in patients with RA refractory to anti-TNF drugs.[13, 15] On the basis of these findings, we aimed to clarify whether different TNF drugs can improve endothelial function better than conventional DMARDs in a series of Japanese patients with RA.