JAC Advance Access originally published online on November 3, 2005
Journal of Antimicrobial Chemotherapy 2005 56(6):1087-1093; doi:10.1093/jac/dki396
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Impact of tenofovir-containing antiretroviral therapy on chronic hepatitis B in a cohort co-infected with human immunodeficiency virus
1 HIV Research and Treatment Unit at Center for Internal Medicine, Johann Wolfgang Goethe-University Hospital Frankfurt, Germany; 2 Medical Virology Institute, Johann Wolfgang Goethe-University Hospital Frankfurt, Germany; 3 HIV Medical Office Grüneburgweg Frankfurt, Germany; 4 HIV Outpatient Clinic Stresemannallee Frankfurt, Germany
Received 17 August 2005; returned 5 September 2005; revised 29 September 2005; accepted 3 October 2005
* Correspondence address. Klinikum der Johann Wolfgang Goethe-Universität, Medizinische Klinik II—Infektionsambulanz Haus 68, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany. Tel: +49-69-6301-7680; Fax: +49-69-6301-5712; E-mail: C.Stephan{at}em.uni-frankfurt.de
Objectives: We studied the impact of tenofovir disoproxil fumarate, given as an antiretroviral medication, on patients with chronic hepatitis B virus (HBV) co-infection.
Methods: The polymerase gene-sequence evolution and quantitative HBV loads (HBVL) were observed for 48 weeks in patients taking tenofovir-containing antiretroviral therapy. The patients were grouped according to baseline strata: high-replicative virus (>6 log copies/mL), low-replicative virus at detectable virus loads (<6 log) and HBs-antigen-positive, HBV-DNA-negative individuals.
Results: Thirty-one patients were evaluated. The median decline in 20 patients with high-replicative HBV infection was –5.37 log (range: 3.57–7); 11 out of 20 decreased to undetectable levels (lower limit of detection = < 200 copies/mL) and another three were below 400 copies/mL. Out of six patients with detectable HBV-DNA at week 48 (HBVL result: range 3.36–4.32 log10), we were able to carry out a re-sequence in four patients. We did not observe relevant emerging resistance mutations, or a relevant virus load re-increase from nadir (>+0.5 log). The patients with low-replicative virus (n = 9) and the baseline DNA-negative patients (n = 2) had an undetectable HBV-DNA at week 48. Two patients became HBeAg-negative; one DNA-negative patient became HBsAg-negative.
Conclusions: Tenofovir is effective in treating HBV infection in HIV patients. Patients with high-replicative virus may benefit from this treatment strategy by a reduction in replicative status, a precondition for improved hepatic function. A few patients showed low-level HBV replication. Indicators for clinical HBV-resistance to tenofovir were not observed.
Keywords: tenofovir disoproxil fumarate , lamivudine , YMDD mutation , HBV , HIV
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