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

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Chronic cirrhotic hepatitis B patients with a high incidence of hepatic

decompensation after viral breakthrough with lamivudine-resistant mutants and

during rescue treatment

Authors: Moon Kyung Joo a; Jong Eun Yeon a; Ji Hoon Kim a; Young Kul Jung a;

Sun Jae Lee a; Jeong Han Kim a; Hyung Joon Yim a; Kwan Soo Byun a; Jong-Jae

Park a; Jae Seon Kim a; Young-Tae Bak a

Affiliation: a Department of Internal Medicine, Korea University College of

Medicine, Seoul, Korea

DOI: 10.1080/00365520802273033

Publication Frequency: 12 issues per year

Published in: Scandinavian Journal of Gastroenterology

First Published on: 29 July 2008

Subjects: Gastroenterology; Gastrointestinal & Abdominal Surgery;

Formats available: HTML (English) : PDF (English)

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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.

Keywords: ALAT flare; hepatic decompensation; lamivudine resistance