[Biomarkers of vascular inflammation and subclinical atherosclerosis in the metabolic syndrome].
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.


METHODS
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.
Gómez-Fernández
Pablo
P
Sección de Nefrología, Servicio de Bioquímica y Radiodiagnóstico, Hospital General, Jerez, Cádiz, España. pgomezf@senefro.org
Eady Alonso
Miriam
M
Ruiz
Asunción
A
Conde Lozano
M Rosario
MR
Sánchez-Margalet
Víctor
V
Almaraz Jiménez
Miguel
M
D001161:Arteriosclerosis / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood*; D001774:Blood Chemical Analysis; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008875:Middle Aged; D012044:Regression Analysis
D015415:Biomarkers; D016207:Cytokines