*Department of Internal Medicine and Nephrologic Diseases Section of Infectious Diseases University of Bologna S. Orsola-Malpighi Hospital Bologna, Italy †Proteomic Core Facility and Research Group-CIRB University of Bologna S. Orsola-Malpighi Hospital Bologna, Italy
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To the Editor:The increased incidence of cardiovascular diseases in patients with HIV infection has been recently demonstrated1 mostly in subjects with prolonged exposure to protease inhibitors2 or recent administration of some nucleoside analogues, especially abacavir and didanosine.3 An increased risk of cardiovascular complications has been associated in HIV-negative population with elevated circulating levels of adhesion molecules released by the vascular endothelium.4,5 An elevation in plasma levels of endothelial cell-derived markers has been reported also in HIV-positive patients, particularly in subjects with an elevated plasma viral load and a more advanced disease, whereas its association with antiretroviral therapy is still controversial.6-8Aim of our cross-sectional study is to evaluate plasma levels of soluble vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and P-selectin in 99 HIV-infected patients versus 51 HIV-negative healthy individuals.Patients were stratified into the following 3 groups: HIV-positive patients naive to antiretroviral therapy (group A), HIV-positive patients on continued antiretroviral therapy (group B), and HIV-negative controls (group C). Serum concentrations of VCAM-1, ICAM-1, E-selectin, and P-selectin were evaluated by a specific enzyme-linked immunosorbent assay. Subjects with cardiovascular diseases, cerebrovascular diseases, diabetes mellitus, or taking lipid-lowering drugs were excluded from the study.Ninety-nine individuals with HIV-1 infection (50 in group A and 49 in group B) and 51 subjects without HIV infection (group C) participated in this study after providing their written informed consent. All study subjects had been free of any kind of acute illness for the 3 months preceding their participation in the study. In group A, males were 45, their median age was 40 years (range, 32-56 years), the mean CD4 lymphocyte count was 625 cells per cubic millimeter, and the mean HIV viral load was 34,000 copies per milliliter. Forty subjects were smokers (80%), the mean systolic blood pressure was 116 mm Hg, mean low-density lipoprotein (LDL) cholesterol level was 105 mg/dL, and the mean calculated 10-year risk of coronary events (as assessed by the Framingham equation) was 4.7%. In group B, males were 31, their median age was 46 years (range, 31-66 years), the mean CD4 lymphocyte count was 729 cells per cubic millimeter, and plasma HIV RNA was undetectable in 31 subjects. Thirty-one patients were cigarette smokers (63%), their mean systolic blood pressure was 127 mm Hg, mean LDL cholesterol level was 124 mg/dL, and their mean 10-year risk of coronary events was calculated to be 5.6%. All patients enrolled in this group had not changed antiretroviral medications in the preceding 3 months. Concomitant antiretroviral therapy included a protease inhibitor in 23 subjects and a nonnucleoside reverse transcriptase inhibitor in 20 patients; the median overall duration of therapy was 119 months. In group C, males were 38, their median age was 32 years (range, 19-57 years), smokers were 31 (61%), mean systolic blood pressure was 112 mm Hg, mean LDL cholesterol level was 95 mg/dL, and their mean 10-year estimated risk of coronary events was 3.1%.Mean value ± SD of VCAM-1 was 1236.9 ± 760.9 ng/mL in group A, 1496.6 ± 871.4 in group B, and 852.9 ± 627.9 ng/mL in group C (Fig. 1). Plasma levels of VCAM-1 were significantly higher in groups A and B than in group C (P = 0.0495 and P = 0.0004, respectively). Mean value ± SD of ICAM-1 was 700.8 ± 238.5 ng/mL in group A, 687.1 ± 265.1 in group B, and 790.8 ± 270.3 in group C. Plasma levels of ICAM-1 did not differ significantly in all considered groups.