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AASLD 2011 abstract 1376. Bone Mineral Density Loss in Tenofovir treated
Chronic Hepatitis B Virus (HBV) patients is a consequence of Vitamin D
deficiency and not Tenofovir therapy
U. Gill1; S. Al-shamma1; K. B. Burke1; V. A. Ross2; R. Marley1; P. Kooner1;
G. R. Foster1; P. T. Kennedy1
1. Department of Hepatology, Barts and The London NHS Trust, London, United
Kingdom.
2. Pharmacy, Barts and The London NHS Trust, London, United Kingdom.
BACKGROUND: Tenofovir Disoproxil Fumarate (TDF) is now an established
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 patients. Furthermore, BMD loss has also
been described in chronic liver disease in addition to being reported with
certain patient characteristics. The aim of this study was to determine the
impact of TDF on BMD in an ethnically diverse CHB population undergoing
treatment with this agent. PATIENTS & METHODS: 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 & -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 version 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 low 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).
CONCLUSIONS: 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 agent.
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