Body-mass index is associated with fibrosis regression during long-term nucleoside analogue therapy in chronic hepatitis B

Abstract

Background: Factors influencing changes in liver stiffness measurements during long‐term nucleoside analogue therapy for chronic hepatitis B (CHB) have not been thoroughly investigated.

Aim: To identify determinants of on‐treatment fibrosis regression in CHB.

Methods: We performed follow‐up liver stiffness and controlled attenuation parameter measurements on nucleoside analogue‐treated CHB patients with severe liver fibrosis, according to EASL‐ALEH criteria, diagnosed by transient elastography in 2006–2008. Anthropometric measurements and different metabolic parameters were recorded.

Results: Among 257 patients with severe liver fibrosis by initial transient elastography, 123 (47.9%) were recruited for reassessment. Median treatment duration was 87.5 (interquartile range 75.3–102.2) months; 97.5% had undetectable HBV DNA. There was a significant reduction in median liver stiffness from 14.6 to 8.3 kPa (P < 0.001). A total of 29.3% had fibrosis regression, with lower rates of 17.9%, 14.9% and 11.5% noted in patients with body‐mass index (BMI) ≥25 kg/m2, metabolic syndrome and diabetes, respectively. Absence of BMI ≥25 kg/m2, diabetes and metabolic syndrome, when compared with presence of any one of these three factors, was associated with increased fibrosis regression (43.1% vs. 16.9%, P = 0.001). Multivariate analysis found a lower BMI to be the only factor independently associated with fibrosis regression (P = 0.034, odds ratio 0.68, 95% CI 0.48–0.97). No association was noted between controlled attenuation parameter measurements and fibrosis regression (P > 0.05).

Conclusion: An increased BMI hindered fibrosis regression in patients with chronic hepatitis B during nucleoside analogue treatment, suggesting that control of metabolic risk factors, in addition to virologic suppression via antiviral therapy, might be needed to halt the fibrogenic process in chronic hepatitis B.