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Osteoporosis, Mineral Metabolism, and Serum Soluble Tumor Necrosis Factor Receptor p55 in Viral Cirrhosis

Department of Gastroenterology (J.L.G.-C., F.G.-R., R.F.-P., F.C.-C., E.R.-E.) and Immunology Unit (E.G.O.), University Hospital San Cecilio, 18012 Granada, Spain

Address all correspondence and requests for reprints to: Dr. Jorge L. Gonzalez-Calvin, Department of Gastroenterology, University Hospital San Cecilio, 18012 Granada, Spain. E-mail: jorgegonzalezc{at}meditex.es.

Liver cirrhosis is a risk factor for osteoporosis. Nevertheless, little is known about the mechanisms of bone mass loss in patients with viral cirrhosis. TNF is a potent bone-resorbing agent. Serum concentrations of soluble TNF receptor p55 (sTNFR-55) correlate with clinical activity in liver cirrhosis. Our aim was to evaluate the possible role of sTNFR-55 in the pathogenesis of osteoporosis in patients with viral cirrhosis and its relationship with bone turnover markers. We studied 40 consecutive patients with viral cirrhosis and no history of alcohol intake and 26 healthy volunteers. Bone mineral density (BMD) was measured by dual x-ray absorptiometry in the lumbar spine (LS) and femoral neck (FN). Patients with viral cirrhosis had reduced BMD (expressed as the z-score) in all sites [LS, –1.5 ± 0.22 (P < 0.001); FN, –0.37 ± 0.15 (P < 0.01)]. Serum concentrations of sTNFR-55 and urinary deoxypyridinoline, a biochemical marker of bone resorption, were significantly higher in patients with osteoporosis than in patients without osteoporosis (P < 0.001 and P < 0.05, respectively). Serum levels of sTNFR-55 correlated inversely with BMD in LS (r = –0.62; P < 0.005) and FN (r = –0.47; P < 0.05) and positively with urinary deoxypyridinoline (r = 0.72, P < 0.001). Our findings show that high serum concentrations of sTNFR-55 play a role in the pathogenesis of viral cirrhosis-associated bone mass loss and provide evidence of increased bone resorption related to the high serum sTNFR-55 levels.