The Clinical Meaning of the Emergence of Viral Breakthrough during Lamivudine Treatment in Patients with Hepatitis B Virus Related Chronic Liver Disease.
- Author:
Chan Bog PARK
1
;
Hyun Jeung LIM
;
Byung Cheol YUN
;
Sang Uk LEE
;
Byung Hoon HAN
Author Information
1. Department of Internal Medicine, Kosin University College of Medicine, Korea. bhhan@ns.kosinmed.or.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Hepatitis B/Chronic;
Lamivudine;
Breakthrough
- MeSH:
Acute Disease;
Adult;
Aged;
Antiviral Agents/*therapeutic use;
DNA, Viral/blood;
English Abstract;
Female;
Hepatitis B e Antigens/blood;
Hepatitis B virus/genetics/isolation & purification;
Hepatitis B, Chronic/complications/drug therapy/*virology;
Humans;
Lamivudine/*therapeutic use;
Male;
Middle Aged;
Reverse Transcriptase Inhibitors/*therapeutic use
- From:The Korean Journal of Hepatology
2004;10(2):108-116
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Viral breakthrough has been considered a major limitation of lamivudine in the treatment of hepatitis B virus related chronic liver disease. Its clinical meaning has not been thoroughly assessed. METHODS: 64 patients who showed viral breakthrough during lamivudine treatment were retrospectively reviewed. We evaluated the rate of HBeAg seroconversion and hepatic decompensation after viral breakthrough. RESULTS: After viral breakthrough, serum alanine transaminase (ALT) elevation more than 1.2X upper limit of normal (ULN) was noticed in 40 patients (62.5%). Acute flare (serum ALT elevation >X5 ULN, or serum bilirubin >3 mg/dL) occured in 15 patients (23.4%). During the period of follow up (15.0 +/- 9.7 months; range, 0-31 months) since viral breakthrough, decreased serum HBV-DNA level to below the detection limit and serum ALT normalization was seen in 15 patients (23.4%). HBeAg seroconversion was noticed in 7 (13.7%) of a total of 51 HBeAg positive patients at base line; in 4 (15.4%) of 26 patients with non-hepatic failure (chronic hepatitis or Child-Pugh class A liver cirrhosis) at base line; and in 2 (40.0%) of 5 patients with non-hepatic failure at base line and acute flare after viral breakthrough. During this period, terminal hepatic decompensation (Child-Pugh class C) or death was noticed in 9 (90.0%) of 10 patients who had hepatic decompensation (Child-Pugh class B or C) at baseline and acute flare after viral breakthrough. CONCLUSIONS: Acute flare after viral breakthrough seemed to continue during HBeAg seroconversion and rarely developed into terminal hepatic decompensation or death in patients with non-hepatic decompensation at baseline. Its incidence is not only high but lethal to most patients with hepatic decompensation at baseline.
