Severe exacerbation of chronic hepatitis B after emergence of lamivudine resistance in a cirrhotic patient: immediate switch to adefovir dipivoxil appears to be indicated.


Journal Article

INTRODUCTION: Lamivudine is a treatment option for the therapy of chronic hepatitis B with an excellent safety profile. Unfortunately, viral resistance to lamivudine is common in the course of therapy. The lamivudine resistant mutants are usually less pathogenic than the wild type, but development of viral resistance can also lead to acute exacerbation of the underlying hepatitis. The recently FDA approved nucleoside analogue adefovir dipivoxil has potent antiviral activity against lamivudine-resistant mutants and can prevent viral replication effectively. CASE REPORT: A 31-year-old man with pre-existing compensated liver cirrhosis developed resistance to lamivudine therapy leading to subacute liver failure. After referral adefovir dipivoxil 10 mg daily was initiated within an early access protocol. Since initiating therapy with adefovir dipivoxil progression of the subacute liver failure was delayed accompanied by a rapid decrease of ALT and decline of HBV viral load. Even so, the clinical course was not reverted but showed slower deterioration. This enabled the patient to undergo living-related liver transplantation. Adefovir dipivoxil was well tolerated in the acute phase of the disease and did not cause nephrotoxicity or favour the development of hepatorenal syndrome. CONCLUSION: Adefovir dipivoxil resulted in a delay of hepatic decompensation and enabled liver transplantation as final treatment option for this patient. Earlier initiation might even have prevented the need of liver transplantation. Thus, in patients with pre-existing liver cirrhosis an early switch to adefovir dipivoxil appears indicated after emergence of lamivudine resistance.

Full Text

Cited Authors

  • Wiegand, J; Tischendorf, JJ; Nashan, B; Klempnauer, J; Flemming, P; Niemann, P; Rohde, P; Manns, MP; Trautwein, C; Tillmann, HL

Published Date

  • January 2004

Published In

Volume / Issue

  • 42 / 1

Start / End Page

  • 15 - 18

PubMed ID

  • 14997399

Pubmed Central ID

  • 14997399

International Standard Serial Number (ISSN)

  • 0044-2771

Digital Object Identifier (DOI)

  • 10.1055/s-2004-812683


  • eng

Conference Location

  • Germany