Hepatocellular carcinoma reduced, HBsAg loss increased, and survival improved after finite therapy in hepatitis B patients with cirrhosis

Wen Juei Jeng, Rong Nan Chien, Yi Cheng Chen, Chih Lang Lin, Chia Ying Wu, Yen Chun Liu, Chien Wei Peng, Chung Wei Su, Cheng Er Hsu, Yun Fan Liaw*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

9 Scopus citations

Abstract

BACKGROUND AND AIMS: Long-term nucleos(t)ide analog (Nuc) treatment can reduce HCC in patients with HBV-related liver cirrhosis (HBV-LC). Earlier small cohort studies showed a comparable 5-year incidence of HCC in HBeAg-negative patients with HBV-LC who stopped and those continued Nuc therapy. This study aimed to validate these findings using a large cohort with 10-year follow-up.

APPROACH AND RESULTS: From 2 centers, 494 HBeAg-negative patients with HBV-LC who stopped (finite group) and 593 who continued (continuous group) Nuc therapy were recruited. HCC, HBsAg loss, liver-related mortality/transplantation, and overall survival rates were compared between 2 groups with 1:1 propensity score matching of sex, treatment history, types of Nuc, age, transaminases, platelet count, and HBsAg levels at end of therapy in finite group or 3-year on-therapy in continuous groups. During a median follow-up of 6.2 (3.4-8.9) years, the annual and 10-year HCC incidence were lower in finite group (1.6 vs. 3.3%/y and 10-y 15.7% vs. 26.8%, respectively; log-rank test, p <0.0001). The finite group showed greater HBsAg decline/year (-0.116 vs. -0.095 log 10 IU/mL, p =0.0026) and 7.6 times higher 10-year incidence of HBsAg loss (22.7% vs. 3%, p <0.0001). Multivariate Cox regression showed finite therapy an independent factor for HBsAg loss (adjusted HR: 11.79) but protective against HCC (adjusted HR: 0.593), liver-related mortality/transplantation (adjusted HR: 0.312), and overall mortality (adjusted HR: 0.382).

CONCLUSIONS: Finite Nuc therapy in HBeAg-negative HBV-LC may reduce HCC incidence, increase HBsAg loss, and improve survival. Greater HBsAg decline/loss may reflect enhanced immunity and contribute to the reduction of hepatic carcinogenesis.

Original languageEnglish
Pages (from-to)690-703
Number of pages14
JournalHepatology
Volume79
Issue number3
DOIs
StatePublished - 01 03 2024

Bibliographical note

Copyright © 2023 American Association for the Study of Liver Diseases.

Keywords

  • Humans
  • Carcinoma, Hepatocellular/drug therapy
  • Hepatitis B Surface Antigens
  • Hepatitis B virus/genetics
  • Hepatitis B e Antigens
  • Hepatitis B, Chronic/complications
  • Liver Neoplasms/drug therapy
  • Antiviral Agents/therapeutic use
  • Liver Cirrhosis/complications
  • DNA, Viral

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