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P61 Bone mineral density loss in tenofovir treated Chronic Hepatitis B Virus (HBV) patients is a consequence of Vitamin D deficiency and not Tenofovir therapy
  1. U S Gill1,
  2. S Al-shamma1,
  3. K Burke1,
  4. V Ross2,
  5. R T C Marley1,
  6. P Kooner1,
  7. G R Foster1,
  8. P T F Kennedy1
  1. 1Department of Hepatology, Barts and The London NHS Trust
  2. 2Pharmacy, Barts and The London NHS Trust


Introduction Tenofovir Disoproxil Fumarate (TDF) is now established as a very potent oral antiviral (OAV) agent in the treatment of chronic hepatitis B (CHB). However, as treatment with this OAV is often indefinite and potentially lifelong, concerns remain about its long-term safety. Bone Mineral Density (BMD) loss has been described in TDF treated HIV patients, but limited data exist for HBV treated patients. Furthermore, BMD loss has also been described in chronic liver disease in addition to being reported with certain patient characteristics.

Aim The aim of this study was to determine the impact of TDF on BMD in an ethnically diverse HBV infected population undergoing long-term treatment with this agent.

Method CHB patients treated with TDF for a minimum of 12 months were recruited to this single centre study. Patients were prospectively offered a dual x-ray absorptiometry (DEXA) scan. Serum bone profile and Vitamin D levels were requested simultaneously. BMD loss was defined by WHO criteria; T-score < −2.5 (osteoporosis) and between −1 and −2.5 (osteopenia). 107 consecutive TDF treated patients were included (78 males), median age 45 (range 26–64). A control group, 27 CHB patients (19 males), median age 32 (range 20–61), with no TDF exposure were also studied. Data on gender, ethnicity, BMI, fibrosis stage, co-morbidities and drug history were recorded in all subjects. Analysis was performed with SPSS V.19.

Results BMD loss was present in 44% of the treatment group (osteopenia 81%, osteoporosis 19%) and in 44% of the control group (osteopenia 83%, osteoporosis 17%) (p=0.21). In the ethnically diverse population studied, there was more marked BMD loss in the non-white population (47%, treated group; 45%, controls) compared with the white population (30%, treated group; 40%, controls). By univariate analysis age, gender, ethnicity, fibrosis stage, BMI, co-morbidities and low Vitamin D level were all significant for reduced BMD (p≤0.05, all variables). On multivariate analysis gender, ethnicity, BMI, fibrosis, co-morbidities and Vitamin D all met statistical significance for a reduction in BMD, but Vitamin D deficiency only was significant for the presence of osteoporosis (p=0.0001).

Conclusion Our results demonstrate the prevalence of reduced BMD in CHB patients of diverse ethnicity and identify Vitamin D deficiency and not TDF as the likely cause. This cross-sectional study does not exclude the potential for BMD loss with TDF and further longitudinal studies are required to determine its effect on BMD over time. Vitamin D deficiency should be appropriately treated to avoid any potential for BMD loss associated with TDF when considering treatment with this OAV agent.

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