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Effects of the Change From Stavudine to Tenofovir in Human Immunodeficiency Virus-Infected Children Treated With Highly Active Antiretroviral Therapy: Studies on Mitochondrial Toxicity and Thymic Function

Rosso, Raffaella MD, PhD*; Nasi, Milena PhD†; Di Biagio, Antonio MD*; Repetto, Ernestina MD*; Dentone, Chiara MD*; Pinti, Marcello PhD†; Nemes, Elisa BSc†; Ferraresi, Roberta PhD†; Mussini, Cristina MD‡; Esposito, Roberto MD‡; Viscoli, Claudio MD*; Cossarizza, Andrea MD, PhD†

Pediatric Infectious Disease Journal: January 2008 - Volume 27 - Issue 1 - pp 17-21
doi: 10.1097/INF.0b013e31814689be
Original Studies

Background: Changing from drugs that have significant mitochondrial toxicity to less toxic compounds may be of benefit in human immunodeficiency virus (HIV)-positive patients who receive highly active antiretroviral therapy. Few data on mitochondrial toxicity of antiviral drugs are available in HIV-positive children.

Methods: Eighteen HIV-positive children (median age, 10.9 years) receiving a stavudine-containing regimen were randomized to maintain stavudine (arm A) or change to tenofovir (arm B), while preserving the remaining drugs. Glucose, lipidic, and viro-immunologic factors were assessed at months 0, 1, 3, 6, 12, and 18. Thymic output and mtDNA content were measured in peripheral blood mononuclear cells at 0 and 6 months, mtDNA in isolated CD4+ and CD8+ T cells after 18 months.

Results: From baseline to month 6, arms A and B showed similar thymic output and mtDNA. After 18 months, a significant decrease in plasma HDL was observed in arm B, along with a small increase in blood glucose; mtDNA showed no difference. In the 2 arms other factors did not show significant differences from the baseline and from the previous values at 18 months.

Conclusions: Changing from stavudine to tenofovir was well-tolerated, and viro-immunologic success was maintained.

From the *Infectious Diseases Clinics, San Martino Hospital, University of Genoa, Genoa, Italy; †Department of Biomedical Sciences, University of Modena and Reggio Emilia, Modena, Italy; and ‡Infectious Diseases Clinics, Azienda Ospedaliero-Universitaria, Modena, Italy.

Accepted for publication June 22, 2007.

The first 2 authors have contributed equally to this work. The authors declare no conflict of interest.

Address for correspondence: Andrea Cossarizza, Department of Biomedical Sciences, Via Campi, 287, 41100 Modena, Italy. E-mail: cossarizza.andrea@unimore.it.

© 2008 Lippincott Williams & Wilkins, Inc.