Hepatitis B Surface Antigen Levels Can Be Used to Rule Out Cirrhosis in Hepatitis B e Antigen-Positive Chronic Hepatitis B: Results From the SONIC-B Study.


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
01 06 2022
Historique:
received: 23 10 2019
accepted: 18 04 2020
pubmed: 23 4 2020
medline: 19 11 2022
entrez: 23 4 2020
Statut: ppublish

Résumé

Serum hepatitis B surface antigen (HBsAg) levels correlate with the duration of chronic hepatitis B virus (HBV) infection and may predict the extent of hepatic fibrosis. We analyzed data from the SONIC-B database, which contains data from 8 global randomized trials and 2 large hepatology centers. Relationship between HBsAg levels and presence of significant fibrosis (Ishak 3-4) or cirrhosis (Ishak 5-6) were explored, and clinically relevant cutoffs were identified to rule out cirrhosis. The dataset included 2779 patients: 1866 hepatitis B e antigen (HBeAg)-positive; 322 with cirrhosis. Among HBeAg-positive patients, lower HBsAg levels were associated with higher rates of significant fibrosis (odds ratio [OR], 0.419; P < .001) and cirrhosis (OR, 0.435; P < .001). No relationship was observed among HBeAg-negative patients. Among HBeAg-positive patients, genotype-specific HBsAg cutoffs had excellent negative predictive values (>97%) and low misclassification rates (≤7.1%) and may therefore have utility in ruling out cirrhosis. Diagnostic performance of the HBsAg cutoffs was comparable among patients in whom cirrhosis could not be ruled out with fibrosis 4 (FIB-4). Hepatitis B virus genotype-specific HBsAg cutoffs may have utility in ruling out presence of cirrhosis in HBeAg-positive patients with genotypes B, C, and D and can be an adjunct to FIB-4 to reduce the need for further testing.

Sections du résumé

BACKGROUND
Serum hepatitis B surface antigen (HBsAg) levels correlate with the duration of chronic hepatitis B virus (HBV) infection and may predict the extent of hepatic fibrosis.
METHODS
We analyzed data from the SONIC-B database, which contains data from 8 global randomized trials and 2 large hepatology centers. Relationship between HBsAg levels and presence of significant fibrosis (Ishak 3-4) or cirrhosis (Ishak 5-6) were explored, and clinically relevant cutoffs were identified to rule out cirrhosis.
RESULTS
The dataset included 2779 patients: 1866 hepatitis B e antigen (HBeAg)-positive; 322 with cirrhosis. Among HBeAg-positive patients, lower HBsAg levels were associated with higher rates of significant fibrosis (odds ratio [OR], 0.419; P < .001) and cirrhosis (OR, 0.435; P < .001). No relationship was observed among HBeAg-negative patients. Among HBeAg-positive patients, genotype-specific HBsAg cutoffs had excellent negative predictive values (>97%) and low misclassification rates (≤7.1%) and may therefore have utility in ruling out cirrhosis. Diagnostic performance of the HBsAg cutoffs was comparable among patients in whom cirrhosis could not be ruled out with fibrosis 4 (FIB-4).
CONCLUSIONS
Hepatitis B virus genotype-specific HBsAg cutoffs may have utility in ruling out presence of cirrhosis in HBeAg-positive patients with genotypes B, C, and D and can be an adjunct to FIB-4 to reduce the need for further testing.

Identifiants

pubmed: 32318704
pii: 5823493
doi: 10.1093/infdis/jiaa192
pmc: PMC9159342
doi:

Substances chimiques

Hepatitis B e Antigens 0
Hepatitis B Surface Antigens 0
DNA, Viral 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1967-1973

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America.

Auteurs

Milan J Sonneveld (MJ)

Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.

Bettina E Hansen (BE)

Toronto Centre for Liver Disease, University Health Network, Toronto, Canada.
IHPME, University of Toronto, Toronto, Canada.

Willem P Brouwer (WP)

Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.

Henry L-Y Chan (HL)

Department of Medicine and Therapeutics and Institute of Digestive Disease, the Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.

Teerha Piratvisuth (T)

NKC Institute of Gastroenterology and Hepatology, Songklanagarind Hospital, Prince of Songkla University, Hat Yai, Thailand.

Ji-Dong Jia (JD)

Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.

Stefan Zeuzem (S)

Medical Clinic 1, Johann Wolfgang Goethe University Medical Center, Frankfurt, Germany.

Rong-Nan Chien (RN)

Liver Research Unit, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan.

Robert J de Knegt (RJ)

Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.

Cynthia Wat (C)

Roche Product Ltd., Welwyn Garden City, United Kingdom.

Vedran Pavlovic (V)

Roche Product Ltd., Welwyn Garden City, United Kingdom.

Anuj Gaggar (A)

Gilead Sciences, Foster City, California, USA.

Qing Xie (Q)

Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Maria Buti (M)

Hospital Universitari Vall d'Hebron and CIBEHED del Instituto Carlos III, Barcelona, Spain.

Robert A de Man (RA)

Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.

Harry L A Janssen (HLA)

Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
Toronto Centre for Liver Disease, University Health Network, Toronto, Canada.

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