Chakri Naruebodindra Medical Institute, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Samut Prakan, Thailand.
Center of Research Excellence in Immunoregulation, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
AIDS Res Ther. 2023 Feb 27;20(1):13. doi: 10.1186/s12981-023-00506-2.
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.
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.
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/mm. 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-DRCD38CD4 T cells and PD1CD4 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).
Pitavastatin treatment increases basic FGF levels, and lowers HLA-DRCD38CD4 T cells, and PD1CD4 T cells. Further study on the effects of pitavastatin on preventing cardiovascular diseases in PLHIV should be pursued.
尽管接受抗逆转录病毒疗法（ART）的艾滋病毒感染者（PLHIV）病毒得到抑制，但仍存在慢性炎症。与炎症相关的非传染性疾病，包括动脉粥样硬化，已成为 HIV 感染的公认并发症。我们研究了匹伐他汀对接受 ART 的 PLHIV 中与动脉粥样硬化相关的炎症生物标志物的影响。
在患有血脂异常且接受阿扎那韦/利托那韦（ATV/r）治疗的 HIV 感染者中进行了一项随机、双盲、交叉研究，以评估 2 毫克/天匹伐他汀治疗与安慰剂的疗效。研究了接受 12 周匹伐他汀或安慰剂治疗的 PLHIV 中的高敏 C 反应蛋白（hs-CRP）、细胞因子和细胞标志物。
共招募了 24 名中位（四分位间距）年龄为 46（41-54）岁的 HIV 感染者，中位 CD4 T 细胞计数为 662（559-827）个/mm。ATV/r 的中位使用时间为 36（24-48）个月。与基线相比，在第 12 周时，匹伐他汀治疗与安慰剂治疗之间的碱性成纤维细胞生长因子（FGF）水平有显著变化（27.1 与 20.5 pg/mL；p=0.023）。然而，在第 12 周时，hs-CRP 和其他血浆细胞因子水平与基线相比没有显著变化。关于细胞标志物，与安慰剂相比，接受 12 周匹伐他汀治疗的 PLHIV 中 HLA-DRCD38CD4 T 细胞和 PD1CD4 T 细胞的百分比从基线显著下降（-0.27 与 0.02%；p=0.049 和-0.23 与 0.23%；p=0.022）。
匹伐他汀治疗可增加碱性 FGF 水平，并降低 HLA-DRCD38CD4 T 细胞和 PD1CD4 T 细胞。应进一步研究匹伐他汀对预防 PLHIV 心血管疾病的作用。
