The prognosis of decompensated cirrhosis resulting from chronic hepatitis B
is poor, and the benefits of treatment with interferon are outweighed by s
erious side effects and by the risk of fatal exacerbation of disease activi
ty. Lamivudine rapidly reduces hepatitis B virus (HBV)-DNA in serum to unde
tectable levels. We have treated 35 patients with chronic hepatitis B and d
ecompensated cirrhosis with lamivudine 100 mg or 150 mg orally once daily.
Pretreatment, all mere positive for HBV-DNA in serum, Ten had Child-Pugh cl
ass 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 (m
ean = 19 months). In a majority of these 23 cases, there was a slow but mar
ked improvement in liver function, which was most apparent after 9 months o
f treatment, with a decrease in serum bilirubin from 67 +/- 13 to 30 +/- 4
mu mol/L (P <.05, baseline vs. 9 months), an increase in serum albumin from
27 +/- 1 to 34 +/- 1 g/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 d
id not deteriorate, We conclude that inhibition of viral replication with l
amivudine results in a significant improvement of liver function in patient
s with decompensated HBV cirrhosis, but the long-term benefits remain uncer
tain.