Chronic cirrhotic hepatitis B patients with a high incidence of hepatic decompensation after viral breakthrough with lamivudine-resistant mutants and during rescue treatment

Abstract

Objective. To compare the rate of biochemical and hepatic decompensation after viral breakthrough (V-BT) caused by lamivudine (LMV)-resistant HBV mutants and during rescue treatment for patients with liver cirrhosis (LC) and chronic hepatitis B (CHB).

Material and methods. We reviewed the medical records of 205 CHB patients who developed V-BT with LMV-resistant HBV mutants (134 in the CHB group, 71 in the LC group).

Results. Sixty-five of the 205 patients had an alanine aminotransferase (ALAT) flare-up (32%) and 21 (10%) had hepatic decompensation. The ALAT flare-up among the CHB and LC groups occurred in 43 (32%) and 22 patients (31%), respectively, and there was no significant difference between the two groups. Hepatic decompensation occurred in 5 (4%) and 16 (23%) patients with CHB and LC, respectively, and these differences were significant (p=0.001). A total of 187 patients were treated by rescue therapy (CHB 121, LC 66) and 13 cases with hepatic decompensation occurred only in LC patients during rescue therapy. Among them, 11 patients had serum ALAT levels two times higher than the upper normal limit (UNL) and the HBV-DNA was more than 107 copies/ml at the baseline of rescue therapy. In contrast, the cumulative ALAT normalization and viral response rates were reached significantly earlier in patients with a serum HBV-DNA of 107 copies/ml compared with those with an HBV-DNA 107 copies/ml (p=0.0221 and 0.0002, respectively).

Conclusion. Earlier rescue therapy for cirrhotic patients with genotypic resistance due to LMV-resistant mutants may improve patient outcome.