Key result
Ischemic-proliferative retinopathy in type I diabetes is linked to ~80% lower nitrites than controls.
Why the study?
The study investigated prostacyclin and nitric oxide and their platelet second messengers cAMP and cGMP in type I diabetes patients with or without retinopathy to understand platelet function differences.
Observational (n=117)
Patients with type I diabetes and edematous retinopathy exhibit higher NO production and greater impairment of platelet function compared to those with ischemic-proliferative retinopathy.
Answers are grounded in this paper and cite their sources.
May indicate dysregulated platelet signaling in type 1 diabetic retinopathy; leaves open causal role and clinical relevance.
The aim of this study was investigate prostacyclin and nitric oxide (NO) and their platelet second messengers cAMP and cGMP, in patients with type I diabetes with or without retinopathy. We compared 20 healthy volunteers and 97 patients with type I diabetes: 24 with no signs of diabetic retinopathy (DR), 43 with ischemicproliferative DR, and 30 with edematous DR. The following parameters were recorded: platelet aggregometry, nitrites/nitrates, 6-keto-prostaglandin-F(1alpha), and intraplatelet cAMP and cGMP. Platelet aggregation was greater in patients with edematous DR. The platelets in patients with diabetes were more resistant to inhibition by prostaglandin E(1) or sodium nitropruside. Nitrite concentration in patients with ischemic-proliferative DR was 80% lower than the value in healthy controls, but there was no significant difference between the control group and patients with edematous DR. In the latter group, stimulation of neutrophils with L-arginine increased nitrite + nitrate production by 44 +/- 3.6%, whereas in patients with ischemic-proliferative DR, the increase was 9.8 +/- 0.8%. We conclude that NO production is higher in patients with type I diabetes and edematous retinopathy than in those with ischemic-proliferative retinopathy. This finding, together with the possibly greater production of free radicals, may explain the greater impairment of platelet function in the former patients.
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J.P. De La Cruz (2001) conducted an observational in Type I diabetes and retinopathy (n=117). Type I diabetes with ischemic-proliferative or edematous retinopathy vs. Healthy volunteers was evaluated on Platelet aggregometry, nitrites/nitrates, 6-keto-prostaglandin-F(1alpha), and intraplatelet cAMP and cGMP. Patients with type I diabetes and edematous retinopathy had higher nitric oxide production than those with ischemic-proliferative retinopathy, who had 80% lower nitrite concentrations than controls.
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