BACKGROUND/AIMS: We investigated the efficacy of entecavir in lamivudine-experienced and -naïve patients with persistently high HBV DNA during adefovir treatment. METHODS: Fourteen chronic hepatitis B patients (57% lamivudine-experienced) with a viral load above 5log(10)copies/mL after 12months of adefovir therapy and thereafter were treated with entecavir 1mg daily. RESULTS: During a median follow-up of 15months (range: 8-23months) one of six lamivudine-naïve and none of the eight lamivudine-experienced patients achieved undetectable HBV DNA (<373copies/mL). HBeAg loss occurred in none of the subjects. Two lamivudine-experienced patients demonstrated the rtM204I mutation; no other entecavir-resistant substitutions were detected (rtI169, rtT184, rtS202, and rtM250). Two of three patients with genotypic adefovir resistance at baseline demonstrated a rapid virologic response to entecavir, but undetectable HBV DNA was not achieved. To attain a better antiviral response the dosage of entecavir was increased to 2mg daily in two patients, resulting in further viral load decline for both of them. CONCLUSIONS: Entecavir monotherapy dosed at 1mg resulted in a slow reduction of viral load in both lamivudine-experienced and -naïve patients with persistently high HBV DNA during adefovir therapy. Increasing the dosage of entecavir led to further HBV DNA decline.
BACKGROUND/AIMS: We investigated the efficacy of entecavir in lamivudine-experienced and -naïve patients with persistently high HBV DNA during adefovir treatment. METHODS: Fourteen chronic hepatitis Bpatients (57% lamivudine-experienced) with a viral load above 5log(10)copies/mL after 12months of adefovir therapy and thereafter were treated with entecavir 1mg daily. RESULTS: During a median follow-up of 15months (range: 8-23months) one of six lamivudine-naïve and none of the eight lamivudine-experienced patients achieved undetectable HBV DNA (<373copies/mL). HBeAg loss occurred in none of the subjects. Two lamivudine-experienced patients demonstrated the rtM204I mutation; no other entecavir-resistant substitutions were detected (rtI169, rtT184, rtS202, and rtM250). Two of three patients with genotypic adefovir resistance at baseline demonstrated a rapid virologic response to entecavir, but undetectable HBV DNA was not achieved. To attain a better antiviral response the dosage of entecavir was increased to 2mg daily in two patients, resulting in further viral load decline for both of them. CONCLUSIONS:Entecavir monotherapy dosed at 1mg resulted in a slow reduction of viral load in both lamivudine-experienced and -naïve patients with persistently high HBV DNA during adefovir therapy. Increasing the dosage of entecavir led to further HBV DNA decline.
Authors: Hana Park; Jun Yong Park; Seung Up Kim; Do Young Kim; Kwang-Hyub Han; Chae Yoon Chon; Sang Hoon Ahn Journal: World J Gastroenterol Date: 2013 Impact factor: 5.742
Authors: Hee Bok Chae; Mee Jin Kim; Eui Geun Seo; Yong Hyeok Choi; Hee Seung Lee; Joung Ho Han; Soon Man Yoon; Seon Mee Park; Sei Jin Youn Journal: Korean J Hepatol Date: 2012-03-22