Liver and Bile

Hepatology. 2024;79(3):690–703

Jeng WJ, Chien RN, Chen YC, Lin CL, Wu CY, Liu YC, Peng CW, Su CW, Hsu CE, Liaw YF

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

Background and aims: Long-term nucleos(t)ide analogue (NA) treatment can reduce hepatocellular carcinoma (HCC) in patients with hepatitis B virus-related liver cirrhosis (HBV-LC). Earlier small cohort studies showed a comparable 5-year incidence of HCC in hepatitis B e antigen (HBeAg)-negative patients with HBV-LC who stopped and those continued NA 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) NA therapy were recruited. HCC, hepatitis B surface antigen (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 NA, 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%/year and 10-year 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 log10 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 hazard ratio [aHR] = 11.79) but protective against HCC (aHR = 0.593), liver-related mortality/transplantation (aHR = 0.312), and overall mortality (aHR = 0.382).

Conclusions: Finite nucleos(t)ide analogue therapy in hepatitis B e antigen-negative hepatitis B virus-related liver cirrhosis may reduce incidence of hepatocellular carcinoma, increase hepatitis B surface antigen (HBsAg) loss, and improve survival. Greater HBsAg decline/loss may reflect enhanced immunity and contribute to the reduction of hepatic carcinogenesis.

Prof. Dr. Y.-F. Liaw, Liver Research Unit, Chang Gung Memorial Hospital, Linkou Branch, Taipei, Taiwan, E-Mail: liveryfl@gmail.com

DOI: 10.1097/hep.0000000000000575

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