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Systemic inflammation and obesity are associated with retinopathy development in type 2 but not in type 1 diabetes

Purpose. Diabetic retinopathy (DR), a microvascular and visually devastating diabetic complication, is the leading cause of new blindness among working-age adults in developed countries. Its pathogenesis is insufficiently understood and presumed to possibly involve chronic, low-grade inflammation. The aim of this study was to investigate risk factors and role of systemic inflammation and obesity in development of retinopathy in type 1 and type 2 diabetes, and determine the differences in these two types of disease with possible impact on future research and treatment guidelines. Setting/Venue. Department of Ophthalmology, Department of Diabetes and Endocrinology, Vuk Vrhovac University Clinic for Diabetes, Endocrinology and Metabolic Diseases, Merkur University Hospital, Zagreb, Croatia. Methods. This cross-sectional study included 84 patients with type 1 and 107 patients with type 2 diabetes. Basic and anthropometric parameters assessed were sex, age, diabetes duration, body mass index (BMI), waist circumference (WC) and waist-to-hip ratio (WHR). C- reactive protein (CRP), fibrinogen (FIB), glycated hemoglobin (HbA1c), fasting and postprandial blood glucose (fBG, ppBG), total cholesterol, HDL and LDL cholesterol, triglycerides (TG) and serum creatinine were determined using routine laboratory methods. HbA1cmedian was obtained by statistical analysis of data from the National Diabetes Registry. Glomerular filtration rate was estimated using CKD-EPI formula. Albumin excretion rate (AER) was measured from a 24- hr urine sample. Blood pressure was measured with a mercury sphygmomanometer after a 10-min resting period. Ophthalmologic examination included indirect slit lamp fundoscopy and color fundus photography after mydriasis of two fields of both eyes according to the EURODIAB retinal photography methodology. Results. Patients were divided into three groups: group 1 (no retinopathy), group 2 (mild/moderate NPDR) and group 3 (severe NPDR/PDR). In both types of diabetes group 3 had longer diabetes duration than group 1 (type 1 p=0.002 ; type 2 p<0.001). Group 3 in type 1 had higher HbA1cmedian (p<0.001) and AER (p=0.002), while in type 2 had higher BMI, WC, WHR, SBP, CRP, FIB, ppBG and TG than group 1. DR was positively associated with diabetes duration (p<0.001), HbA1cmedian (p<0.001) and AER (0.008) in type 1, and diabetes duration (p<0.001), HbA1cmedian (p=0.018), AER (0.001), CRP (p=0.048) and TG (p=0.041) in type 2 diabetes. Logistic regression analyses showed that diabetes duration (OR=1.22, CI 1.04-1.45, p=0.011) and prolonged poor glycemic control (HbA1cmedian) (OR=1.73, CI 1.25-2.34, p=0.022) were the main predictors of DR in type 1 diabetes. Diabetes duration (OR=1.25, CI 1.12-1.39, p<0.001), fBG (OR=1.45, CI 1.04-2.00, p=0.024) and TG (OR=2.08, CI 1.09-3.98, p=0.025) were the main predictors of DR in type 2 diabetes. Conclusion. Diabetes duration, poor glycemic control and nephropathy are the main risk factors for DR in both types of diabetes. Systemic inflammation and visceral obesity were found to be related to the development of DR in type 2 but not in type 1 diabetes. These findings might hypothesize different pathogenesis of retinopathy in these two different types of diabetes and suggest different treatment guidelines. Further researches focusing on the use of different treatment approaches in different types of diabetes might therefore identify best first-line treatment of retinopathy in type 1 and type 2 diabetes.

systemic inflammation, type 1 and type 2 diabetes, retinopathy

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