RESUMEN
Stored plasma specimens from 164 participants in the ANRS 138 trial were analyzed to determine interleukin 6 (IL-6), high-sensitivity C-reactive protein (hsCRP), and D-dimer levels at baseline and weeks 24 and 48. These virologically suppressed, treatment-experienced patients were randomly assigned to undergo an immediate switch (IS) or a deferred switch (DS; at week 24) from an enfuvirtide-based antiretroviral therapy (ART) regimen to a raltegravir-based regimen. At week 24, a significant decrease from baseline was observed in the IS arm, compared with the DS arm, for IL-6 level (-30% vs +10%; P < .002), hsCRP level (-46% vs +15%; P < .0001), and D-dimer level (-40% vs +6%; P < .0001). At week 48, there was a reproducible decrease in levels of all biomarkers in the DS arm.
Asunto(s)
Biomarcadores/sangre , Coagulación Sanguínea/efectos de los fármacos , Proteína gp41 de Envoltorio del VIH/uso terapéutico , Infecciones por VIH/tratamiento farmacológico , Inflamación/sangre , Fragmentos de Péptidos/uso terapéutico , Pirrolidinonas/uso terapéutico , Adulto , Fármacos Anti-VIH/uso terapéutico , Proteína C-Reactiva/análisis , Recuento de Linfocito CD4 , Enfuvirtida , Femenino , Productos de Degradación de Fibrina-Fibrinógeno/análisis , Infecciones por VIH/sangre , Infecciones por VIH/virología , VIH-1 , Humanos , Inflamación/virología , Interleucina-6/sangre , Masculino , Persona de Mediana Edad , ARN Viral/sangre , Raltegravir Potásico , Manejo de Especímenes , Carga ViralRESUMEN
BACKGROUND: Cardiovascular events have been reported among HIV-infected patients following antiretroviral therapy. However, the role of HIV itself in determining vascular damage is less described. Chronic inflammatory state might impair some regulatory endothelium properties leading to its activation, apoptosis or erosion. OBJECTIVES: To evaluate the balance between endothelial progenitor cells and microparticles in HIV-infected antiretroviral drug-naive patients. DESIGN: A case-control study comparing HIV-infected patients (n = 35) with sex-matched and age-matched healthy controls (n = 33). METHODS: Endothelial progenitor cells populations expressing CD34, CD133 and KDR were quantified by flow cytometry. Endothelial-derived microparticles, expressing CD51, and platelet-derived microparticles, expressing CD31/CD42, were also measured. Endothelial function was estimated by flow-mediated dilation. RESULTS: Lower percentages of endothelial progenitor cells (CD34/KDR) were observed in HIV-infected individuals compared with controls (0.02 vs. 0.09%, P = 0.045). In addition, endothelial microparticles concentration was higher in HIV-infected individuals (1963 vs. 436 microparticles/µl platelet-poor plasma, P = 0.003), with similar number of platelet-derived microparticles among groups. Furthermore, flow-mediated dilation was lower among HIV-infected individuals compared with controls [mean (SEM): 10 (1) and 16% (2), respectively; P = 0.03]. CONCLUSION: Our findings suggest an imbalance between endothelial progenitor cells mobilization and endothelial apoptosis. The alteration in the turnover of endothelial cells may contribute to cardiovascular events in HIV-infected patients.