title: Low-grade inflammation, endothelial activation and carotid intima-media thickness in type 2 diabetes.
abstract: OBJECTIVE
  The objective of this study was to assess the relationship between inflammation, endothelial activation and incipient atherosclerosis in type 2 diabetes.
  
  
  METHODS
  Cross-sectional study. Setting and subjects. We studied 239 type 2 diabetic patients [71 with clinical cardiovascular disease (CVD)] and 78 healthy control subjects, aged 50-75 in a single research centre.
  
  
  METHODS
  Carotid intima-media thickness (IMT) was determined by ultrasound. Circulating intracellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, ultra-sensitive C-reactive protein, human serum amyloid A, interleukin-6, monocyte colony-stimulating factor, secretory nonpancreatic phospholipase A(2) type IIA, glucose, HbA1c, and lipid/lipoprotein variables were measured.
  
  
  RESULTS
  Carotid IMT was significantly thicker in diabetic patients than healthy controls across the whole age range. IMT was also thicker in diabetic patients with, than without, CVD, but this difference disappeared after controlling for confounding factors. Concentrations of the inflammatory and endothelial markers except IL-6 were significantly higher in the diabetic patients than in healthy controls, but comparable in diabetic patients with and without CVD. The main determinants of IMT in the diabetic patients were blood pressure, age and diabetes duration.
  
  
  CONCLUSIONS
  Low-grade inflammation and endothelial activation are increased in diabetic patients but do not associate with IMT or clinical CVD. The inflammatory reaction seems to be rather a feature of the metabolic syndrome than a direct determinant of atherosclerosis.
authors.affiliation: Department of Medicine, Division of Cardiology, University of Helsinki, Helsinki, Finland.
authors.forename: E S
authors.initials: ES
authors.lastname: Leinonen
authors.forename: A
authors.initials: A
authors.lastname: Hiukka
authors.forename: E
authors.initials: E
authors.lastname: Hurt-Camejo
authors.forename: O
authors.initials: O
authors.lastname: Wiklund
authors.forename: S S
authors.initials: SS
authors.lastname: Sarna
authors.forename: L
authors.initials: L
authors.lastname: Mattson Hultén
authors.forename: J
authors.initials: J
authors.lastname: Westerbacka
authors.forename: R M
authors.initials: RM
authors.lastname: Salonen
authors.forename: J T
authors.initials: JT
authors.lastname: Salonen
authors.forename: M-R
authors.initials: MR
authors.lastname: Taskinen
mesh_terms: D000367:Age Factors; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000473:pathology*; D003925:Diabetic Angiopathies / Q000097:blood / Q000473:pathology*; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000032:analysis; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology; D014463:Ultrasonography; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015415:Biomarkers; D019040:E-Selectin; D015850:Interleukin-6; D000685:Serum Amyloid A Protein; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein