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DNA changes no indicator of mitochondrial toxicity in HIV patients
  NEW YORK (Reuters Health) - Measuring mitochondrial DNA (mtDNA) in peripheral blood mononuclear cells (PBMCs) is not an effective way to gauge mitochondrial dysfunction in HIV patients with lipoatrophy from exposure to nucleoside analogs, Australian researchers report in the August 15th issue of the Journal of Infectious Diseases.
Nucleoside reverse-transcriptase inhibitors (NRTIs) have a wide variety of adverse side effects, including a decrease in peripheral subcutaneous fat, and mitochondrial toxicity has been proposed as the mechanism behind such adverse effects, Dr. Jennifer F. Hoy of Alfred Hospital in Melbourne, and colleagues note.
The researchers had conducted a 24-week study to determine whether switching HIV-infected patients from stavudine or zidovudine to abacavir would reverse lipoatrophy without compromising virological control. They did find small increases in subcutaneous peripheral fat in patients switched to abacavir.
The team then launched a substudy to determine whether an assay they had developed would identify an increase in PBMC mtDNA content accompanying the improvements in lipoatrophy. However, no such association was found. MtDNA levels were also not tied to venous lactate levels -- another test of mitochondrial dysfunction.
These findings, the researchers conclude, corroborate those of other reports that indicate that measurement of mtDNA in PBMCs "does not differentiate individuals on the basis of proposed mitochondrial dysfunction resulting in lipodystrophy."
J Infect Dis 2004;190:688-692.


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