Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Fábrega, E. et al.

Fábrega, Orive, García-Suarez, García-Unzueta, Antonio Amado, Pons-Romero,

Osteoprotegerin and RANKL in alcoholic liver cirrhosis.

BACKGROUND/AIMS: The mechanisms leading to osteoporosis in alcoholic liver disease remain poorly understood. Recently identified soluble circulating osteoprotegerin (OPG), is the osteoclastogenesis inhibitory factor. It acts as a decoy receptor for osteoclast activating factor, receptor activator of nuclear factor-kappaB ligand (RANKL), and impairs osteoclast function. The aim of our study was to investigate the OPG/RANKL system in alcoholic cirrhotic patients and their correlation with biochemical marker of bone turnover. PATIENTS AND METHODS: Serum OPG, RANKL, osteocalcin (OC), C-terminal cross-linking telopeptide of type I collagen (CTX-I), bone alkaline phosphatase activity (bALP), and urinary hydroxyproline were measured in 30 patients with alcoholic cirrhosis, and in 20 age- and sex-matched healthy controls. RESULTS: OPG levels were significantly increased in patients with alcoholic cirrhosis compared with healthy subjects (5.9 pmol/l, range 2.7-9.0 vs 4.1 pmol/l, range 1.2-6.6; P < 0.001). RANKL levels were significantly higher in patients with cirrhosis (0.48 pmol/l, range 0.01-1.34) than in healthy subjects (0.11 pmol/l, range 0.01-0.90). There was a positive correlation between serum OPG and RANKL (r = 0.37; P < 0.001), bALP (r = 0.66; P < 0.001) and urinary hydroxyproline (r = 0.51; P < 0.05) but not with OC and CTX-I. CONCLUSIONS: OPG might partly represent a compensating mechanism to the negative balance of bone remodelling in patients with alcoholic cirrhosis.[1]

References

Osteoprotegerin and RANKL in alcoholic liver cirrhosis. Fábrega, E., Orive, A., García-Suarez, C., García-Unzueta, M., Antonio Amado, J., Pons-Romero, F. Liver Int. (2005) [Pubmed]

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