Gut and Liver 2010; 4(4): 530-536 https://doi.org/10.5009/gnl.2010.4.4.530 A Low Viral Load Predicts a Higher Initial Virologic Response to Adefovir in Patients with Lamivudine-Resistant Chronic Hepatitis B
Author Information
Su Rin Shin*, Kwang Cheol Koh, Geum-Youn Gwak, Moon Seok Choi, Joon Hyoek Lee, Seung Woon Paik, and Byung Chul Yoo
*Department of Medicine, Kangnam Sacred Heart Hospital, Hallym University College of Medicine, and Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

Kwang Cheol Koh
© The Korean Society of Gastroenterology, the Korean Society of Gastrointestinal Endoscopy, the Korean Society of Neurogastroenterology and Motility, Korean College of Helicobacter and Upper Gastrointestinal Research, Korean Association the Study of Intestinal Diseases, the Korean Association for the Study of the Liver, Korean Pancreatobiliary Association, and Korean Society of Gastrointestinal Cancer. All rights reserved.

Abstract
Background/Aims: Adefovir (ADV) is the preferred drug for treating lamivudine (LAM)-resistant hepatitis B. However, not all patients who face virologic breakthrough during LAM treatment respond to ADV. The aim of this study was to determine the factors associated with efficacy of ADV in LAM-resistant hepatitis B patients. Methods: The medical records of 231 patients who received ADV due to LAM-resistance were reviewed. Efficacy was assessed by the initial virologic response (IVR), defined as hepatitis B virus (HBV) DNA not being undetectable by real-time PCR at 6 months of ADV treatment. Results: Seventy patients (30%) achieved IVR. While 'add-on' modality, hepatitis B e antigen (HBeAg) negativity, and low baseline HBV DNA levels were associated with IVR in univariate analysis, multivariate analysis revealed HBeAg status and the DNA level to be the significant factors. The probability of IVR achievement increased sharply per each log10 copies/mL decrement in the baseline viral load, which was 133 times in patients who had HBV DNA <105 copies/mL compared with those who had ≥108 copies/mL. Conclusions: Factors associated with the IVR were HBeAg negativity and a low baseline viral load. Therefore, when virologic breakthrough with genotypic resistance emerges during LAM therapy, ADV treatment should be considered immediately before further increases in viral load. Additional long-term follow-up data are warranted. (Gut Liver 2010;4:530-536)
Keywords: Chronic hepatitis B; Lamivudine; Antiviral drug resistance; Adefovir; Viral load
Abstract
Background/Aims: Adefovir (ADV) is the preferred drug for treating lamivudine (LAM)-resistant hepatitis B. However, not all patients who face virologic breakthrough during LAM treatment respond to ADV. The aim of this study was to determine the factors associated with efficacy of ADV in LAM-resistant hepatitis B patients. Methods: The medical records of 231 patients who received ADV due to LAM-resistance were reviewed. Efficacy was assessed by the initial virologic response (IVR), defined as hepatitis B virus (HBV) DNA not being undetectable by real-time PCR at 6 months of ADV treatment. Results: Seventy patients (30%) achieved IVR. While 'add-on' modality, hepatitis B e antigen (HBeAg) negativity, and low baseline HBV DNA levels were associated with IVR in univariate analysis, multivariate analysis revealed HBeAg status and the DNA level to be the significant factors. The probability of IVR achievement increased sharply per each log10 copies/mL decrement in the baseline viral load, which was 133 times in patients who had HBV DNA <105 copies/mL compared with those who had ≥108 copies/mL. Conclusions: Factors associated with the IVR were HBeAg negativity and a low baseline viral load. Therefore, when virologic breakthrough with genotypic resistance emerges during LAM therapy, ADV treatment should be considered immediately before further increases in viral load. Additional long-term follow-up data are warranted. (Gut Liver 2010;4:530-536)
Keywords: Chronic hepatitis B; Lamivudine; Antiviral drug resistance; Adefovir; Viral load
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