Core promoter/pre-core mutations are associated with lamivudine-induced HBeAg loss in chronic hepatitis B with

Yasuhiro Asahina1, Namiki Izumi, Masakatsu Uchihara

  • 1Division of Gastroenterology and Hepatology, Musashino Red Cross Hospital, 1-26-1 Kyonan-cho, Musashino-shi, Tokyo 180-8610, Japan.

Journal of Hepatology
|December 4, 2003
PubMed

Insights

Lamivudine treatment significantly increased hepatitis B e antigen (HBeAg) loss in genotype C patients, especially those with specific mutations. However, the drug

Area of Science:

  • Hepatology
  • Virology
  • Genetics

Background:

  • Chronic hepatitis B (CHB) is a significant global health concern.
  • Hepatitis B e antigen (HBeAg) seroconversion is a key treatment goal.
  • Lamivudine is a nucleoside analog used in CHB treatment.

Purpose of the Study:

  • To identify factors influencing lamivudine efficacy in CHB patients.
  • To investigate the role of basic core promoter (BCP) and pre-core (PreC) mutations.

Main Methods:

  • A study involving 60 HBeAg-positive CHB patients with genotype C.
  • Thirty patients received lamivudine treatment; 30 served as controls.
  • Evaluation of BCP and PreC mutations, fibrosis, and HBeAg loss.

Main Results:

  • Lamivudine therapy significantly increased HBeAg loss rates compared to controls.
  • Patients with BCP-mutant/PreC-mutant (MM) and BCP-mutant/PreC-wild (MW) patterns showed higher HBeAg loss.
  • The BCP-wild/PreC-wild (WW) pattern was associated with lower lamivudine efficacy.
  • Severe fibrosis was more common in MW and MM patterns.
  • Histological activity, HBV-DNA levels, BCP/PreC mutations, and fibrosis were factors for HBeAg loss.

Conclusions:

  • Lamivudine efficacy in genotype C CHB varies based on BCP/PreC mutation status.
  • Earlier HBeAg loss is expected in patients with MM and MW patterns.
  • Lamivudine efficacy is limited in patients with the WW pattern.
Abstract

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