title: Soluble interleukin-2 receptor as a marker for progression of coronary artery calcification in type 1 diabetes.
abstract: BACKGROUND
  Soluble interleukin-2 receptor (sIL2r), a marker of T cell activation, is elevated in inflammatory processes, such as rheumatoid arthritis, hepatitis and neoplasm. We explored a potential association between plasma sIL2r levels and progression of coronary artery calcification (CAC), a marker for subclinical atherosclerosis, in a prospectively followed cohort of type 1 diabetic and non-diabetic subjects, aged 20-59 years, with no history of coronary artery disease.
  
  
  METHODS
  CAC progression was assessed by electron beam tomography over 2.6 years (range 1.6-3.2). Plasma sIL2r levels were measured in a nested case-control substudy of 98 subjects (67 diabetic, 31 non-diabetic) with and 173 subjects (84 diabetic, 89 non-diabetic) without significant CAC progression. Log-transformed sIL2r levels were analyzed by conditional logistic regression to compare subjects with and without significant CAC progression.
  
  
  RESULTS
  SIL2r was a significant predictor for CAC progression after adjusting for presence of baseline CAC, age, gender, diabetes status, baseline calcium volume score and adiponectin (OR 1.99, 95% CI 1.09-3.61, p = 0.02 for a doubling of sIL2r level). Addition of BMI, LDL, HDL, hypertension, smoking status, HbA1c, CRP, fibrinogen, homocysteine and PAI-1 to regression models weakened but did not remove sIL2r as a predictor of CAC progression. There was no indication that this effect was different by diabetes status (p = 0.6 for diabetes-sIL2r interaction).
  
  
  CONCLUSIONS
  Elevated plasma sIL2r is associated with CAC progression independent of traditional coronary artery disease risk factors in type 1 diabetic and non-diabetic young adults. SIL2r should be considered as a novel marker of inflammation leading to coronary artery disease.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Aurora, 80045, USA. Paul.Wadwa@uchsc.edu
authors.forename: R Paul
authors.initials: RP
authors.lastname: Wadwa
authors.forename: Gregory L
authors.initials: GL
authors.lastname: Kinney
authors.forename: Lorraine
authors.initials: L
authors.lastname: Ogden
authors.forename: Janet K
authors.initials: JK
authors.lastname: Snell-Bergeon
authors.forename: David M
authors.initials: DM
authors.lastname: Maahs
authors.forename: Elaine
authors.initials: E
authors.lastname: Cornell
authors.forename: Russell P
authors.initials: RP
authors.lastname: Tracy
authors.forename: Marian
authors.initials: M
authors.lastname: Rewers
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D015415:Biomarkers / Q000097:blood*; D002114:Calcinosis / Q000097:blood / Q000473:pathology*; D016022:Case-Control Studies; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000209:etiology* / Q000473:pathology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications*; D003925:Diabetic Angiopathies / Q000175:diagnosis* / Q000473:pathology; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000097:blood*
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D015375:Receptors, Interleukin-2