Background: The main process involved in hepatic osteodystrophy seems to be osteoporosis, but decreased 25-hydroxylation of vitamin D might lead to osteomalacia and secondary hyperparathyroidism.
Methods and Results: We studied bone mineral density (BMD) by using DEXA-Expert Lunar, biochemical markers of bone turnover and calcium-parathyroid hormone (PTH)-vitamin D axis in 100 patients with chronic viral hepatitis secondary to hepatitis C virus: 49 non-cirrhotic (NCir) and 51 with cirrhosis (Cir) confirmed by liver biopsy and/or clinical and biochemical features. When compared to the age-matched population, 25% of the patients had low BMD at the lumbar spine (LS), 26.2% at Ward's triangle, 15.5% at the femoral neck (FN), and 20.2% at the trochanter. No difference was found either between Cir and NCir groups or between sexes. Urinary N-telopeptide was increased in 31.86% of the patients, and negatively correlated with BMD at the LS and trochanter (P < 0.02). Serum bone-specific alkaline phosphatase was elevated in 21% of the patients and negatively correlated with BMD at the trochanter and Ward's triangle (P < 0.02). Fasting 25-hydroxyvitamin D was low in only three Cir patients, with no difference between the Cir and NCir groups, but it was higher in men (51.8 ± 16.0 ng/mL) compared to women (40.4 ± 14.4 ng/mL; P = 0.001). Fasting serum calcium was lower in Cir than NCir patients, P = 0.019. Fasting intact PTH was elevated in 42% of the patients, but the mean serum levels were similar in Cir and NCir groups.
Conclusion: We found no evidence of vitamin D deficiency, but cannot exclude the participation of PTH in the high bone turnover and bone loss in the population with chronic viral hepatitis.