Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B

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.