Could Mitochondrial DNA Quantitation Be a Surrogate Marker for Drug Mitochondrial Toxicity?

Could Mitochondrial DNA Quantitation Be a Surrogate Marker for Drug Mitochondrial Toxicity?

Carmen de Mendoza 1, Matilde Sánchez-Conde 2, Esteve Ribera 3, Pere Domingo 2, Vicente Soriano 4

1 Puerta de Hierro University Hospital, Madrid, Spain; 2 NULL; 3 Department of Infectious Diseases, Hospital Universitari Vall d’Hebron and Universitat Autònoma de Barcelona, Barcelona, Spain; 4 UNIR Health Sciences School and Medical Center, Universidad Internacional de La Rioja, Madrid, Spain

*Correspondence: Carmen de Mendoza, Email not available

Abstract

Nucleoside reverse transcriptase inhibitors have been proven to inhibit mitochondrial DNA (mtDNA) polymerase gamma, resulting in decreased mtDNA synthesis and consequential risk for the development of mitochondrial dysfunction in HIV-infected individuals. The depletion of mtDNA seems to correlate with the development of symptomatic hyperlactatemia and lipoatrophy. A validated quantitative mitochondrial DNA assay could be useful to monitor and prevent mitochondrial damage in HIV-infected patients, especially in those under antiretroviral therapy with nucleoside analogues. This review analyzes the current methods to determine mitochondrial damage and the available data to support their utility in clinical practice.

Keywords: Mitochondrial DNA. HIV. Nucleoside reverse transcriptase inhibitors. Hyperlactatemia. Lipoatrophy.

Contents

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