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Persistent Low Level of Hepatitis B Virus Promotes Fibrosis Progression During Therapy.

Authors
  • Sun, Yameng1
  • Wu, Xiaoning1
  • Zhou, Jialing1
  • Meng, Tongtong1
  • Wang, Bingqiong1
  • Chen, Shuyan1
  • Liu, Hui2
  • Wang, Tailing3
  • Zhao, Xinyan1
  • Wu, Shanshan1
  • Kong, Yuanyuan1
  • Ou, Xiaojuan1
  • Wee, Aileen4
  • Theise, Neil D5
  • Qiu, Chao6
  • Zhang, Wenhong6
  • Lu, Fengmin7
  • Jia, Jidong8
  • You, Hong9
  • 1 Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center of Digestive Diseases, Beijing, China. , (China)
  • 2 Department of Pathology, Beijing You-an Hospital, Capital Medical University, Beijing, China. , (China)
  • 3 Department of Pathology, China-Japan Friendship Hospital, Beijing, China. , (China)
  • 4 Department of Pathology, National University Hospital, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. , (Singapore)
  • 5 Department of Pathology, New York University School of Medicine, New York, New York.
  • 6 Department of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China. , (China)
  • 7 State Key Laboratory of Natural and Biomimetic Drugs, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China. , (China)
  • 8 Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center of Digestive Diseases, Beijing, China. Electronic address: [email protected] , (China)
  • 9 Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center of Digestive Diseases, Beijing, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
Publication Date
Oct 01, 2020
Volume
18
Issue
11
Identifiers
DOI: 10.1016/j.cgh.2020.03.001
PMID: 32147592
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Progression of liver fibrosis still occurs in some patients with chronic hepatitis B virus (HBV) infection despite antiviral therapy. We aimed to identify risk factors for fibrosis progression in patients who received antiviral therapy. We conducted a longitudinal study of patients with chronic HBV infection and liver biopsies collected before and after 78 weeks of anti-HBV therapy. Fibrosis progression was defined as Ishak stage increase ≥ 1 or as predominantly progressive classified by P-I-R system (Beijing Classification). Levels of HBV DNA and HBV RNA in blood samples were measured by real-time quantitative PCR. HBV RNA in liver tissue was detected by in situ hybridization. A total of 239 patients with chronic HBV infection with paired liver biopsies were included. Among the 163 patients with significant fibrosis at baseline (Ishak ≥ stage 3), fibrosis progressed in 22 patients (13%), was indeterminate in 24 patients (15%), and regressed in 117 patients (72%). Univariate and multivariate analyses revealed that independent risk factors for fibrosis progression were higher rate of detected HBV DNA at week 78 (odds ratio, 4.84; 95% CI, 1.30-17.98; P = .019) and alcohol intake (odds ratio, 23.84; 95% CI, 2.68-212.50; P = .004). HBV DNA was detected in blood samples from a significantly higher proportion of patients with fibrosis progression (50%) at week 78 than patients with fibrosis regression (19%) or indeterminate fibrosis (26%) (P = .015), despite low viremia (20-200 IU/mL) in all groups. The decrease of serum HBV RNA from baseline in the fibrosis regression group was larger than that in the fibrosis progression group. In a longitudinal study of patients with chronic HBV infection, we associated liver fibrosis progression at week 78 of treatment with higher rates of detected HBV DNA. We propose that a low level of residual HBV may still promote fibrosis progression, and that patients' levels of HBV DNA should be carefully monitored. Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

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