Endothelial Progenitors Cells and Microparticles in HIV-infected patients

Background: HIV infection is an inflammatory disease and can cause endothelial disfunction and increases the cardiovascular risk. It plays a critical role in coronary artery disease, but the assessment of the endothelial disfunction has been problematical. Exposure to cardiovascular risk factors alters the regulatory functions of the endothelium that progresses from a quiescent state to activation, apoptosis and death. Recently, it has been shown that endothelial cells (EC) release microparticles (MP) on activation or apoptosis and that evaluation of MP can provide useful information on EC status in patients with an increased cardiovascular risk. Identification of circulating endothelial cells and microparticles has raised considerable interest as non-invasive markers of vascular disfunction. Methods: We studied these new markers of cardiovascular risk, as endothelial progenitors cells and microparticles in HIV-infected naive patients and compared with HIV negative controls matched for age and sex.Standard laboratory study included: lipid profile, glycaemia, C-reactive protein and apolipoprotein B. The endothelial progenitors (EPC) cells and microparticles (MP) were measure by flow citometry. The EPC were identified using the following markers: CD34+ (surface protein), KDR (vascular endothelial growth receptor 2) for definition and CD133+ for immature lineage cells. The MP were characterized with CD31+ (MP platelet and endothelial derived), CD42+ (MP platelet derived) and CD51+ (MP endothelial derived). Results: Thirty patients were included, 15 in each group, 73,3% were male with mean age 30,9 years. The lipid profile was significant only in the HDL-c and LDL-c between the groups. In the HIV-infected group we observed 0,01% of CD34+/KDR+ and it was not isolated CD34+/CD133+ neither CD133+/KDR+. In this group it was also observed more release of MP CD51+ and CD31+/CD42+ comparing to the control group, any MP CD31+/CD42- were found. Conclusion: Our results suggest a possible imbalance between EPC and MP. This new finding in HIV-naive patient may be associated with increased cardiovascular disease in the long term follow-up of these patients, and can be aggravated after antiretroviral therapy. Abstracts for SupplementInternational Journal of Infectious DiseasesVol. 14Preview Full-Text PDF Open Archive