Enrique Bernal, Jose Saban, Angeles Munoz, Irene Marin, Ana Garcia-Medina, Tomas Vicente and Alfredo Cano
Although HIV and antiretroviral therapy (ART) have been linked with an increased cardiovascular risk, the pathological pathways remain unknown. We assessed whether secretory phospholipase A2 (sPLA2), high-sensitivity C-reactive protein (hs-CRP), vascular cell adhesion molecule (VCAM), thiobarbituric acid reactive species (TBARS), Superoxide dismutases (SOD), adiponectin and resistin were elevated in HIV infected patients with detectable and undetectable viral load compared to a control group matched for age, sex and cardiovascular risk factors. We evaluated its correlation with traditional and no traditional cardiovascular risk factors and carotid intima-media thickness. Levels of sPLA2 (median [IQR]) were 8.35 (5.36, 9.6) pg/ml, hsCRP were 3.3 (IQR, 1.27, 5.28) mg/L, VCAM 945.6 (IQR, 655.9, 1404.05) ng/ml and TBARS 1.69 (IQR, 1.39, 1.97) uM/L in HIV infected group compared to levels of sPLA2 1.22 (IQR, 0.69, 2.62) pg/ml (p<0.001), hsCRP 3.05 (IQR, 2.68, 3.27) mg/L (p=0.05), VCAM 678.35 (IQR, 530.39, 831.04) ng/ml (p<0.001) and TBARS 7.47 (IQR, 5.03, 10.4) uM/L (p<0.001) in control group. Levels of VCAM (median [IQR]) were 1047.19 (IQR, 609.06, 1084.1) ng/ml (p=0.015) and sPLA2 were 7.6 (IQR, 5.25, 9.6) pg/ml (p<0.001) in HIV infected patients with undetectable viral load compared to control group. There was a good correlation between all analyzed biomarkers and cardiovascular risk factors. In conclusion, HIV infection induces chronic inflammation and endothelial activation that is not completely suppressed by the treatment.
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