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Pediatric Infectious Disease Journal:
Original Studies

Lamivudine treatment for chronic hepatitis B infection in children unresponsive to interferon

HARTMAN, CORINA MD; BERKOWITZ, DRORA MD; SHOUVAL, DANIEL MD; ESHACH-ADIV, ORLY MD; HINO, BIAN MD; RIMON, NURIT PhD; SATINGER, IEHUDITH PhD; KRA-OZ, TZIPI PhD; DAUDI, NILY PhD; SHAMIR, RAANAN MD

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Abstract

Background/aims. Lamivudine is a potent inhibitor of hepatitis B virus (HBV) replication. This prospective open study reports the results of lamivudine treatment in children with chronic hepatitis B infection who did not respond to previous interferon treatment.

Patients and methods. Lamivudine, 3 mg/kg/day (maximum, 100 mg/day), was given for 52 weeks to 20 children and adolescents, ages 8.5 to 19 years, with chronic hepatitis B infection who had been treated with interferon 2 to 5 years earlier. We evaluated virologic and biochemical responses, the occurrence of YMDD mutants and adverse effects.

Results. All children were HBV DNA+, hepatitis B e antigen (HBeAg)+/anti-hepatitis B e antibody at start of treatment. At the end of 1 year, HBV DNA declined by 95% in all patients, and 8 of 18 (44%) had sustained undetectable HBV DNA by hybridization assay. Median pretreatment alanine aminotransferase (ALT) ×1.5 upper limit of normal decreased to ALT ×0.9 upper limit of normal after 1 year. One child became HBeAg-negative. YMDD mutants were detected in 11 of 17 (65%) children after 1 year of lamivudine treatment. Among children with YMDD mutant variants, 54% maintained normal ALT values and 45% had undetectable HBV DNA by hybridization assay. No adverse effects were observed.

Conclusions. Children with chronic hepatitis B infection treated with lamivudine after failure of interferon therapy had decreased HBV replication and improved ALT values. However, lamivudine treatment resulted in an exceptionally high rate of lamivudine-resistant mutants and low HBeAg seroconversion rate.

© 2003 Lippincott Williams & Wilkins, Inc.

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