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Article: Prospective study on lamivudine-resistant hepatitis B in renal allograft recipients

TitleProspective study on lamivudine-resistant hepatitis B in renal allograft recipients
Authors
KeywordsHepatitis B
Kidney transplantation
Lamivudine
Issue Date2004
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJT
Citation
American Journal Of Transplantation, 2004, v. 4 n. 7, p. 1103-1109 How to Cite?
AbstractThe natural history of lamivudine-resistant hepatitis B virus (HBV) infection in renal transplant recipients (RTx) is unclear, despite its increasing incidence. Twenty-nine HBsAg-positive RTx with rising HBV DNA received lamivudine therapy. The course of lamivudine-resistant HBV infection was studied prospectively. During 68.7 ± 12.5 months of follow-up, 14 (48.3%) patients developed lamivudine resistance, at 10-35 months (mean 16.9 ± 7.0). All showed mutant sequences at codons 552 and 528 of the YMDD motif, while 13 patients demonstrated wild-type sequence at codon 555. Lamivudine resistance was unrelated to patient demographics, HBeAg status/sero-conversion, or genotype. Following resistance, HBV DNA and alanine aminotransferase showed an initial increase followed by spontaneous gradual reduction. The subsequent peak HBV DNA was lower (1.25 ± 1.09 × 109 vs. 6.26 ± 12.23 × 109 copies/mL, p = 0.011), while that of alanine aminotransferase was higher (196 ± 117 vs. 77 ± 47 iμ/I, p = 0.005), compared with pretreatment levels. Post-resistance hepatitic flare occurred in 11 (78.6%) patients. This was transient in four (36.4%), but became chronic in six (54.5%) patients. Decompensation was noted in one patient during this flare, but all survived. We conclude that drug resistance is prevalent in lamivudine-treated RTx. Despite a lower ensuing peak viremia compared with baseline, hepatitic flare is common. While most patients have spontaneous resolution, a minority may develop potentially fatal decompensation during the preceding exacerbation.
Persistent Identifierhttp://hdl.handle.net/10722/162929
ISSN
2015 Impact Factor: 5.669
2015 SCImago Journal Rankings: 2.792
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, TMen_HK
dc.contributor.authorTse, KCen_HK
dc.contributor.authorTang, CSOen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorHo, SKNen_HK
dc.date.accessioned2012-09-05T05:25:28Z-
dc.date.available2012-09-05T05:25:28Z-
dc.date.issued2004en_HK
dc.identifier.citationAmerican Journal Of Transplantation, 2004, v. 4 n. 7, p. 1103-1109en_HK
dc.identifier.issn1600-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162929-
dc.description.abstractThe natural history of lamivudine-resistant hepatitis B virus (HBV) infection in renal transplant recipients (RTx) is unclear, despite its increasing incidence. Twenty-nine HBsAg-positive RTx with rising HBV DNA received lamivudine therapy. The course of lamivudine-resistant HBV infection was studied prospectively. During 68.7 ± 12.5 months of follow-up, 14 (48.3%) patients developed lamivudine resistance, at 10-35 months (mean 16.9 ± 7.0). All showed mutant sequences at codons 552 and 528 of the YMDD motif, while 13 patients demonstrated wild-type sequence at codon 555. Lamivudine resistance was unrelated to patient demographics, HBeAg status/sero-conversion, or genotype. Following resistance, HBV DNA and alanine aminotransferase showed an initial increase followed by spontaneous gradual reduction. The subsequent peak HBV DNA was lower (1.25 ± 1.09 × 109 vs. 6.26 ± 12.23 × 109 copies/mL, p = 0.011), while that of alanine aminotransferase was higher (196 ± 117 vs. 77 ± 47 iμ/I, p = 0.005), compared with pretreatment levels. Post-resistance hepatitic flare occurred in 11 (78.6%) patients. This was transient in four (36.4%), but became chronic in six (54.5%) patients. Decompensation was noted in one patient during this flare, but all survived. We conclude that drug resistance is prevalent in lamivudine-treated RTx. Despite a lower ensuing peak viremia compared with baseline, hepatitic flare is common. While most patients have spontaneous resolution, a minority may develop potentially fatal decompensation during the preceding exacerbation.en_HK
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJTen_HK
dc.relation.ispartofAmerican Journal of Transplantationen_HK
dc.subjectHepatitis Ben_HK
dc.subjectKidney transplantationen_HK
dc.subjectLamivudineen_HK
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAlanine Transaminase - Metabolismen_US
dc.subject.meshAmino Acid Motifsen_US
dc.subject.meshCodonen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshDna, Viral - Geneticsen_US
dc.subject.meshDrug Resistance, Viralen_US
dc.subject.meshFemaleen_US
dc.subject.meshFollow-Up Studiesen_US
dc.subject.meshHepatitis - Virologyen_US
dc.subject.meshHepatitis B - Etiologyen_US
dc.subject.meshHepatitis B Virus - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunosuppressive Agents - Pharmacologyen_US
dc.subject.meshKidney Transplantation - Adverse Effectsen_US
dc.subject.meshLamivudine - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshProspective Studiesen_US
dc.subject.meshReverse Transcriptase Inhibitors - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.titleProspective study on lamivudine-resistant hepatitis B in renal allograft recipientsen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1600-6143.2004.00467.xen_HK
dc.identifier.pmid15196068-
dc.identifier.scopuseid_2-s2.0-3042703006en_HK
dc.identifier.hkuros99047-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3042703006&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1103en_HK
dc.identifier.epage1109en_HK
dc.identifier.isiWOS:000221968700014-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridTse, KC=7102609864en_HK
dc.identifier.scopusauthoridTang, CSO=8681865300en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridHo, SKN=36839065300en_HK

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