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Wednesday, January 9, 2013

Serum Sclerostin in Alcoholics: A Pilot Study

Sclerostin is an endogenous inhibitor of the Wnt/β-catenin pathway secreted by osteocytes, which inhibits osteoblast function, differentiation and survival. As a consequence, sclerostin tends to decrease bone mass. Alcoholics frequently present osteoporosis, mainly due to decreased bone synthesis. The behaviour of sclerostin in these patients is unknown. The aim of this work was to analyse the relationship between serum sclerostin levels and bone mineral density (BMD), ethanol consumption, nutritional status, liver function derangement and biomarkers of bone homeostasis in alcoholic patients. 

We included 31 alcoholic patients, of whom 11 were infected with Hepatitis C virus (HCV) and 7 age and sex-matched controls. All underwent densitometry, and serum sclerostin, osteocalcin, collagen telopeptide, parathyroid hormone (PTH), vitamin D, cortisol and testosterone were determined. 

Sclerostin levels were significantly higher in patients (30.95 ± 18.91 pmol/l) than controls (t = 4.4; P < 0.001), especially in non-HCV patients; they showed an inverse correlation with osteocalcin, prothrombin activity and serum albumin, and a direct correlation with bilirubin and telopeptide, but not with BMD, nutritional status or ethanol intake. 

Serum sclerostin was raised in alcoholic patients, and it correlated with decreased markers of bone synthesis and increased markers of bone breakdown. The elevation in sclerostin levels was clearly related with liver function, but not with ethanol intake, nutritional status or concomitant HCV infection.

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