The relationships between serum sclerostin, bone mineral density, and vascular calcification in rheumatoid arthritis.

Abstract

Recent data indicate that the secreted glycoprotein sclerostin may be involved in vascular calcification (VC). The objective of the study was to establish whether serum sclerostin levels are associated with VC in patients with rheumatoid arthritis (RA). This was a cross-sectional study. The study was conducted with ambulatory care. We compared 75 RA patients with 75 age- and gender-matched control participants. Coronary artery calcification (CAC) and abdominal aortic calcification (AAC) scores were evaluated by computed tomography. Serum sclerostin levels (determined with an ELISA) were assessed. A statistical analysis was performed to identify the determinants of serum sclerostin and VC. AAC and CAC were more prevalent and more severe in patients with RA than in controls. Higher levels of AAC (P = .02) and a higher lumbar bone mineral density (BMD; P = .03) were identified as independent determinants of higher serum sclerostin levels in RA patients, whereas male gender (P = .03), higher lumbar BMD (P < .0001), and low estimated glomerular rate (P < .001) were identified as determinants in controls. In RA patients, a multivariate logistic regression analysis indicated that older age [P < .01, with an odds ratio (OR) per year 1.10] and male gender (P = .02, OR 6.79) were independent determinants of CAC and that older age (P < .001, OR 1.16) were independent determinants of AAC. In controls, the independent determinants were older age (P < .01, OR 1.19), hypertension (P < .01, OR 7.31), and lumbar BMD (P = .03, OR per 30 mg/cm(2) increment of 1.14) for CAC and older age (P = .01, OR 1.11) for AAC. Serum sclerostin levels were significantly and independently associated with AAC in RA patients.