Chinese Hepatolgy ›› 2024, Vol. 29 ›› Issue (7): 834-839.

• Viral Hepatitis • Previous Articles     Next Articles

Research on risk factors for hepatitis B virus (HBV) reactivation in HBeAg-positive pregnant chronic hepatitis B carriers after treatment cessation

LIU Ming, GUO Yan, CHEN Wen-ting, KUANG Xue-mei, LI Shi-lian, JIE Li, XIA Jie, MAO Qing, ZHU Yan   

  1. Department of Infectious Diseases, Southwest Hospital, Army Medical University, Chongqing 400038, China
  • Received:2024-03-30 Online:2024-07-31 Published:2024-08-27
  • Contact: ZHU Yan,Email:cqueenzy@126.com

Abstract: Objective To observe the dynamic changes of HBV RNA, HBV DNA, qHBsAg, qHBeAg and biochemical parameters from initiated antiviral therapy to 96 weeks postpartum in HBeAg-positive pregnant chronic hepatitis B carriers, and to analyze the risk factors for hepatitis flares within 96 weeks after treatment cessation. Methods Pregnant HBeAg-positive patients receiving antiviral prophylaxis and ceasing treatment postpartum were included. HBV RNA, HBV DNA, qHBsAg, qHBeAg, and biochemical parameters were measured at antiviral therapy baseline, at 36 weeks of gestation, at treatment withdrawal postpartum, and/or at 24 weeks postpartum. Virological and biochemical parameters were regularly examined until 96 weeks postpartum. Results 146 patients with a median treatment duration of 16.4 weeks were enrolled. HBV DNA levels and qHBeAg gradually decreased during antiviral therapy, while HBV RNA gradually increased. qHBsAg levels decreased at 36 weeks of gestation compared to baseline, but increased at treatment withdrawal postpartum. All these indicators rebounded and approached or exceeded baseline levels at 24 weeks postpartum. HBeAg seroconversion at 96 weeks postpartum occurred in 5 patients while none experienced HBsAg clearance. The proportion of hepatitis flares was highest at treatment withdrawal postpartum and 24 weeks postpartum (30.1% vs. 30.8%) but only 14 patients (9.59%) required antiviral intervention due to hepatitis flares. According to whether antiviral treatment was restarted, patients were divided into recurrence group (n=14) and non-recurrence group (n=132). Ten patients in the relapse group experienced hepatitis flares after 6 months of treatment cessation, with a median relapse time of 13.5 months. The difference in the type of antiviral therapy drugs and the magnitude of HBeAg decline from baseline to 36 weeks of gestation between the two groups is statistically significant. Conclusion HBeAg-positive pregnant chronic hepatitis B carriers have a certain proportion of hepatitis flares during receiving antiviral prophylaxis and ceasing treatment. The peak occurs at treatment withdrawal postpartum and at 24 weeks postpartum. However, only a small number of patients require further antiviral intervention. The vast majority (71.4%) of postpartum hepatitis flares occured more than 6 months, so it is recommended to be strengthened long-term regular follow-up after treatment discontinuation. The decline levels of HBeAg from the antiviral baseline to the 36 weeks of gestation are independent risk factors for predicting hepatitis flares after treatment cessation.

Key words: Chronic hepatitis B, Pregnant women who are chronic HBV carriers, Mother-to-child, transmission, HBV RNA, Hepatitis flares