Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B
- Abstract
- BACKGROUND/AIMS: To investigate the association between the baseline profiles and dynamics of hepatitis B virus (HBV) DNA polymerase gene mutations and the long-term virological response of lamivudine (LAM)-adefovir (ADV) combination therapy in patients with LAM-resistant chronic hepatitis B. METHODS: Seventy-five patients who received LAM-ADV combination therapy for more than 12 months were analyzed. Restriction fragment mass polymorphism assays were used to detect and monitor the dynamics of LAM- and ADV-resistant mutations. RESULTS: The median duration of LAMADV combination therapy was 26 months (range, 12 to 58 months). The baseline mutation profiles, rtM204I (p=0.992), rtM204I/V (p=0.177), and rtL180M (p=0.051), were not correlated with the cumulative virological response, and the baseline HBV DNA level (p=0.032) was the only independent predictive factor for cumulative virological response. Tests for LAM- and ADV-resistant mutations were performed in 12 suboptimal responders in weeks 48 and 96. The population of rtM204 mutants persisted or increased in 8 of 12 patients, and rtA181T mutants newly emerged as a minor population in four patients until 96 weeks. Nevertheless, the viral loads progressively decreased during rescue therapy, and these dynamics did not correlate with virological response. CONCLUSIONS: The baseline profile and dynamics of LAM-resistant mutations during LAM-ADV combination therapy are not associated with a virological response.
- All Author(s)
- J. Kim
; S. H. Lee
; H. S. Kim
; K. Choi
; S. W. Jeong
; S. G. Kim
; J. Y. Jang
; Y. S. Kim
; B. S. Kim
- Issued Date
- 2015
- Type
- Article
- Keyword
- Hepatitis B virus; Lamivudine resistance; Restriction fragment mass polymorphism; Mutation
- Publisher
- 대한소화기학회
- ISSN
- 1976-2283
- Citation Title
- Gut and Liver
- Citation Volume
- 9
- Citation Number
- 1
- Citation Start Page
- 103
- Citation End Page
- 108
- Language(ISO)
- eng
- DOI
- 10.5009/gnl14018
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/2973
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