Diverse effects of hepatic steatosis on fibrosis progression and functional cure in virologically quiescent chronic hepatitis B.

Autor: Mak LY; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong., Hui RW; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong., Fung J; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong., Liu F; Department of Gastroenterology and Hepatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China., Wong DK; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong., Cheung KS; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; Department of Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China., Yuen MF; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong. Electronic address: mfyuen@hkucc.hku.hk., Seto WK; Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong; Department of Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China. Electronic address: wkseto@hku.hk.
Jazyk: angličtina
Zdroj: Journal of hepatology [J Hepatol] 2020 Oct; Vol. 73 (4), pp. 800-806. Date of Electronic Publication: 2020 Jun 03.
DOI: 10.1016/j.jhep.2020.05.040
Abstrakt: Background & Aims: Concomitant non-alcoholic fatty liver disease is common in patients with chronic hepatitis B (CHB) infection, although its impact on liver-related outcomes remains controversial. We aimed to study the effect of hepatic steatosis on the risk of fibrosis progression and the likelihood of HBsAg seroclearance.
Methods: Treatment-naïve patients with CHB, normal alanine aminotransferase and low viraemia (serum HBV DNA <2,000 IU/ml) were prospectively recruited for baseline and 3-year transient elastography assessment. Fibrosis staging was defined according to the EASL-ALEH guidelines, with fibrosis progression defined as ≥1 stage increment of fibrosis. Hepatic steatosis and severe hepatic steatosis were defined as controlled attenuation parameter (CAP) ≥248 dB/m and ≥280 dB/m, respectively.
Results: A total of 330 patients (median age 50.5 years, 41.2% male, median HBV DNA 189 IU/ml) were recruited. Twenty-two patients (6.7%) achieved HBsAg seroclearance during follow-up, and the presence of hepatic steatosis was associated with a significantly higher chance of HBsAg seroclearance (hazard ratio 3.246; 95% CI 1.278-8.243; p = 0.013). At baseline, 48.8% and 28.8% of patients had steatosis and severe steatosis, respectively, while 4.2% had F3/F4 fibrosis at baseline, increasing to 8.7% at 3 years. The rate of liver fibrosis progression in patients with persistent severe steatosis was higher than in those without steatosis (41.3% vs. 23%; p = 0.05). Persistent severe hepatic steatosis was independently associated with fibrosis progression (odds ratio 2.379; 95% CI 1.231-4.597; p = 0.01).
Conclusions: CAP measurements have predictive value in patients with virologically quiescent CHB. The presence of hepatic steatosis was associated with a higher risk of fibrosis progression but, paradoxically, a 3-fold increase in HBsAg seroclearance rate.
Lay Summary: Co-existing fatty liver disease in patients with chronic viral hepatitis B infection leads to worsening liver fibrosis, but also increases the chance of cure from hepatitis B virus. Routine bedside assessment of liver fat content is important for risk assessment in treatment-naïve patients with chronic hepatitis B.
Competing Interests: Conflict of interest J Fung has been a consultant for Gilead Sciences. MF Yuen is an Associate Editor of Journal of Hepatology, and received speaker fees and received research funding from Bristol-Myers Squibb and Gilead Sciences. WK Seto is an advisory board member, received speaker fees and research funding from Gilead Sciences. All other authors: none to declare. Please refer to the accompanying ICMJE disclosure forms for further details.
(Copyright © 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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