Guest guest Posted February 14, 2006 Report Share Posted February 14, 2006 Gut. 2006 Feb 4; [Epub ahead of print] Resistance to adefovir dipivoxil (ADV) in lamivudine- resistant chronic hepatitis B patients treated with ADV. Yeon JE, Yoo W, Hong SP, Chang YJ, Yu SK, Kim JH, Seo YS, Chung HJ, Moon MS, Kim SO, Byun KS, Lee CH. Korea University Medical College Guro Hospital, Korea, Republic of. BACKGROUND: Adefovir dipivoxil (ADV) is a potent nucleotide analogue against both the wild-type and lamivudine (LMV)-resistant HBV. The cumulative incidences of ADV resistant mutations in the nucleoside/-tide treatment na?e chronic hepatitis B patients (CHB) at weeks 48, 96, 144 were 0, 0.8-3% and ~5.9%, respectively. AIMS: The aim of this study was to characterize the genotypic and phenotypic mutation profiles to ADV in 67 LMV-resistant CHB patients who were treated with ADV. METHODS: The serum HBV DNA was quantified by real time PCR. The ADV mutant was detected by using matrix-assisted laser desorption/ionization time of flight mass spectrometry-based genotyping assays, termed Restriction Fragment Mass Polymorphism (RFMP). RESULTS: RFMP analysis revealed that a total of 11 amino acid substitutions developed in the rt domain of the HBV polymerase in 9 patients. The cumulative incidence of genotypic ADV resistance at months 12 and 24 was 6.4% and 25.4%, respectively. The rtA181V, rtN236T and rtA181T mutations were detected in 5, 4 and 2 of the 67 patients at treatment months 12~17, 3~19 and 7~20, respectively. Serial quantification of the serum HBV DNA revealed that two patients with the rtA181V mutation that were with or without the rtN236T mutation and one patient with the rtA181T mutation displayed the HBV DNA rebound. CONCLUSION: The emergence of the ADV mutation in LMV resistant patients who are treated with ADV appeared to present earlier and more frequent than was reported in the previous studies on nucleoside/-tide treatment na?e patients. PMID: 16461777 _________________________________________________________________ On the road to retirement? Check out MSN Life Events for advice on how to get there! http://lifeevents.msn.com/category.aspx?cid=Retirement Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 14, 2006 Report Share Posted February 14, 2006 Gut. 2006 Feb 4; [Epub ahead of print] Resistance to adefovir dipivoxil (ADV) in lamivudine- resistant chronic hepatitis B patients treated with ADV. Yeon JE, Yoo W, Hong SP, Chang YJ, Yu SK, Kim JH, Seo YS, Chung HJ, Moon MS, Kim SO, Byun KS, Lee CH. Korea University Medical College Guro Hospital, Korea, Republic of. BACKGROUND: Adefovir dipivoxil (ADV) is a potent nucleotide analogue against both the wild-type and lamivudine (LMV)-resistant HBV. The cumulative incidences of ADV resistant mutations in the nucleoside/-tide treatment na?e chronic hepatitis B patients (CHB) at weeks 48, 96, 144 were 0, 0.8-3% and ~5.9%, respectively. AIMS: The aim of this study was to characterize the genotypic and phenotypic mutation profiles to ADV in 67 LMV-resistant CHB patients who were treated with ADV. METHODS: The serum HBV DNA was quantified by real time PCR. The ADV mutant was detected by using matrix-assisted laser desorption/ionization time of flight mass spectrometry-based genotyping assays, termed Restriction Fragment Mass Polymorphism (RFMP). RESULTS: RFMP analysis revealed that a total of 11 amino acid substitutions developed in the rt domain of the HBV polymerase in 9 patients. The cumulative incidence of genotypic ADV resistance at months 12 and 24 was 6.4% and 25.4%, respectively. The rtA181V, rtN236T and rtA181T mutations were detected in 5, 4 and 2 of the 67 patients at treatment months 12~17, 3~19 and 7~20, respectively. Serial quantification of the serum HBV DNA revealed that two patients with the rtA181V mutation that were with or without the rtN236T mutation and one patient with the rtA181T mutation displayed the HBV DNA rebound. CONCLUSION: The emergence of the ADV mutation in LMV resistant patients who are treated with ADV appeared to present earlier and more frequent than was reported in the previous studies on nucleoside/-tide treatment na?e patients. PMID: 16461777 _________________________________________________________________ On the road to retirement? Check out MSN Life Events for advice on how to get there! http://lifeevents.msn.com/category.aspx?cid=Retirement Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 14, 2006 Report Share