Clinical correlations between chronic hepatitis C infection and decreasing bone mass density after treatment with interferon-alpha

• Published in: Asian Pacific Journal of Tropical Biomedicine
• Main Authors: Vahid Babaei, Masoud Ghorbani, Nastaran Mohseni, Hojjat Afraid, Yassaman Saghaei, Shahram Teimourian
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wolters Kluwer Medknow Publications 2017
• Subjects: Hepatitis C; Interferon alpha; Bone mass density; Liver fibrosis; Bone mass loss; Arctic medicine. Tropical medicine; RC955-962; Biology (General); QH301-705.5; Arctic
• Online Access: https://doi.org/10.1016/j.apjtb.2016.11.027; https://doaj.org/article/f2e9ab80d1014fe9961be45ff12d1f40

Objective: To compare the bone mass density in chronic hepatitis patients before and after interferon-α treatment. Methods: A total of 70 patients with chronic hepatitis C were treated with interferon-α and were evaluated. The treatment dosage was three million IU three times a week for one year. All the patients underwent bone mass density detection at lumbar spine and femoral neck before and after the interferon-α treatment. All the necessary information such as age, sex, and laboratory test, history of occurrence of fractures, lifestyle, and menopause status was collected by interviewers face-to-face from participants at the research visit. Smoking was categorized by whether participants were nonsmokers or smokers. Menopause was designated if there had been complete cessation of menses for more than 12 months. All statistical analyses were performed by SPSS version 14 (SPSS, Inc., Chicago, IL, USA). Results: Among 70 patients, 52% were male, 48% were female and the mean age was (57.0 ± 9.6) years (range: 24–79). Twenty-nine percent of the patients had a history of smoking. The mean body mass index was (24.4 ± 3.6) kg/m2 (range: 18.4–35.3). Of the 70 cases, 21 had high fibrosis-4. The prevalence of overall fracture history was 2.9% (two patients). Conclusions: Chronic hepatitis C virus infection did increase the risk of development of metabolic bone disease in this cohort. Indeed, greater reduction of bone mass density occurs in advanced liver fibrosis. The bone loss in earlier stages of chronic hepatitis C infection is likely to result from increased bone reduction rather than decreased bone formation. Overall, these observations suggest an important role for chronic hepatitis C virus infection in increased bone turnover in osteodystrophy pathogenesis.