RESUMEN
BACKGROUND/AIMS: Lamivudine, an oral nucleoside analogue, effectively suppresses HBV replication and improves liver enzymes as well as liver histology. Long-term lamivudine therapy can induce the emergence of drug resistant HBV strains in some patients. The aim of this study was to evaluate the effects of lamivudine, the breakthrough rate, and the relapse rate of discontinuing therapy after HBeAg loss. METHODS: A total of 190 patients with HBeAg and HBV DNA positive showing abnormal serum levels of aminotransferases for at least 6 months received 100 mg of lamivudine once daily. The duration of lamivudine therapy was from 6-36 months (mean 14 months). Responder was defined as the ALT normalization with sustained suppression of HBV DNA and HBeAg loss. Therapy was to be stopped after HBeAg loss. Post-treatment monitoring continued for 1-21 months (mean 6 months). RESULTS: The cumulative HBeAg loss rates at 12 months and 18 months were 35% and 43%, respectively. Pretreatment serum HBeAg quantitation, and the duration of lamivudine therapy were independent predictive factors for HBeAg loss. The cumulative breakthrough rates at 18 and 24 months were 38% and 57%, respectively. Pretreatment HBV DNA level was the only predictable factor for breakthrough. Therapy was discontinued after HBeAg loss in 52 patients. Most episodes of relapse (15/16) occurred within 6 months after cessation of lamivudine. The cumulative relapse rates at 3 months and 6 months were 21% and 50%, respectively. A predictive factor for post-treatment relapse after HBeAg loss was the duration of lamivudine therapy. CONCLUSIONS: These results suggested the pretreatment quantitative HBeAg in serum and duration of lamivudine therapy are independent predictive factors for HBeAg loss. The HBeAg response of lamivudine-induced HBeAg loss was not durable after discontinuing therapy.