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Mediators of Inflammation
Volume 2014 (2014), Article ID 681635, 11 pages
http://dx.doi.org/10.1155/2014/681635
Research Article

Differential Associations of Inflammatory and Endothelial Biomarkers with Disease Activity in Rheumatoid Arthritis of Short Duration

1Department of Internal Medicine and Gerontology, Jagiellonian University Medical College/University Hospital, ul. Śniadeckich 10, 31-531 Cracow, Poland
2Department of Rheumatology and Balneology, Jagiellonian University Medical College/University Hospital, ul. Śniadeckich 10, 31-531 Cracow, Poland
32nd Department of Cardiology, Jagiellonian University Medical College/University Hospital, ul. Kopernika 17, 31-501 Cracow, Poland
4Division of Rheumatology, Department of Internal Medicine and Gerontology, Jagiellonian University Medical College/University Hospital, ul. Śniadeckich 10, 31-531 Cracow, Poland
5Department of Clinical Biochemistry, Jagiellonian University Medical College/University Hospital, ul. Kopernika 15b, 31-501 Cracow, Poland

Received 15 November 2013; Revised 3 January 2014; Accepted 17 January 2014; Published 3 March 2014

Academic Editor: Oreste Gualillo

Copyright © 2014 Ewa Klimek et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objectives. To estimate endothelial dysfunction in patients with rheumatoid arthritis (RA) of short duration in relation to disease activity based on the assessment of 28 joints (DAS28). Methods. We studied 29 patients (22 women, mean age 41 (SD, 9) years) with RA of short duration and 29 healthy controls. The RA subjects were divided into those with low (DAS28: 2.6–5.1, ) or high ( , ) disease activity. Exclusion criteria included clinically overt atherosclerosis and other coexistent diseases. Biochemical markers of inflammatory activation and endothelial dysfunction were measured. Results. There were no significant intergroup differences in the majority of classical cardiovascular risk factors. High-sensitivity C-reactive protein, tumor necrosis factor-α, and interleukin-6 were increased in RA subjects. Compared to the controls, levels of soluble vascular cell adhesion molecule-1, von Willebrand factor, and pentraxin-3 were significantly elevated in RA subjects with low disease activity, exhibiting no further significant rises in those with high disease activity. Asymmetric dimethyl-L-arginine, soluble E-selectin, monocyte chemotactic protein-1, and osteoprotegerin were increased only in RA patients with high disease activity. Conclusions. Our findings might suggest a dissociation of pathways governing generalized and joint-specific inflammatory reactions from those involved in endothelial activation and inflammation within the vascular wall.