Serum sclerostin in hepatitis C virus infected patients.
BACKGROUND
Sclerostin inhibits osteoblast functions, differentiations, and survival rates. As an endogenous inhibitor of the Wnt/β-catenin pathway, the sclerostin should be related to decreased bone masses, although several studies indicate opposite results. In addition, it may be related to insulin resistances and carbohydrate metabolisms, a relation shared with other markers of bone metabolisms, such as osteocalcin. Hepatitis C virus (HCV) infected patients may present osteoporosis, and frequently show liver steatosis, which is a consequence of insulin resistance. The behaviour of sclerostin in these patients is yet unknown. The aim of this work is to analyse the relationships between serum sclerostin and osteocalcin levels and bone mineral density (BMD), liver functions, the intensity of liver steatosis and biochemical markers of bone homeostasis and insulin resistance in HCV-infected patients.


METHODS
Forty HCV patients with 20 years of age and gender-matching controls were included in this study and underwent bone densitometry. Serum sclerostin, osteocalcin, collagen telopeptide, adiponectin, leptin, insulin, resistin, tumor necrosis factor (TNF)-α, and interleukin (IL)-6 were determined. Liver fat was histomorphometrically assessed.


RESULTS
Sclerostin levels were slightly higher in patients than in controls, and were directly related to BMD at different parts of the skeleton, also to the serum telopeptide, and to the liver steatosis and TNF-α. On the contrary, osteocalcin showed a significant direct relationship with serum adiponectin, and an inverse one with IL-6.


CONCLUSIONS
Serum sclerostin levels were within the normal range in HCV patients, and correlated directly with BMD and serum telopeptide. In addition, the relationships of sclerostin and osteocalcin with variables associated with insulin resistance suggested the role of bones for intermediary metabolisms.
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
Emilio
E
González-Reimers
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
Javier
J
López-Prieto
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
Ricardo
R
Pelazas-González
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
M Remedios
MR
Alemán-Valls
Department of Laboratory, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
María
M
José de la Vega-Prieto
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
Carlos
C
Jorge-Ripper
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
M Carmen
MC
Durán-Castellón
Department of Internal Medicine, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, Canary Islands, Spain.
F
F
Santolaria-Fernández
Fatty liver; Hepacivirus; Insulin resistance; Osteocalcin