Department of Gastroenterology, Virgen de las Nieves University Hospital, Granada, Spain.
Osteoporos Int. 2014 Jun;25(6):1709-15. doi: 10.1007/s00198-014-2663-z. Epub 2014 Mar 28.
Patients with chronic hepatitis C have low bone mineral density and increased bone resorption related to serum transaminase levels. Elevated serum soluble tumor necrosis factor (sTNFR-55) receptor levels may play a role in the bone mass loss in these patients. Bone mass is improved and bone turnover normalized in patients who respond to antiviral therapy with interferon and ribavirin.
Low bone mineral density (BMD) has been described in patients with chronic hepatitis C (HCV). The study objective was to evaluate the effect of antiviral therapy on BMD and bone metabolism in non-cirrhotic HCV patients with sustained virological response.
We conducted a prospective study in 36 consecutive outpatients from the general community with non-cirrhotic HCV and an early and sustained virological response to peginterferon-alfa and ribavirin therapy. Determinations of BMD (dual X-ray absorptiometry at lumbar spine and femoral neck) and biochemical measurements of bone metabolism and sTNFR-55 were made at baseline, after 24 and 48 weeks of antiviral therapy, and at 48 weeks after the end of treatment.
Patients had a significantly reduced BMD, which significantly increased during the follow-up. Serum levels of sTNFR-55 and bone turnover markers were increased at baseline and significantly reduced at all subsequent time points. We found an inverse correlation between BMD and both serum aminotransferase levels and urine deoxypyridinoline (D-pyr) and a positive correlation between serum aminotransferases and both urine D-Pyr and serum sTNFR-55.
Patients with chronic hepatitis C have low bone mass associated with increased bone resorption, and some relationship can be expected between serum aminotransferase levels and the degree of bone mass loss. Bone mass may be improved and bone turnover normalized in patients who respond to antiviral therapy. Elevated serum sTRFR-55 levels may play a role in the bone mass loss of these patients.
评估抗病毒治疗对非肝硬化慢性丙型肝炎（HCV）患者骨密度（BMD）和骨代谢的影响。
我们对 36 例来自普通社区的非肝硬化 HCV 患者进行了前瞻性研究，这些患者对聚乙二醇干扰素-α和利巴韦林治疗有早期和持续的病毒学应答。在基线、抗病毒治疗 24 周和 48 周以及治疗结束后 48 周时，测定 BMD（腰椎和股骨颈双能 X 线吸收法）和骨代谢及可溶性肿瘤坏死因子受体-55（sTNFR-55）的生化指标。
患者的 BMD 明显降低，在随访期间明显增加。sTNFR-55 血清水平和骨转换标志物在基线时升高，所有后续时间点均显著降低。我们发现 BMD 与血清转氨酶水平和尿脱氧吡啶啉（D-pyr）呈负相关，与血清转氨酶水平和尿 D-Pyr 与血清 sTNFR-55 呈正相关。
慢性丙型肝炎患者存在低骨量和骨吸收增加，血清转氨酶水平与骨量丢失程度之间可能存在一定的相关性。抗病毒治疗应答的患者骨量可能得到改善，骨转换恢复正常。升高的血清 sTRFR-55 水平可能在这些患者的骨量丢失中起作用。
