Assessment of Biomarkers of Cardiovascular Risk Among HIV Type 1-Infected Adolescents: Role of Soluble Vascular Cell Adhesion Molecule As an Early Indicator of Endothelial Inflammation

Abstract

Cardiovascular disease (CVD) biomarkers were examined in a cohort of HIV-infected and HIV-uninfected adolescents who participated in Adolescent Trials Network study 083 utilizing samples from the Reaching for Excellence in Adolescent Care cohort, a longitudinal study of youth infected through adult risk behavior. Nonfasting blood samples from 97 HIV-infected and 81 HIV-uninfected adolescents infected by adult risk behaviors were analyzed for total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), very low-density lipoprotein (VLDL), triglycerides, apolipoprotein A-I, high-sensitivity C-reactive protein (hsCRP), soluble vascular adhesion molecule-1 (sVCAM-1), myeloperoxidase, and neopterin at baseline and 18 months later. Results were analyzed using ANOVA, Wilcoxon signed-rank, and paired t tests. Among infected subjects 67 received antiretroviral therapy and 30 were treatment naive. The HIV-infected and HIV-uninfected subjects were similar in gender, ethnicity, and cardiovascular risk factors such as smoking and obesity. In all groups lipid parameters were within accepted guidelines for cardiovascular risk. Among HIV-infected youth on antiretroviral therapy (ART), HDL and apoprotein A-I were significantly lower when compared to uninfected youth. hsCRP was not elevated and thus not predictive for risk in any group. sVCAM-1 levels were significantly elevated in both HIV-infected groups: 1,435 ng/ml and 1,492 ng/ml in untreated and treated subjects, respectively, and 1,064 ng/ml in the uninfected group (p<0.0001). Across all groups neopterin correlated with sVCAM at 18 months (Spearman correlation coefficient 0.58, p<0.0001). Only 9% of ART-treated subjects fully suppressed virus. Lipid profiles and hsCRP, traditional markers of cardiovascular disease, are not abnormal among HIV-infected youth but elevated sVCAM may be an early marker of atherosclerosis.

Serum activities of oxidative burst enzymes in HIV infected subjects

“…This study assesses the activities of respiratory burst enzymes in order to ascertain if HAART impacts negatively or otherwise on these enzymes in HIV positive subjects on these drugs. It was observed from this study that there were significantly higher (p < 0.001) activities of CAT and myeloperoxidase in HIV positive subjects on HAART than HIV positive HAART naïve subjects, which was consistent with previous studies [22]. It was reported that myeloperoxidase activity was significantly higher in HIV infected subjects on HAART than HAART naïve subjects [22].…”

“…It was observed from this study that there were significantly higher (p < 0.001) activities of CAT and myeloperoxidase in HIV positive subjects on HAART than HIV positive HAART naïve subjects, which was consistent with previous studies [22]. It was reported that myeloperoxidase activity was significantly higher in HIV infected subjects on HAART than HAART naïve subjects [22]. But Ross et al [23] observed elevated myeloperoxidase activity in HIV infected adults both on HAART and HAART naïve.…”

“…on HAART and HAART naïve subjects [22]. The data from our study may be due to immune-activation, inflammation and opportunistic infection in HIV infections.…”

Albuminuria Is Associated with Elevated Acute Phase Reactants and Proinflammatory Markers in HIV-Infected Patients Receiving Suppressive Combination Antiretroviral Therapy

“…38 In the HIV population, VCAM-1 was significantly elevated in both HIV-infected adolescents who received antiretroviral therapy and who were treatment naive. 39 Other studies showed higher VCAM-1 and E-selectin levels in adult HIV patients with and without treatment, 40,41 and they were a potential marker of disease progression and death. 42,43 Recently, VCAM-1 was found to be associated with greater carotid intima media thickness in another study from our group.…”

The Influence of Nonalcoholic Fatty Liver Disease on the Platelet Hemostasis and Endothelial Function State in Patients with Stable Coronary Heart Disease

“…У свою чергу, активація тромбоцитів пов'язана з ендоте-ліальною дисфункцією та в подальшому -з ремо-делюванням судинної стінки [2]. Зокрема, збіль-шення рівня молекул адгезії сприяє проникненню лейкоцитів у судинну стінку та накопиченню в ній ліпідів, що відображає ступінь пошкодження ендо-теліальних клітин і порушення мікроциркуляції в тканинах [9,17]. Це викликає розвиток ендотеліаль-ної дисфункції, яка вважається одним із чинників розвитку ІХС.…”