BACKGROUND/AIMS: Lamivudine is highly effective in suppressing hepatitis B virus replication and hepatitis B induced necroinflammatory activity. The objective of this study was to evaluate the virological and biochemical responses to lamivudine by patients with HBV associated chronic liver disease. In particular we stressed the importance of lamivudine therapy by patients with decompensated liver cirrhosis. METHODS: We conducted a one-year trial of lamivudine in 80 patients with HBV associated chronic liver disease (chronic hepatitis 44, cirrhosis 36). We classified these patients according to the severity of hepatic dysfunction as chronic B hepatitis (Group A) or liver cirrhosis (Group B). These patients were treated for 12 months with 100 mg daily doses of lamivudine. RESULTS: The seroconversion rate of HBeAg was 23.5% in group A patients and 26.7% in group B patients. The negative conversion of HBV-DNA was sustained for one year in 79.5% of patients in group A and 86.1% in group B. The normalization rates of serum ALT were 90.9% in group A and 88.9% in group B patients. No serious side effect after discontinuance of the treatment was found. There were 12 ALT breakthrough cases and all of them showed mutation of YMDD motif. However, they did not deteriorate clinically in spite of ALT elevation and HBV-DNA reappearance. The Child-Pugh scores improved even in patients with decompensated liver cirrhosis. CONCLUSION: One-year lamivudine treatment resulted in excellent virological and biochemical improvements and was well tolerated in the patients with HBV associated chronic liver disease, even in decompensated cirrhosis. We conclude that lamivudine is relatively safe in chronic hepatitis B and liver cirrhosis treatment.
Fibrosis ; Hepatitis B ; Hepatitis B e Antigens ; Hepatitis B virus ; Hepatitis B, Chronic ; Hepatitis* ; Humans ; Lamivudine* ; Liver Cirrhosis* ; Liver Diseases ; Liver*

BACKGROUND: Helicobacter pylori colonizes the gastric surface epithelium and the mucus gel layer. It has been known that H. pylori infection decreased the gastric mucin expression. The aim of this study was to determine the effect of H. pylori eradication on mucin expression (MUC5AC, MUC6 and MUC1) in the gastric epithelium. METHODS: This study included 20 patients positive for H. pylori whom successful eradication was performed between March 1998 and December 1999. H. pylori status was determined by histology, rapid urase test and urea breath test. Gastric antral biopsy specimens were examined by immunohistochemistry for mucin (MUC5AC, MUC6 and MUC1) expression. The distribution of epithelial cells expressing MUC5AC was calculated at two sites (surface mucous cells, pyloric glands). Two scores system (weak-strong) was used to assess staining intensity. RESULTS: There was a gradient of MUC5AC expression, higher to lower from the surface to the glands. Increased MUC5AC expression in the surface mucous cell (p=0.013) and in the glands (p=0.008) was found after H. pylori eradication. MUC6 and MUC1 distribution was not changed after H. pylori eradication. CONCLUSION: MUC5AC expression was increased after H. pylori eradication. These results suggest that MUC5AC may relate in the pathogenesis of H. pylori.
Biopsy ; Breath Tests ; Colon ; Epithelial Cells ; Epithelium ; Gastric Mucins ; Helicobacter pylori* ; Helicobacter* ; Humans ; Immunohistochemistry ; Mucins* ; Mucus ; Urea