Effect of liver dysfunction on circulating sclerostin

Abstract

Sclerostin is a Wnt inhibitor produced specifically by osteocytes. It decreases bone formation by repressing osteoblast differentiation and proliferation. Whether circulating sclerostin level is affected by liver function is not currently clear. The aim of the study was to evaluate this relationship. Our cross-sectional study included 47 patients with liver cirrhosis and 50 healthy controls. Serum sclerostin level was analyzed by ELISA. Serum sclerostin levels were significantly higher in patients with cirrhosis than in controls (50.8 ± 38.2 vs. 35.1 ± 8.8 pmol/L, p = 0.008). After further adjustment for age, sex, body mass index, serum creatinine, and presence of diabetes, cirrhosis patients had higher sclerostin than controls. Subgroup analysis found that patients with Child–Pugh class B or C had higher sclerostin levels than patients with class A or controls after adjusting for multiple confounding factors. Multiple regression analysis showed that gender (p = 0.022), presence of diabetes (p < 0.001), albumin (p = 0.010), and serum creatinine (p = 0.037) were independent factors for circulating sclerostin level. Circulating sclerostin was higher in patients with advanced liver cirrhosis than in healthy controls or patients with early liver cirrhosis. The elevated sclerostin levels clearly correlated with markers of liver dysfunction such as albumin. The relationship between circulating sclerostin and liver function indicates a possible role of the liver in sclerostin metabolism.