Recently the medical community got to acknowledge that, although not as relevant as in women, male osteoporosis is an epidemiologically relevant feature of the disease and one out of three osteoporosis fractures occurs in the male population. Aim of this study was to evaluate bone mineral density and bone metabolism markers in a selected series of male patients affected only by viral, non-advanced chronic liver disease. This illness is known to affect patients metabolism, possibly leading to hypermetabolism affecting also the bone turnover. The eccessive bone turnover activity can lead to an alteration of bone trabeculae, and to their perforation. This fact leads to a damage of bone micro-architecture and, consequently, to the reduction of proper mechanical characteristics of the bone segment and to increased risk of fracture. The present study shows that viral chronic liver disease in man is associated with reduced bone mineral density. In fact BMD at LS was significantly lower in liver patients as compared to controls (p<0.05) and BMD at FN showed a trend to reduction even though the difference between patients and controls was not statistically significant (Table I). Data are obtained using two different groups of controls: 1) age, BMI-matched healthy volunteers, 2) population-based reference values. Osteoporosis has been described in patiens treated with orthotopic liver transplantation, as well as in subjects affected by advanced liver cirrhosis, primary biliary cirrhosis, cholestatic or alcoholic liver diseases, hemochromatosis and in corticosteroid treated patients, but little is known about bone mineral density in viral non advanced liver disease. A recent paper on this issue reported in viral cirrhosis in men a high prevalence of osteoporosis suggesting that it is a major cause of reduced bone mineral density in men. However, in this study three heterogeneous groups of patients, aged 3874, affected by different severity of liver disease, according to Child’s classification and Pugh’s score were studied: a significant correlation between BMD at lumbar spine and severity of liver disease was found. An advanced age and a more severe liver disease could both affect the results, therefore, in the present study we examined 25 male patients selected on the basis of very restricted criteria: it was a homogeneous group, without confounding factor affecting bone metabolism, B and C Child’s classes of liver cirrhosis and subsets aged > 60 years were excluded.
Previous papers reported low serum levels of PTH, 25-OHD, and calcium in advanced liver cirrhosis graded as Child’s C class. In contrast we did not find any difference between patients and controls for all biochemical parameters of bone metabolism. These discrepancies may be explained by patient selection and different pathogenetic mechanisms. In fact, the pathogenesis of reduced bone density in chronic liver disease remains not clear. Reduced osteoblastic function with diminished bone formation has been suggested as the main factor responsible for osteoporosis in alcoholic liver cirrhosis: it is defined “low turnover osteoporosis” and low serum concentrations of IGF-1 are associated with this condition. In contrast, a “high turnover osteoporosis” is characterized by normal or reduced bone formation coupled with increased resorption. In this case synthesis of matrix and its mineralization are normal, but osteoblasts are unable to fill the numerous resorption cavities. “High turnover osteoporosis” has been mainly reported in patients with chronic cholestatic liver disease as primary sclerosing cholangitis, and primary biliary cirrhosis.
In our patients serum levels of IGF-1 are normal since they are affected by non advanced liver disease and it is known that IGF-1 levels are related to the severity of liver disease. Our patients did not show any difference, as compared to controls, in bone remodelling markers as serum PTH, 25-OHD, calcium and sexual hormones, as well as urinary hydroxypro line. When you need your medication buy on online pharmacy american
Neverthless, a high prevalence of osteoporosis and osteopenia was found in our selected group of male patients and bone mass reduction was more severe at LS (trabecular bone) than at FN (cortical and trabecular bone) in keeping with the above mentioned papers, probably because the rate of turnover in cortical bone is much lower than in trabecular bone. In conclusion our data, obtained on the basis of severe inclusion criteria, excluding confounding factor affecting bone metabolism, suggest that liver disease “per se” indipendently on its severity and lasting, can reduce the bone mass. The exclusion of female sex and advanced age, and the study of a very homogeneous group of male patients not alcohol consumers, never treated with steroids or drugs affecting bone mass, without clinical or laboratory signs of cholestasis suggest that osteoporosis is a frequent finding in males with non advanced viral liver disease and that more attention has to be paid to bone metabolism in liver patients.