Association between subclinical atherosclerosis and serum TWEAK, CD163 and FN14 levels in rheumatoid arthritis patients

Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disease with unknown etiology. Coronary artery disease (CAD) is known to increase in RA patients and starts years before clinical symptom release. The increase cardiovascular risk is driven by inflammation that is common pathway in both disease. TWEAK is a type 2 transmembrane glycoprotein of TNF family that has multiple functions such as angiogenesis, regulation of tissue production-destruction, proinflammatory cytokine release. TWEAK and Fn14 receptor interaction has an important role in pathogenesis of atherosclerosis. The aim of our study was to evaluate subclinical atherosclerosis and its association with serum sTWEAK, Fn14 and CD163 levels in RA patients. One hundred RA patients, 50 SpA patients and 50 healthy volunteers were included for this study. Serum soluble TWEAK, CD163 and Fn14 levels were measured by ELISA tecnique. Subclinical atherosclerosis was evaluated by measuring carotis intima media thickness (cIMT), aortic strain, stiffness and elasticity. At the end of the study, TWEAK levels were found significantly lower (p=0.05), and Fn14 levels were significantly higher (p<0.01) in RA patients compare to both control groups. In addition Fn14 levels were higher in RA patients with biological drug users and seropositive subgroup. Fn14 levels were correlated with disease duration (r=0.38, p<0.01). CD163 levels were similar in all groups. Although there was not any difference in cIMT measurements among groups, aortic stiffness was increased (p=0.03), aortic strain and elasticity were decreased (p=0.03, p=0.02) in RA patients compare to healthy controls. Multivariate analysis shows that, cardiovascular paramethers was only associated with age. In conclusion; we noted increased subclinic atherosclerosis in RA patients. Also we demonstrated, lower serum sTWEAK with higher serum Fn14 levels in RA patients which support vascular damage. However, more studies are needed to demonstrate association between atherosclerosis and these biomarkers in RA patients.