Brief Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Aug 14, 2011; 17(30): 3526-3530
Published online Aug 14, 2011. doi: 10.3748/wjg.v17.i30.3526
Virological response to adefovir monotherapy and the risk of adefovir resistance
Dong Hyun Sinn, Hyang Ie Lee, Geum-Youn Gwak, Moon Seok Choi, Kwang Cheol Koh, Seung Woon Paik, Byung Chul Yoo, Joon Hyeok Lee
Dong Hyun Sinn, Geum-Youn Gwak, Moon Seok Choi, Kwang Cheol Koh, Seung Woon Paik, Byung Chul Yoo, Joon Hyeok Lee, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 135-710 Seoul, South Korea
Hyang Ie Lee, Department of Internal Medicine, Eulji University Hospital, 302-799 Daejeon, South Korea
Author contributions: Sinn DH analyzed the data and wrote the draft manuscript; Lee HI collected data and was also involved in writing the draft manuscript; Gwak GY, Choi MS, Koh KC, Paik SW and Yoo BC provided the data, and was involved in study design; Lee JH designed the study, provided the data and undertook critical revision of the manuscript.
Correspondence to: Joon Hyeok Lee, Professor, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, 135-710 Seoul, South Korea. liverjhlee@skku.edu
Telephone: +82-2-34103409 Fax: +82-2-34106983
Received: February 14, 2011
Revised: March 29, 2011
Accepted: April 5, 2011
Published online: August 14, 2011
Abstract

AIM: To evaluate virological response to adefovir (ADV) monotherapy and emergence of ADV-resistant mutations in lamivudine (LAM)-resistant chronic hepatitis B patients.

METHODS: Seventy-seven patients with documented LAM resistance who were treated with 10 mg/d ADV for > 96 wk were analyzed for ADV resistance.

RESULTS: At week 48 and 96, eight (10%) and 14 (18%) of 77 LAM-resistant patients developed the ADV-resistant strain (rtA181V/T and/or rtN236T mutations), respectively. Hepatitis B virus (HBV) DNA levels during therapy were significantly higher in patients who developed ADV resistance than in those who did not. Incidence of ADV resistance at week 96 was 11%, 8% and 6% among patients with complete virological response (HBV DNA level < 60 IU/mL); 0%, 5% and 19% among patients with partial virological response (HBV DNA level ≥ 60 to 2000 IU/mL); and 32%, 34% and 33% among patients with inadequate virological response (HBV DNA levels > 2000 IU/mL) at week 12, week 24 and week 48, respectively. HBV DNA levels > 2000 IU/mL at week 24 showed best performance characteristics in predicting ADV resistance.

CONCLUSION: Development of ADV resistance mutations was associated with HBV DNA levels, which could identify patients with LAM resistance who are likely to respond to ADV monotherapy.

Keywords: Hepatitis B virus, Viral DNA, Adefovir, Lamivudine, Drug resistance