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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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.

Original languageEnglish
Pages (from-to)1514-1521
Number of pages8
JournalScandinavian Journal of Gastroenterology
Volume43
Issue number12
DOIs
Publication statusPublished - 2008 Dec 1

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Lamivudine
Chronic Hepatitis B
Liver
Incidence
Liver Cirrhosis
Alanine Transaminase
Therapeutics
DNA
Secondary Prevention
Serum
Medical Records

Keywords

  • ALAT flare
  • Hepatic decompensation
  • Lamivudine resistance

ASJC Scopus subject areas

  • Gastroenterology

Cite this

@article{9bb4cf6e7d3f48e2a208f1321425a906,
title = "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.",
keywords = "ALAT flare, Hepatic decompensation, Lamivudine resistance",
author = "Joo, {Moon Kyung} and Yeon, {Jong Eun} and Kim, {Ji Hoon} and Jung, {Young Kul} and Lee, {Sun Jae} and Kim, {Jeong Han} and Yim, {Hyung Joon} and Byun, {Kwan Soo} and Park, {Jong Jae} and Kim, {Jae Seon} and Young-Tae Bak",
year = "2008",
month = "12",
day = "1",
doi = "10.1080/00365520802273033",
language = "English",
volume = "43",
pages = "1514--1521",
journal = "Scandinavian Journal of Gastroenterology",
issn = "0036-5521",
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TY - JOUR

T1 - Chronic cirrhotic hepatitis B patients with a high incidence of hepatic decompensation after viral breakthrough with lamivudine-resistant mutants and during rescue treatment

AU - Joo, Moon Kyung

AU - Yeon, Jong Eun

AU - Kim, Ji Hoon

AU - Jung, Young Kul

AU - Lee, Sun Jae

AU - Kim, Jeong Han

AU - Yim, Hyung Joon

AU - Byun, Kwan Soo

AU - Park, Jong Jae

AU - Kim, Jae Seon

AU - Bak, Young-Tae

PY - 2008/12/1

Y1 - 2008/12/1

N2 - 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.

AB - 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.

KW - ALAT flare

KW - Hepatic decompensation

KW - Lamivudine resistance

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U2 - 10.1080/00365520802273033

DO - 10.1080/00365520802273033

M3 - Article

VL - 43

SP - 1514

EP - 1521

JO - Scandinavian Journal of Gastroenterology

JF - Scandinavian Journal of Gastroenterology

SN - 0036-5521

IS - 12

ER -