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Conference Paper: Clinical course of lamivudine-resistant HBV infection in renal allograft recipients

TitleClinical course of lamivudine-resistant HBV infection in renal allograft recipients
Authors
Issue Date2003
PublisherWiley-Blackwell Publishing, Inc.
Citation
The 2003 American Transplant Congress (ATC), Washington, DC., 31 May-4 June 2003. In American Journal of Transplantation, 2003, v. 3 n. S5, p. 502, abstract no. 1365 How to Cite?
AbstractWe have reported that pre-emptive lamivudine therapy based on HBV DNA level markedly reduced liver-related mortality in HBsAg+ renal transplant recipients (RTR). However, the progressive emergence of lamivudine-resistant HBV variants presents a major concern, and yet the natural history of lamivudine-resistant HBV infection in immunosuppressed subjects remains obscure. Since Jan 1996 we have treated 29 of 53 HBsAg+ RTR pre-emptively with lamivudine based on their increasing HBV DNA levels. All the patients had maintenance immunosuppression with low-dose prednisolone and cyclosporin or tacrolimus. All the patients had effective suppression of HBV DNA after treatment. This is a prospective cohort study to examine the clinical course of patients who have developed lamivudine-resistant HBV variants. 14 patients (48.3%) developed lamivudine-resistance with resurgence of HBV DNA during treatment, whereas treatment was successfully withdrawn (i.e. without relapse) after 24.6±11.9 mon in 9 patients (31.0%). The duration of lamivudine therapy and the posttransplant follow-up for the 14 patients were 56.7±12.5 and 97.4±44.9 mon respectively. Lamivudine-resistance emerged after 16.9±7.0 mon (range 10-35) of treatment, with 78.6% within the first 18 mon. Patients with lamivudine-resistant variants showed similar age, gender, baseline eAg status, and post-lamivudine eAg sero-conversion (25.0 vs 33.3%, P=1.00) compared to those who did not develop resistance. Liver biochemistry deteriorated in 11 (78.6%) patients after the emergence of lamivudineresistance, which was transient in 4 (36.4%) but became chronic in 6 (54.5%) patients. The remaining patient developed severe exacerbation, but responded to the addition of famciclovir. Peak HBV DNA after the emergence of resistance was lower (1.26±1.09x109 vs 6.26±12.23x109 copies/ml, P=0.011), while peak ALT was higher (196±117 vs 77±47 iu/l, P=0.005), compared to the respective pre-treatment levels. None of the patients with lamivudine-resistant HBV had liver-related mortality or hepatocellular carcinoma, while the latter affected 2 patients in the other group. We conclude that half of lamivudine-treated HBsAg+ RTR are complicated by drug resistance. Although the subsequent peak HBV DNA is lower than the pre-treatment level, exacerbation of hepatitis is common, and half of these patients develop chronic active hepatitis. Thus, lamivudine-resistant HBV variants will present an escalating clinical problem in immunosuppressed RTR, before the advent of effective therapy.
Persistent Identifierhttp://hdl.handle.net/10722/102434
ISSN
2015 Impact Factor: 5.669
2015 SCImago Journal Rankings: 2.792

 

DC FieldValueLanguage
dc.contributor.authorChan, DTMen_HK
dc.contributor.authorYip, PSen_HK
dc.contributor.authorTang, CSOen_HK
dc.contributor.authorFang, Gen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorHo, KNen_HK
dc.date.accessioned2010-09-25T20:30:29Z-
dc.date.available2010-09-25T20:30:29Z-
dc.date.issued2003en_HK
dc.identifier.citationThe 2003 American Transplant Congress (ATC), Washington, DC., 31 May-4 June 2003. In American Journal of Transplantation, 2003, v. 3 n. S5, p. 502, abstract no. 1365-
dc.identifier.issn1600-6135-
dc.identifier.urihttp://hdl.handle.net/10722/102434-
dc.description.abstractWe have reported that pre-emptive lamivudine therapy based on HBV DNA level markedly reduced liver-related mortality in HBsAg+ renal transplant recipients (RTR). However, the progressive emergence of lamivudine-resistant HBV variants presents a major concern, and yet the natural history of lamivudine-resistant HBV infection in immunosuppressed subjects remains obscure. Since Jan 1996 we have treated 29 of 53 HBsAg+ RTR pre-emptively with lamivudine based on their increasing HBV DNA levels. All the patients had maintenance immunosuppression with low-dose prednisolone and cyclosporin or tacrolimus. All the patients had effective suppression of HBV DNA after treatment. This is a prospective cohort study to examine the clinical course of patients who have developed lamivudine-resistant HBV variants. 14 patients (48.3%) developed lamivudine-resistance with resurgence of HBV DNA during treatment, whereas treatment was successfully withdrawn (i.e. without relapse) after 24.6±11.9 mon in 9 patients (31.0%). The duration of lamivudine therapy and the posttransplant follow-up for the 14 patients were 56.7±12.5 and 97.4±44.9 mon respectively. Lamivudine-resistance emerged after 16.9±7.0 mon (range 10-35) of treatment, with 78.6% within the first 18 mon. Patients with lamivudine-resistant variants showed similar age, gender, baseline eAg status, and post-lamivudine eAg sero-conversion (25.0 vs 33.3%, P=1.00) compared to those who did not develop resistance. Liver biochemistry deteriorated in 11 (78.6%) patients after the emergence of lamivudineresistance, which was transient in 4 (36.4%) but became chronic in 6 (54.5%) patients. The remaining patient developed severe exacerbation, but responded to the addition of famciclovir. Peak HBV DNA after the emergence of resistance was lower (1.26±1.09x109 vs 6.26±12.23x109 copies/ml, P=0.011), while peak ALT was higher (196±117 vs 77±47 iu/l, P=0.005), compared to the respective pre-treatment levels. None of the patients with lamivudine-resistant HBV had liver-related mortality or hepatocellular carcinoma, while the latter affected 2 patients in the other group. We conclude that half of lamivudine-treated HBsAg+ RTR are complicated by drug resistance. Although the subsequent peak HBV DNA is lower than the pre-treatment level, exacerbation of hepatitis is common, and half of these patients develop chronic active hepatitis. Thus, lamivudine-resistant HBV variants will present an escalating clinical problem in immunosuppressed RTR, before the advent of effective therapy.-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing, Inc.-
dc.relation.ispartofAmerican Journal of Transplantationen_HK
dc.titleClinical course of lamivudine-resistant HBV infection in renal allograft recipientsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChan, DTM: dtmchan@hku.hken_HK
dc.identifier.emailTang, CSO: csotang@HKUCC.hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityChan, DTM=rp00394en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1034/j.1600-6143.3.s5.15c.x-
dc.identifier.hkuros132012en_HK
dc.identifier.volume3-
dc.identifier.issuesuppl. 5-
dc.identifier.spage502, abstract no. 1365-
dc.identifier.epage502, abstract no. 1365-

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