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Randomized Controlled Trial
. 2023 Feb 27;20(1):13.
doi: 10.1186/s12981-023-00506-2.

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

Sirawat Srichatrapimuk  1 , Artit Wongsa  2 , Somnuek Sungkanuparph  1 , Sasisopin Kiertiburanakul  3 , Boonrat Tassaneetrithep  2 , Angsana Phuphuakrat  4
Affiliations
Randomized Controlled Trial

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

Sirawat Srichatrapimuk et al. AIDS Res Ther. .

Abstract

Background: Chronic 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.

Methods: A 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.

Results: A 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/mm3. 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).

Conclusions: Pitavastatin 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.

Keywords: Atherosclerosis; Dyslipidemia; HIV infection; Inflammatory biomarker; Pitavastatin.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Flowchart of subjects in the randomized crossover trial
Fig. 2
Fig. 2
Inflammatory markers that revealed significant difference of changes from baseline to week 12 of pitavastatin vs. placebo in PLHIV receiving ritonavir-boosted atazanavir; (A) basic FGF, (B) HLA-DR+CD38-CD4+ T cells, (C) PD-1+CD4+ T cells. Y axis shows median change from the baseline
See this image and copyright information in PMC

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