Conclusions
The major mechanism in which PI-mediated was triggering atherogenesis could be through alteration of lipid metabolism and endothelial function, but no evidence of accelerated pro-inflammatory response was attested.
Results
Compared with non-PI, patients in the boosted-PI group had more evidence of dyslipidemia. No statistical difference in the prevalence of subclinical atherosclerosis was found between the two groups. Circulating levels of inflammatory markers, C-reactive protein (CRP) (5.4±9.1 vs. 14.9 ± 19.4 mg/L, p = 0.019) and lectin-liked oxidized lipoprotein receptor-1 (LOX-1) (387 ± 299 vs. 554 ± 324 pg/mL, p = 0.042) were lower in boosted-PI group. Contrastingly, Vascular adhesion molecules-1 (VCAM-1) (160.2 ± 80.0 vs. 147.8 ± 66.3 ng/mL, p = 0.010), and osteoprotegerin (OPG) (153.7 ± 57.1 vs. 126.4 ± 35.8, p = 0.031) were higher. After adjustment in the multivariate analysis, PI treatment is the only independent parameter associated with the changes of CRP, LOX-1, VCAM-1, and OPG. Subgroup analysis showed that ARV treatment effects differed among participant having dyslipidemia. Conclusions: The major mechanism in which PI-mediated was triggering atherogenesis could be through alteration of lipid metabolism and endothelial function, but no evidence of accelerated pro-inflammatory response was attested.