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JAC Advance Access originally published online on March 12, 2008
Journal of Antimicrobial Chemotherapy 2008 61(6):1340-1343; doi:10.1093/jac/dkn097
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Changes in metabolic toxicity after switching from stavudine/didanosine to tenofovir/lamivudine—a Staccato trial substudy

Jintanat Ananworanich1,2,*, Reto Nuesch3, Hélène C. F. Côté4, Stephen J. Kerr1,5, Andrew Hill6, Thidarat Jupimai1, Naphassanant Laopraynak1, Sukontha Saenawat1, Kiat Ruxrungtham1,7 and Bernard Hirschel8

1 The HIV Netherlands Australia Thailand Research Collaboration (HIV-NAT), Bangkok, Thailand 2 South East Asia Research Collaboration with Hawaii (SEARCH), Bangkok, Thailand 3 Outpatient Clinic of Internal Medicine and Division of Infectious Diseases University Hospital Basel, Switzerland 4 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada 5 National Centre in HIV Epidemiology and Clinical Research, The University of New South Wales, Sydney, Australia 6 Liverpool University, Liverpool, UK 7 Chulalongkorn University, Bangkok, Thailand 8 Geneva University Hospital, Geneva, Switzerland

Received 2 November 2007; returned 25 November 2007; revised 28 January 2008; accepted 17 February 2008

* Correspondence address. The HIV Netherlands Australia Thailand Research Collaboration (HIV-NAT), 104 Rajdumri Road, Pathumwan, Bangkok 10330, Thailand. Tel: +66-2-255-7335; Fax: +66-2-252-5779; E-mail: jintanat.a{at}hivnat.org

Objectives: Stavudine is widely used in Thailand and is associated with mitochondrial toxicity. Here, we evaluated the effect of switching from stavudine/didanosine to tenofovir/lamivudine on measures of metabolic and mitochondrial toxicity in Thai patients.

Methods: Thirty-five Thai patients with full HIV RNA suppression were switched from stavudine/didanosine to tenofovir/lamivudine while receiving saquinavir/ritonavir 1600/100 mg once daily. Patients were assessed at the time of switch and 24 and 48 weeks after for lipids, liver enzymes, lactate, mitochondrial DNA content and limb/total fat mass by dual energy X-ray absorptiometry (DEXA) scanning.

Results: Forty-eight weeks after the switch, there were significant reductions in lipids and lactate, but no change in liver enzymes. There was reversal of lipoatrophy, as shown by rises in limb fat mass (+0.38 kg, P = 0.006) and total fat mass (+0.69 kg, P = 0.02) on DEXA scan. Patients perceived weight improvement, but did not report reversal of lipoatrophy of individual body parts. The mitochondrial DNA/nuclear DNA ratio rose (+1.06, P < 0.0001).

Conclusions: After the nucleoside reverse transcriptase inhibitor switch, reversal of mitochondrial toxicity was consistent with switch studies of mainly Caucasian patients, although the peripheral mononuclear cell mitochondrial DNA rise exceeded previous reports.

Keywords: mitochondrial toxicity , NRTIs , Thailand


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