RESUMEN
BACKGROUND AND OBJECTIVE: The metabolic syndrome (MS) is linked to an increase of cardiovascular mortality and morbidity, the pathological substrate of cardiovascular events being atherosclerosis. Inflammatory phenomena play a role in the genesis of atherosclerosis. The aim of this study was to analyze the vascular (adhesins) and systemic [interleukins, amyloid A serum protein (AAS), C reactive protein (PCR)] inflammation markers as well as hemodynamic parameters and the presence or absence of subclinical atherosclerosis measured by intima-media thickness (TIM) determination in MS. PATIENTS AND METHOD: In this transversal study we enrolled 29 patients (18 men,11 women) with a diagnosis of MS. We assessed interleukins (IL-1beta, IL-6, TNF-alpha, TGF-beta, MCP-1), intercellular and intervascular adhesions molecules (sICAM-1, sVCAM-1), systemic inflammation markers (PCR, AAS), microalbuminuria and, as a lipidic oxidation marker, urinary F2 isoprostanes (F2I). TIM was measured by ultrasounds. Ten healthy people with a similar age were included as a control group. RESULTS: Patients with MS, when compared with the control group, showed higher levels of homocysteine (10 [0.5] vs 7.9 [0.5] micromol/l; p < 0.05), sICAM1 (263 [13] vs 203 [14] ng/ml; p < 0.01), IL-6 (7.1 [0.5] vs 4.6 [0.6] pg/ml; p < 0.05), TGF-beta (34 [1.7] vs 26 [1.4] ng/ml; p < 0.01), PCR (0.69 [0.07] vs 0.23 [0.03] mg/dl; p < 0.001), AAS (9.7 [0.7] vs 6.7 [0.7] microg/ml; p < 0.01), microalbuminuria (32 [13] vs 3.2 [0.14] mg/g creatinine; p < 0.05), and F2I (22.4 [2.5] vs 9.1 [0.69] pg/mg creatinine; p < 0.001). TIM in the MS group was greater than in the control group (1.14 [0.14] vs 0.79 [0.02] mm; p < 0.05). F2I values were directly correlated with TIM, systolic arterial pressure and pulse pressure. CONCLUSIONS: Our results show that in MS there is an increase of vascular inflammation and lipooxidation markers and a higher prevalence of subclinical atherosclerosis.