Background Vitamin D deficiency was recently acknowledged as an independent predictor of cardiovascular diseases and all-cause mortality in several clinical setting and its serum levels are commonly reduced in Rheumathoid Arthritis. (RA). Patients affected by RA present accelerated atherosclerosis and increased cardiovascular morbidity and mortality with respect to the general population. In RA an impairment of the number and the activity of circulating progenitor cells, including CD34+ cells and endothelial progenitor cells, appears to be involved in development of endothelial damage and cardiovascular diseases.
Objectives This study investigates the association between vitamin D deficiency and circulating progenitor cell number (CPCs).
Methods Circulating progenitor cells number and vitamin D levels were measured in 30 patients affected by RA and in 30 controls matched for age and gender. C-reactive protein (CRP), fibrinogen, erythrocyte sedimentation rate (ESR), carotid intima-media thickness (cIMT), augmentation index (AIx), pulse wave velocity (PWV) were also evaluated. We investigated the relationships among vitamin D and cell number, inflammatory markers, and vascular parameters.
Results In RA patients the levels of vitamin D were reduced with respect to controls (21.5±6.9 vs 37.6±13.2 ng/ml, p <0.001); CPCs number (1.80±0.59 vs 2.32± 0.34 cells/µL, p <0.001) was also significantly reduced. PWV and AIx were higher in RA, while cIMT was not different between RA patients and controls. Vitamin D correlate inversely with CPCs number and PWV (rs -0.49 p < 0.005 and rs -0.56, p< 0.001 respectively). In RA we identify no association between vitamin D and cIMT, CRP, ESR, fibrinogen. CPCs number correlates with CRP (rs -0.50, p<0.005) and ESR (rs= -0.57, p<0.001).
Conclusions Our findings suggest that Vitamin D deficiency is a common finding in RA and is associated with reduced CPCs counts. Future studies are needed to determine whether vitamin D supplementation could improve CPCs levels and arterial stiffness indices in patients affected by rheumathoid arthritis.
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Disclosure of Interest None Declared