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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

Pediatric Infectious Disease Journal: March 2003 - Volume 22 - Issue 3 - pp 224-228
Original Studies

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.

From the Division of Pediatric Gastroenterology and Nutrition, Meyer Children’s Hospital of Haifa (CH, DB, OEA, BH, RS), and Laboratory of Virology (NR, IS, TKO), Rambam Medical Center, Bruce Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa; and Liver Unit (DS, ND), Division of Medicine, Hadassah University Hospital, Jerusalem, Israel.

Accepted for publication Nov. 13, 2002.

Address for reprints: Raanan Shamir, M.D., Division of Pediatric Gastroenterology and Nutrition, Mayer Children’s Hospital of Haifa, Rambam Medical Center, POB 9602, Haifa 31096, Israel. Fax 972-4-8542485, E-mail shamirr@netvision.net.il.

© 2003 Lippincott Williams & Wilkins, Inc.