The increase of retinal vessel oxygen saturation in diabetic retinopathy points to a diabetic microvascular alteration. This may be due to occlusions and obliterations in the capillary bead and the formation of arterio-venous shunt vessels. On the other hand, hyperglycaemia-induced endothelial dysfunction, with subsequent suppression of the endothelial NO-synthase and disturbance of the vascular auto-regulation, may contribute to retinal tissue hypoxia.
OBJECTIVE—Stimulation of the retina with flickering light increases retinal vessel diameters in humans. Nitric oxide is a mediator of the retinal vasodilation to flicker. The reduction of vasodilation is considered an endothelial dysfunction. We investigated the response of retinal vessels to flickering light in diabetic patients in different stages of diabetic retinopathy.
RESEARCH DESIGN AND METHODS—We studied 53 healthy volunteers, 68 type 1 diabetic patients, and 172 type 2 diabetic patients. The diameter of retinal vessels was measured continuously online with the Dynamic Vessel Analyzer (DVA). Diabetic retinopathy was classified using Early Treatment Diabetic Retinopathy Study criteria. Changes in vasodilation are expressed as percent change over baseline values.
RESULTS—After adjustments for age, sex, and antihypertensive treatment, the response of retinal arterioles to diffuse luminance flicker was significantly diminished in patients with type 1 diabetes compared with healthy volunteers. The vasodilation of retinal arterioles and venules decreased continuously with increasing stages of diabetic retinopathy. The retinal arterial diameter change was 3.6 ± 2.1% in the control group, 2.6 ± 2.5% in the no diabetic retinopathy group, 2.0 ± 2.7% in the mild nonproliferative diabetic retinopathy (NPDR) group, 1.6 ± 2.2% in the moderate NPDR group, 1.8 ± 1.9% in severe NPDR group, and 0.8 ± 1.6% in proliferative diabetic retinopathy group.
CONCLUSIONS—Flicker responses of retinal vessels are abnormally reduced in diabetic patients. This decreased response deteriorated with increasing stages of retinopathy. The response was already reduced before clinical appearance of retinopathy. The noninvasive testing of retinal autoregulation with DVA might prove to be of value in early detection of diabetic vessel pathological changes.
In this study, more than half of the patients with diabetes mellitus type 1 had at least one pathologically increased antibody titer apart from diabetes without clinical sign of an additional AIEK. 31% of patients with increased antibodies presented with symptoms of another AIEK (increase by 3.6% within 1 year). Patients with diabetes mellitus type 1 should be screened for other AIEKs. Thyropathy had the greatest prevalence and increased by 3.5% within 1 year's time.
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