Endothelial dysfunction and low-grade inflammation and the progression of retinopathy in Type 2 diabetes.
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.
Spijkerman
A M W
AM
Institute for Research in Extramural Medicine, VU University Medical Center, Amsterdam, The Netherlands. amw.spijkerman@vumc.nl
Gall
M-A
MA
Tarnow
L
L
Twisk
J W R
JW
Lauritzen
E
E
Lund-Andersen
H
H
Emeis
J
J
Parving
H-H
HH
Stehouwer
C D A
CD
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*
D001786:Blood Glucose; D002097:C-Reactive Protein