Mitochondrial DNA copy number in peripheral blood mononuclear cells from patients with lipoatrophy randomized to a non-thymidine analogue containing regimen

Jennifer Hoy, Michelle Gahan, Andrew Carr, Don Smith, Sharon Lewin, Steve Wesselingh, David Cooper

Research output: Contribution to journalArticle

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Abstract

It has been suggested that lipoatrophy associated with exposure to nucleoside analogues is caused by depletion of mitochondrial DNA (mtDNA). The aim of the present study was to determine whether switching treatment from a thymidine analogue to abacavir was associated with an increase in the mtDNA copy number in peripheral blood mononuclear cells (PBMCs). Of 111 patients with lipoatrophy who were randomized to have treatment switched to abacavir or to continue treatment with thymidine analogues, 94 patients had PBMCs obtained at baseline and at weeks 4, 12, and 24, for quantification of the mtDNA copy number. During the 24-week study, there was no significant change in mtDNA copy numbers in PBMCs in either treatment group, despite improvement in peripheral lipoatrophy among patients whose treatment was switched to abacavir
Original languageEnglish
Pages (from-to)688-692
Number of pages5
JournalJournal of Infectious Diseases
Volume190
Issue number4
Publication statusPublished - 2004
Externally publishedYes

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Mitochondrial DNA
Blood Cells
Thymidine
Therapeutics
Nucleosides
abacavir

Cite this

Hoy, Jennifer ; Gahan, Michelle ; Carr, Andrew ; Smith, Don ; Lewin, Sharon ; Wesselingh, Steve ; Cooper, David. / Mitochondrial DNA copy number in peripheral blood mononuclear cells from patients with lipoatrophy randomized to a non-thymidine analogue containing regimen. In: Journal of Infectious Diseases. 2004 ; Vol. 190, No. 4. pp. 688-692.
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abstract = "It has been suggested that lipoatrophy associated with exposure to nucleoside analogues is caused by depletion of mitochondrial DNA (mtDNA). The aim of the present study was to determine whether switching treatment from a thymidine analogue to abacavir was associated with an increase in the mtDNA copy number in peripheral blood mononuclear cells (PBMCs). Of 111 patients with lipoatrophy who were randomized to have treatment switched to abacavir or to continue treatment with thymidine analogues, 94 patients had PBMCs obtained at baseline and at weeks 4, 12, and 24, for quantification of the mtDNA copy number. During the 24-week study, there was no significant change in mtDNA copy numbers in PBMCs in either treatment group, despite improvement in peripheral lipoatrophy among patients whose treatment was switched to abacavir",
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Mitochondrial DNA copy number in peripheral blood mononuclear cells from patients with lipoatrophy randomized to a non-thymidine analogue containing regimen. / Hoy, Jennifer; Gahan, Michelle; Carr, Andrew; Smith, Don; Lewin, Sharon; Wesselingh, Steve; Cooper, David.

In: Journal of Infectious Diseases, Vol. 190, No. 4, 2004, p. 688-692.

Research output: Contribution to journalArticle

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T1 - Mitochondrial DNA copy number in peripheral blood mononuclear cells from patients with lipoatrophy randomized to a non-thymidine analogue containing regimen

AU - Hoy, Jennifer

AU - Gahan, Michelle

AU - Carr, Andrew

AU - Smith, Don

AU - Lewin, Sharon

AU - Wesselingh, Steve

AU - Cooper, David

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AB - It has been suggested that lipoatrophy associated with exposure to nucleoside analogues is caused by depletion of mitochondrial DNA (mtDNA). The aim of the present study was to determine whether switching treatment from a thymidine analogue to abacavir was associated with an increase in the mtDNA copy number in peripheral blood mononuclear cells (PBMCs). Of 111 patients with lipoatrophy who were randomized to have treatment switched to abacavir or to continue treatment with thymidine analogues, 94 patients had PBMCs obtained at baseline and at weeks 4, 12, and 24, for quantification of the mtDNA copy number. During the 24-week study, there was no significant change in mtDNA copy numbers in PBMCs in either treatment group, despite improvement in peripheral lipoatrophy among patients whose treatment was switched to abacavir

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