Reactivation of precore mutant hepatitis B virus leading to fulminant hepatic failure following cytotoxic treatment

Dig Dis Sci. 1992 Aug;37(8):1253-9. doi: 10.1007/BF01296569.


Three hepatitis B virus carriers who were HB(e)Ag negative and having normal liver function developed fulminant hepatitis with evidence of HBV replication following intensive chemotherapy for non-Hodgkin's lymphoma. Each was continuously negative for HB(e)Ag. Analysis of the precore region of HBV isolated from each demonstrated that the HBV of each had a point mutation in the precore region that inhibited the synthesis and the release of hepatitis B(e) antigen. This observation suggests that all HB carriers receiving either immunosuppressive or cytotoxic therapy should be monitored closely even if standard assays suggest that viral replication is not present. Sudden enhanced replication of a HBV mutant as a result of such therapy can be a cause of either very severe hepatitis or occasionally fulminant hepatitis.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Antineoplastic Combined Chemotherapy Protocols / adverse effects*
  • Artificial Organs
  • Base Sequence
  • Carrier State* / microbiology
  • Carrier State* / therapy
  • DNA, Viral / drug effects
  • DNA, Viral / genetics
  • Female
  • Hepatitis B / etiology*
  • Hepatitis B / microbiology
  • Hepatitis B / therapy
  • Hepatitis B e Antigens / blood
  • Hepatitis B e Antigens / drug effects*
  • Hepatitis B e Antigens / genetics
  • Hepatitis B virus / drug effects*
  • Hepatitis B virus / genetics
  • Hepatitis B virus / immunology
  • Humans
  • Lymphoma, Non-Hodgkin / complications
  • Lymphoma, Non-Hodgkin / drug therapy
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Mutation / drug effects*
  • Mutation / genetics
  • Mutation / immunology
  • Virus Activation / drug effects*
  • Virus Activation / genetics
  • Virus Activation / immunology


  • DNA, Viral
  • Hepatitis B e Antigens