The impact of metabolic syndrome and CRP on vascular phenotype in type 2 diabetes mellitus

article







Alizadeh Dehnavi, R.

Beishuizen, E.D.

Ree, M.A. van de

Le Cessie, S.

Huisman, M.V.

Kluft, C.

Princen, H.M.G.

Tamsma, J.T.
Background: The burden of cardiovascular disease in diabetes mellitus type 2 (DM2) patients is variable. We hypothesize that metabolic syndrome (MS) and low-grade systemic inflammation modify the extent of atherosclerosis in DM2. Methods: Vascular phenotype was determined using the following endothelium-related, hemostatic, and sonographic endpoints in 62 DM2 patients with mild dyslipidemia: sVCAM, sE-selectin, von Willebrand factor (VWF), fibrinogen, s-thrombomodulin (sTM), tPA, PAI-1, flow-mediated dilation (FMD), and intima media thickness (IMT). The impact of MS load (number of criteria present), MS components, and CRP on these parameters was assessed. Results: Serum sVCAM, sTM, and tPA levels significantly increased with increasing MS load. IMT also significantly increased from 0.602 ± 0.034 (one MS criterion) to 0.843 ± 0.145 (four MS criteria, p = 0.007). LogCRP significantly correlated with fibrinogen, PAI-1, and IMT. In a multiple regression (MR) model with age and gender as covariates, MS load predicted sVCAM and sTM; CRP predicted PAI-1 and fibrinogen; MS load and CRP simultaneously predicted tPA and IMT. For each MS criterion present, IMT significantly increased by 0.04 mm. An increase in CRP from 1 to 3 mg/L resulted in a significant increase of 0.04 mm. Patients with four MS criteria and inflammation (CRP ≥ 3 mg/L) are predicted to have a 0.21 mm thicker IMT than those without. A second stepwise MR analysis based on gender, traditional risk factors, diabetes-related parameters, renal function, individual MS criteria, and LogCRP as explanatory variables showed a significant effect of systolic and diastolic blood pressure, HDL, and LogCRP on IMT(r2 = 0.36, p < 0.001). Conclusion: MS and low-grade chronic inflammation have an independent impact on vascular phenotype including IMT in DM2. © 2007 European Federation of Internal Medicine.

Chemicals / CAS: C reactive protein, 9007-41-4; endothelial leukocyte adhesion molecule 1, 128875-25-2; fibrinogen, 9001-32-5; plasminogen activator inhibitor 1, 140208-23-7; thrombomodulin, 112049-68-0; tissue plasminogen activator, 105913-11-9; von Willebrand factor, 109319-16-6; Biological Markers; C-Reactive Protein, 9007-41-4; E-Selectin; Fibrinogen, 9001-32-5; Plasminogen Activator Inhibitor 1; Thrombomodulin; Tissue Plasminogen Activator, EC 3.4.21.68; Vascular Cell Adhesion Molecule-1; von Willebrand Factor
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C-reactive proteinDiabetes mellitus type 2Endothelial functionIntima media thicknessMetabolic syndromePAI-1C reactive proteinendothelial leukocyte adhesion molecule 1fibrinogenhigh density lipoproteinplasminogen activator inhibitor 1thrombomodulintissue plasminogen activatorvascular cell adhesion molecule 1von Willebrand factoradultagedarterial wall thicknessarticleatherosclerosischolesterol blood leveldiastolic blood pressuredyslipidemiafemalehumankidney functionmajor clinical studymalemetabolic syndrome Xnon insulin dependent diabetes mellitusphenotyperisk factorsex differencesystolic blood pressureAgedBiological MarkersC-Reactive ProteinDiabetes Mellitus, Type 2E-SelectinFemaleFibrinogenHumansInflammationMaleMetabolic Syndrome XMiddle AgedPhenotypePlasminogen Activator Inhibitor 1ThrombomodulinTissue Plasminogen ActivatorTunica IntimaTunica MediaVascular Cell Adhesion Molecule-1von Willebrand Factor
TNO Identifier
240693
Repository link
https://resolver.tno.nl/uuid:7d7b556c-e0cc-421f-bba4-c9049a9d3d17
ISSN
09536205
Source
European Journal of Internal Medicine, 19(2), pp. 115-121.
Pages
115-121
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