Abstract

Chronic liver disease caused by HBV and HCV infections, due to its great prevalence and serious medical consequences, is at the present time a significant clinical problem. An impaired liver function can provoke severe disturbances in calcium and phosphorus homeostasis, and consequently in the bone metabolism resulting in hepatic osteodystrophy. The aim of this study was to determine whether there are significant differences in bone mineral density (BMD) and/or circadian levels of hormones connected with bone metabolism and bone turnover markers in patients with chronic viral hepatitis. Circadian levels (AUC, area under the curve) of GH, IGF-I, IGFBP-3, osteocalcin (BGLAP), C-terminal telopeptide of type I collagen (ICTP), PTH, 25(OH)D, total calcium and total phosporus were measured in the blood of members of the study group (n = 80). BMD was assessed using the dual-energy X-ray absorptiometry method of the L2-L4 lumbar spine. Data was compared to that of healthy individuals (n = 40). BMD (1.05 g/cm3 vs. 1.20 g/cm3), total calcium concentration (2.20 mmol/L vs. 2.45 mmol/L), total phosphorus concentration (1.06 mmol/L vs. 1.33 mmol/L), IGF-I (AUC 3,982.32 ng/mL vs. 5,167.61 ng/mL), IGFBP-3 (AUC 725.09 ng/L vs. 944.35 ng/L), 25(OH)D (AUC 356.35 ng/mL vs. 767.53 ng/mL) and BGLAP (AUC 161.39 ng/L vs. 298 ng/L) were lower in the study group. GH (AUC 88.3 ng/mL vs. 48.04 ng/mL), iPTH (AUC 1,201.94 pg/mL vs. 711.73 pg/mL) and ICTP (AUC 104.30 μg/L vs. 54.49 μg/L) were higher in patients with hepatitis. Positive correlations were noted between bone mineral density and IGF-I, IGFBP-3, and BGLAP levels. Chronic viral hepatitis causes a decrease in bone mineral density. Impaired liver function disrupts homeostasis of the calcium- vitamin D-parathyroid hormone axis and provokes secondary hyperparathyroidism. Chronic viral hepatitis induces a decrease in the synthesis of IGF-I and IGFBP-3 and an increase in GH secretion. Hepatic osteodystrophy is probably caused by both changes in calciotropic hormones as well as in the somatotropin hormone axis.

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