Background/Aims: HBV-related chronic liver disease patients often present w
ith hepatic decompensation and are not eligible for interferon therapy. Whe
ther long-term lamimdine is effective in these patients was prospectively e
valuated,
Methods: Eighteen patients with HBV-related decompensated cirrhosis, all wi
th quantitative DNA +ve and 10 HBeAg +ve, were given lamivudine 150 mg/d,
Results: Each patient received at least 9 months (mean 17.9) of lamivudine.
Three HBeAg+ve patients (30%) seroconverted to anti-HBe and one lost HBsAg
during the follow-up, An improvement from baseline in the aspartate aminot
ransferase (130 vs 72 IU/l, p<0.04); alanine aminotransferase (111 vs 58 IU
/l, p<0.01) and Child-Pugh score (8.3 vs. 6.7, p<0.013) was seen. Lamivudin
e had no significant side-effects. I-EBV DNA became undetectable in all pat
ients by 8 weeks of therapy In three (17%) patients, HBV DNA again became p
ositive at 9, 9 and 27 months. YMDD mutant was, however, detested in only o
ne (6%), A significant reduction was noted in the morbidity and hospitaliza
tions for complications of liver disease before and after starting lamivudi
ne (1.5+/-0.7 vs, 0.6+/-0.7, p<0.002).
Conclusions: In decompensated HBV-related cirrhosis, lamivudine: i) is effe
ctive in suppressing HBV DNA and seroconversion to anti-HBe (30%), ii) can
achieve significant improvement in clinical and biochemical status of liver
functions.