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Published on: May 31, 2016
The relationships between serum sclerostin, bone mineral density, and vascular calcification in rheumatoid arthritis
J Paccou1, R Mentaverri, C Renard
1Department of Rheumatology (J.P., P.F.), INSERM Unité 1088 (J.P., R.M., C.R., S.L., P.F., Z.A.M., M.B., S.K.), "Pathophysiological mechanisms and consequences of cardiovascular calcification: role of cardiovascular and bone remodelling," Department of Endocrine and Bone Biology (R.M., M.B., S.K.), and Clinical Research Center (S.L.), Division of Clinical Pharmacology, Amiens University Medical Center, F-80054 Amiens, France; and Department of Nephrology (Z.A.M.), and Amboise Paré University Medical Center, Assistance Publique-Hôpitaux de Paris, F-92100 Boulogne Billancourt, France.
Context:
Recent data indicate that the secreted glycoprotein sclerostin may be involved in vascular calcification (VC).
Objective:
The objective of the study was to establish whether serum sclerostin levels are associated with VC in patients with rheumatoid arthritis (RA).
Design:
This was a cross-sectional study.
Setting:
The study was conducted with ambulatory care.
Patients:
We compared 75 RA patients with 75 age- and gender-matched control participants.
Intervention:
Coronary artery calcification (CAC) and abdominal aortic calcification (AAC) scores were evaluated by computed tomography.
Main Outcome Measure:
Serum sclerostin levels (determined with an ELISA) were assessed. A statistical analysis was performed to identify the determinants of serum sclerostin and VC.
Results:
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.
Conclusions:
Serum sclerostin levels were significantly and independently associated with AAC in RA patients.
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