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KMID : 1103920040100020108
Korean Journal of Hepatology
2004 Volume.10 No. 2 p.108 ~ p.116
The Clinical Meaning of the Emergence of Viral Breakthrough during Lamivudine Treatment in Patients with Hepatitis B Virus Related Chronic Liver Disease
¹ÚÂùº¹/Park CB
ÀÓÇöÁ¤/À±º´Ã¶/ÀÌ»ó¿í/ÇѺ´ÈÆ/Lim HJ/Yun BC/Lee SU/Han BH
Abstract
Background: 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.
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