4.0 Article

Effects of pitavastatin on atherosclerotic-associated inflammatory biomarkers in people living with HIV with dyslipidemia and receiving ritonavir-boosted atazanavir: a randomized, double-blind, crossover study

Journal

AIDS RESEARCH AND THERAPY
Volume 20, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12981-023-00506-2

Keywords

Atherosclerosis; Dyslipidemia; HIV infection; Inflammatory biomarker; Pitavastatin

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This study aimed to investigate the effect of pitavastatin on atherosclerotic-associated inflammatory biomarkers in HIV-infected individuals receiving antiretroviral therapy. The results showed that pitavastatin treatment increased basic fibroblast growth factor levels and decreased the percentages of HLA-DR(+)CD38(-)CD4(+) T cells and PD1(+)CD4(+) T cells. Further research on the role of pitavastatin in preventing cardiovascular diseases in HIV-infected individuals should be pursued.
BackgroundChronic inflammation has been described in people living with HIV (PLHIV) receiving antiretroviral therapy (ART) despite viral suppression. Inflammation associated non-communicable diseases, including atherosclerosis, are becoming recognized complication of HIV infection. We studied the effect of pitavastatin on atherosclerotic-associated inflammatory biomarkers in PLHIV receiving ART.MethodsA randomized, double-blind, crossover study was conducted in HIV-infected persons with dyslipidemia and receiving atazanavir/ritonavir (ATV/r) to evaluate the effect of 2 mg/day pitavastatin treatment versus placebo. High-sensitivity CRP (hs-CRP), cytokines, and cellular markers in PLHIV receiving 12 weeks of pitavastatin or placebo were investigated.ResultsA total of 24 HIV-infected individuals with a median (interquartile range) age of 46 (41-54) years were recruited, and the median CD4 T cell count was 662 (559-827) cells/mm(3). The median duration of ATV/r use was 36 (24-48) months. Significant change in levels of basic fibroblast growth factor (FGF) between pitavastatin treatment and placebo at week 12 from baseline was observed (27.1 vs. 20.5 pg/mL; p=0.023). However, there were no significant changes from baseline of hs-CRP and other plasma cytokine levels at week 12 of pitavastatin or placebo. Regarding cellular markers, percentages of HLA-DR(+)CD38(-)CD4(+) T cells and PD1(+)CD4(+) T cells significantly decreased from baseline in PLHIV receiving pitavastatin for 12 weeks, as compared to placebo (- 0.27 vs. 0.02%; p=0.049 and - 0.23 vs. 0.23%; p=0.022, respectively).ConclusionsPitavastatin treatment increases basic FGF levels, and lowers HLA-DR(+)CD38(-)CD4(+) T cells, and PD1(+)CD4(+) T cells. Further study on the effects of pitavastatin on preventing cardiovascular diseases in PLHIV should be pursued.

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