Lamivudine treatment for decompensated cirrhosis resulting... : Hepatology (original) (raw)

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Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B

Villeneuve, Jean-Pierre M.D.*,1; Condreay, Lynn D.2; Willems, Bernard1; Pomier-Layrargues, Gilles1; Fenyves, Daphna1; Bilodeau, Marc1; Leduc, Raymond1; Peltekian, Kevork3; Wong, Florence4; Margulies, Mariana4; Heathcote, Jenny E.4

1Division of Hepatology, Centre Hospitalier de l’Université de Montréal, Montréal, Canada

2Glaxo Wellcome Inc, Durham, NC

3Division of Gastroenterology, Queen Elisabeth II Health Sciences Center, Dalhousie University, Halifax, Canada

4Division of Gastroenterology, The Toronto Hospital, University of Toronto, Toronto, Canada

E-mail:[email protected]

*Address reprint requests to: Centre de recherche du, Centre Hospitalier de l’Université de Montréal, Hôpital Saint-Luc, 264, boul. René-Lévesque est, Montréal, Québec, Canada, H2X 1P1. fax: (514) 281-2492.

Received June 23, 1999; Accepted October 14, 1999; previously published online December 30, 2003

Abstract

The prognosis of decompensated cirrhosis resulting from chronic hepatitis B is poor, and the benefits of treatment with interferon are outweighed by serious side effects and by the risk of fatal exacerbation of disease activity. Lamivudine rapidly reduces hepatitis B virus (HBV)-DNA in serum to undetectable levels. We have treated 35 patients with chronic hepatitis B and decompensated cirrhosis with lamivudine 100 mg or 150 mg orally once daily. Pretreatment, all were positive for HBV-DNA in serum. Ten had Child-Pugh class B and 25 had Child-Pugh class C liver disease. Seven patients underwent liver transplantation within 6 months of treatment initiation, 5 patients died within 6 months, and 23 patients were treated for at least 6 months (mean = 19 months). In a majority of these 23 cases, there was a slow but marked improvement in liver function, which was most apparent after 9 months of treatment, with a decrease in serum bilirubin from 67 ± 13 to 30 ± 4 μmol/L (P< .05, baseline vs. 9 months), an increase in serum albumin from 27 ± 1 to 34 ± 1g/L (P< .05), and a decrease in Child-Pugh score from 10.3 ± 0.4 to 7.5 ± 0.5_(P_< .05). Three patients developed resistance to lamivudine because of a mutation in the YMDD motif, but liver function did not deteriorate. We conclude that inhibition of viral replication with lamivudine results in a significant improvement of liver function in patients with decompensated HBV cirrhosis, but the long-term benefits remain uncertain.