Abstract
Objectives: It is unclear if anti-hepatitis B virus (HBV) treatment can eliminate incident hepatic decompensation. Here we report the incidence and predictors of hepatic decompensation among cirrhotic patients receiving antiviral therapy for chronic hepatitis B. Methods: This is a post hoc analysis of two prospective HBV cohorts from Hong Kong and South Korea. Patients with liver stiffness measurement (LSM) ≥10 kPa and compensated liver disease at baseline were included. The primary endpoint was incident hepatic decompensation (jaundice or cirrhotic complications) with competing risk analysis. Results: 818 patients (mean age, 54.9 years; 519 male [63.4%]) were included in the final analysis. During a mean follow-up of 58.1 months, 32 (3.9%) patients developed hepatic decompensation, among whom 34% were secondary to HCC. Three (0.4%) patients experienced variceal bleeding alone, 27 (3.3%) had non-bleeding decompensation and 13 (1.6%) had more than 2 decompensating events Baseline LSM, diabetes, alanine aminotransferase, platelet, total bilirubin, albumin, prothrombin time, and eGFR were independent predictors of hepatic decompensation. 30/506 (5.9%) patients fulfilling the Baveno VI criteria (LSM ≥20 kPa and/or platelet count <150ⅹ109/L) and 2/312 (0.6%) patients not fulfilling the criteria developed hepatic decompensation (P < .001). Conclusions: Hepatic decompensation is uncommon but not eliminated in patients receiving antiviral therapy for HBV-related cirrhosis, and only a third of decompensating events are secondary to HCC. The Baveno VI criteria, which was originally designed to detect varices needing treatment, can be effectively applied in this population to identify patients at risk of decompensation.
| Original language | English |
|---|---|
| Pages (from-to) | 1950-1958.e7 |
| Journal | Clinical Gastroenterology and Hepatology |
| Volume | 19 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 2021 Sept |
Bibliographical note
Funding Information:Funding This research was supported partly by a grant for the Chronic Infectious Disease Cohort Study (Korea HBV Cohort Study, 4800-4859-304-260: 2016-ER5102-00) from the Korea Center for Disease Control and Prevention. Conflicts of Interest These authors disclose the following: Terry Cheuk-Fung Yip has served as a speaker for Gilead Sciences. Grace Lai-Hung Wong has served as an advisory committee member for Gilead Sciences; and as a speaker for Abbott, Abbvie, Bristol-Myers Squibb, Echosens, Furui, Gilead Sciences, Janssen, and Roche. Henry Lik-Yuen Chan has served as an advisory committee member for AbbVie, Aligos, Aptorum, Altimmune, Arbutus, ContraVir, Intellia, Janssen, Gilead, GRAIL, Medimmune, Roche, Vaccitech, VenatoRx, and Vir Biotechnology; and as a speaker for AbbVie, Gilead, and Roche. Sang Hoon Ahn has served as an advisor and lecturer for Bristol-Myers Squibb, Gilead Sciences, Roche, MSD, AbbVie, and Green Cross; and received unrestricted grant support from Bristol-Myers Squibb, Gilead Sciences, and Roche for the investigator-initiated trials. Vincent Wai-Sun Wong has served as an advisory committee member for 3V-BIO, AbbVie, Allergan, Boehringer Ingelheim, Gilead Sciences, Janssen, Novartis, Novo Nordisk, Perspectum Diagnostics, and Pfizer; and as a speaker for Bristol-Myers Squibb, Echosens, Gilead Sciences, and Merck. The remaining authors declare no conflicts.
Funding Information:
Funding This research was supported partly by a grant for the Chronic Infectious Disease Cohort Study (Korea HBV Cohort Study, 4800-4859-304-260: 2016-ER5102-00) from the Korea Center for Disease Control and Prevention.
Publisher Copyright:
© 2021 AGA Institute
All Science Journal Classification (ASJC) codes
- Hepatology
- Gastroenterology