Posted February 14, 2006 Gut. 2006 Feb 4; [Epub ahead of print] Resistance to adefovir dipivoxil (ADV) in lamivudine- resistant chronic hepatitis B patients treated with ADV. Yeon JE, Yoo W, Hong SP, Chang YJ, Yu SK, Kim JH, Seo YS, Chung HJ, Moon MS, Kim SO, Byun KS, Lee CH. Korea University Medical College Guro Hospital, Korea, Republic of. BACKGROUND: Adefovir dipivoxil (ADV) is a potent nucleotide analogue against both the wild-type and lamivudine (LMV)-resistant HBV. The cumulative incidences of ADV resistant mutations in the nucleoside/-tide treatment na?e chronic hepatitis B patients (CHB) at weeks 48, 96, 144 were 0, 0.8-3% and ~5.9%, respectively. AIMS: The aim of this study was to characterize the genotypic and phenotypic mutation profiles to ADV in 67 LMV-resistant CHB patients who were treated with ADV. METHODS: The serum HBV DNA was quantified by real time PCR. The ADV mutant was detected by using matrix-assisted laser desorption/ionization time of flight mass spectrometry-based genotyping assays, termed Restriction Fragment Mass Polymorphism (RFMP). RESULTS: RFMP analysis revealed that a total of 11 amino acid substitutions developed in the rt domain of the HBV polymerase in 9 patients. The cumulative incidence of genotypic ADV resistance at months 12 and 24 was 6.4% and 25.4%, respectively. The rtA181V, rtN236T and rtA181T mutations were detected in 5, 4 and 2 of the 67 patients at treatment months 12~17, 3~19 and 7~20, respectively. Serial quantification of the serum HBV DNA revealed that two patients with the rtA181V mutation that were with or without the rtN236T mutation and one patient with the rtA181T mutation displayed the HBV DNA rebound. CONCLUSION: The emergence of the ADV mutation in LMV resistant patients who are treated with ADV appeared to present earlier and more frequent than was reported in the previous studies on nucleoside/-tide treatment na?e patients. PMID: 16461777 _________________________________________________________________ On the road to retirement? Check out MSN Life Events for advice on how to get there! http://lifeevents.msn.com/category.aspx?cid=Retirement Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 14, 2006 Report Share Posted February 14, 2006 Gut. 2006 Feb 4; [Epub ahead of print] Resistance to adefovir dipivoxil (ADV) in lamivudine- resistant chronic hepatitis B patients treated with ADV. Yeon JE, Yoo W, Hong SP, Chang YJ, Yu SK, Kim JH, Seo YS, Chung HJ, Moon MS, Kim SO, Byun KS, Lee CH. Korea University Medical College Guro Hospital, Korea, Republic of. BACKGROUND: Adefovir dipivoxil (ADV) is a potent nucleotide analogue against both the wild-type and lamivudine (LMV)-resistant HBV. The cumulative incidences of ADV resistant mutations in the nucleoside/-tide treatment na?e chronic hepatitis B patients (CHB) at weeks 48, 96, 144 were 0, 0.8-3% and ~5.9%, respectively. AIMS: The aim of this study was to characterize the genotypic and phenotypic mutation profiles to ADV in 67 LMV-resistant CHB patients who were treated with ADV. METHODS: The serum HBV DNA was quantified by real time PCR. The ADV mutant was detected by using matrix-assisted laser desorption/ionization time of flight mass spectrometry-based genotyping assays, termed Restriction Fragment Mass Polymorphism (RFMP). RESULTS: RFMP analysis revealed that a total of 11 amino acid substitutions developed in the rt domain of the HBV polymerase in 9 patients. The cumulative incidence of genotypic ADV resistance at months 12 and 24 was 6.4% and 25.4%, respectively. The rtA181V, rtN236T and rtA181T mutations were detected in 5, 4 and 2 of the 67 patients at treatment months 12~17, 3~19 and 7~20, respectively. Serial quantification of the serum HBV DNA revealed that two patients with the rtA181V mutation that were with or without the rtN236T mutation and one patient with the rtA181T mutation displayed the HBV DNA rebound. CONCLUSION: The emergence of the ADV mutation in LMV resistant patients who are treated with ADV appeared to present earlier and more frequent than was reported in the previous studies on nucleoside/-tide treatment na?e patients. PMID: 16461777 _________________________________________________________________ On the road to retirement? Check out MSN Life Events for advice on how to get there! http://lifeevents.msn.com/category.aspx?cid=Retirement Quote Link to comment Share on other sites More sharing options...
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