title: Endothelial dysfunction and low-grade inflammation and the progression of retinopathy in Type 2 diabetes.
abstract: OBJECTIVE
  To study whether microalbuminuria, endothelial dysfunction and low-grade inflammation are associated with the presence and progression of diabetic retinopathy.
  
  
  METHODS
  Patients with Type 2 diabetes (n = 328) attending a diabetes clinic were followed for 10 years and examined annually during the last 7 years. Retinopathy was assessed after pupillary dilatation by direct ophthalmoscopy (baseline) and two-field 60 degrees fundus photography (follow-up). Urinary albumin excretion, and markers of endothelial function (von Willebrand factor, tissue-type plasminogen activator, soluble E-selectin (sE-selectin), and soluble vascular cell adhesion molecule 1) and inflammatory activity (C-reactive protein and fibrinogen) were determined.
  
  
  RESULTS
  The prevalence of retinopathy was 33.8%. The median diabetes duration at baseline was 7 years (interquartile range 2-12 years). The highest tertiles of baseline urinary albumin excretion and glycated haemoglobin (HbA(1c)) were associated with prevalent retinopathy: odds ratio (OR) 95% confidence interval (CI) 2.80 (1.44-5.46) and 2.19 (1.11-4.32), respectively. Progression of retinopathy occurred in 188 patients. The second and third tertiles of baseline sE-selectin were associated with progression of retinopathy [1.44 (1.04-2.01) and 1.61 (1.19-2.18)] but not independently of HbA(1c). None of the other markers was significantly associated with the presence or progression of retinopathy. High baseline HbA(1c) was significantly associated with progression of retinopathy: 1.65 (1.21-2.25).
  
  
  CONCLUSIONS
  In this population of patients with Type 2 diabetes who attended a diabetes clinic, there was some evidence for a role of endothelial dysfunction in the progression of retinopathy. We could not demonstrate a role for low-grade inflammation. Our study emphasizes the importance of glycaemic control in the development and progression of retinopathy.
authors.affiliation: Institute for Research in Extramural Medicine, VU University Medical Center, Amsterdam, The Netherlands. amw.spijkerman@vumc.nl
authors.forename: A M W
authors.initials: AM
authors.lastname: Spijkerman
authors.forename: M-A
authors.initials: MA
authors.lastname: Gall
authors.forename: L
authors.initials: L
authors.lastname: Tarnow
authors.forename: J W R
authors.initials: JW
authors.lastname: Twisk
authors.forename: E
authors.initials: E
authors.lastname: Lauritzen
authors.forename: H
authors.initials: H
authors.lastname: Lund-Andersen
authors.forename: J
authors.initials: J
authors.lastname: Emeis
authors.forename: H-H
authors.initials: HH
authors.lastname: Parving
authors.forename: C D A
authors.initials: CD
authors.lastname: Stehouwer
mesh_terms: D001786:Blood Glucose / Q000378:metabolism*; D002097:C-Reactive Protein / Q000032:analysis; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000378:metabolism; D003930:Diabetic Retinopathy / Q000175:diagnosis* / Q000378:metabolism; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D031300:Retinal Vasculitis / Q000150:complications* / Q000378:metabolism; D012171:Retinal Vessels / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D002097:C-Reactive Protein