Hepatic osteodystrophy in male patients with liver cirrhosis secondary to hepatitis C virus

Introduction and aim of the study: Osteoporosis is an established complication of cholestatic liver cirrhosis. Nevertheless, little is known about the mechanisms of bone mass loss and mineral metabolism in patients with viral cirrhosis. The present study was performed to evaluate bone mineral density and mineral metabolism in patients with liver cirrhosis secondary to hepatitis C virus (HCV). Patients and methods: Eighty male patients with chronic liver disease secondary to hepatitis C virus were studied at Internal Medicine department Al-Azhar University, National Research Center and tropical medicine department Tanta University. Bone mineral density (BMD) was measured by dual x-ray absorptiometry in the lumbar spine. Intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25(OH) D), Insulin like growth factor-1 (IGF-1), liver function testes and serum calcium were measured to all participants. The patients were divided into two groups according to liver biopsy and clinical examination. Group I (40 patients without cirrhosis; Group II (40 patients with liver cirrhosis) in addition to 20 healthy volunteers. Patients with cirrhosis were further classified using the Child- Pugh score into three subgroups: Child A (15 patients), Child B (13 patients) and Child C (12 patients). Results: Serum levels of albumin, bilirubin, ALT, AST and Prothrombin activity were significantly impaired in patients than control and in group II than group I. Serum levels of 25(OH) D and IGF-1 were significantly lower in Child A, B and C than control, in Child B and C than Child A and in Child C than Child B. Serum levels of iPTH were significantly higher in Child A, B and C than control and in Child C than Child A and B. Bone mineral density negatively correlated with serum iPTH (r=-750) and Child-Pugh score (r=-782), positively correlated with serum 25(OH) D (r=550) and IGF-I (r=685), but not correlated with serum calcium. Conclusion: Liver cirrhosis predisposes to bone loss. The severity of metabolic osteopathy worsens as liver function does. The underlying mechanism is represented by an increased bone resorption.