2023
DOI: 10.3390/pathogens12070925
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Evaluation of Lipid Profile and Intima Media Thickness in Antiretroviral-Experienced HIV-Infected Patients Treated with Protease Inhibitor-Based Regimens versus Protease Inhibitor-Sparing Regimens

Salvatore Martini,
Mariantonietta Pisaturo,
Antonio Russo
et al.

Abstract: Background: Antiretroviral therapy has increasingly improved management of HIV infection, ensuring long-term efficacy and tolerability. Each class of antiretrovirals has, however, different characteristics and different tolerability profiles. The literature data show that protease inhibitors (PIs) are associated with a higher incidence of dyslipidemia. The aim of our study was to evaluate whether patients treated with PIs have both greater dyslipidemia and increased intima media thickness (IMT) and atheromatou… Show more

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Cited by 4 publications
(4 citation statements)
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“…Only 30% of subjects treated with PI were receiving a ritonavir-containing regimen at baseline. In our recent study, we evaluated the lipid profile and cIMT in antiretroviral-experienced HIV-positive patients treated with PI-based versus PI-sparing regimens [13]. Our real-life data show that patients treated with PI have a tendency to develop both increased dyslipidemia and increased pathological IMT and atheromatous plaques.…”
Section: Discussionmentioning
confidence: 99%
“…Only 30% of subjects treated with PI were receiving a ritonavir-containing regimen at baseline. In our recent study, we evaluated the lipid profile and cIMT in antiretroviral-experienced HIV-positive patients treated with PI-based versus PI-sparing regimens [13]. Our real-life data show that patients treated with PI have a tendency to develop both increased dyslipidemia and increased pathological IMT and atheromatous plaques.…”
Section: Discussionmentioning
confidence: 99%
“…In general, PI-based regimens have a trend to develop greater atherosclerosis compared to non-PI-based regimens, as demonstrated by the increase in the intima media thickness (IMT) and the development of atheromatous plaques. More specifically, PIs inhibit lipolysis by altering lipoprotein lipase (LPL) activity, resulting in reduced TG uptake in adipocytes and elevated plasma TG levels [72,73]. Furthermore, they inhibit the nuclear localization of sterol response element binding protein-1 (SREBP-1) in adipocytes, resulting in the downregulation of PPARγ, impaired adipocyte differentiation, and insufficient lipid removal from circulation, while concomitantly promoting the nuclear localization of SREBP-1 in hepatocytes, resulting in excessive fatty acids synthesis [74,75].…”
Section: Protease Inhibitorsmentioning
confidence: 99%
“…In contrast, PIs are generally considered to have unfavorable effects in terms of cardiovascular risk. The mechanisms responsible include the triggering of reactive oxygen species production, impaired mitochondrial function, and ubiquitin-proteasome system dysregulation, factors that can in turn initiate transcriptional changes that contribute to the perturbation of lipid metabolism [ 124 ].…”
Section: Modifiable Cvd Risk Factors In Plwhmentioning
confidence: 99%