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Pharmacologic therapies for diabetic retinopathy and diabetic macular edema

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Authors: Ehud Rechtman, Alon Harris, Hanna J Garzozi, Thomas A Ciulla

Published Date January 2007 Volume 2007:1(4) Pages 383 - 391
DOI: http://dx.doi.org/10.2147/OPTH.S

Ehud Rechtman1, Alon Harris2, Hanna J Garzozi3, Thomas A Ciulla4

1Goldschleger Eye Institute, Sheba Medical Center, Tel-Hashomer, Israel; 2Department of Ophthalmology, Indiana University, Indianapolis, IN, USA; 3Department of Ophthalmology, Bnai Zion Medical Center, The Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel; 4Midwest Eye Institute, Indianapolis, IN, USA

Abstract: Diabetic retinopathy (DR) and diabetic macular edema (DME) are leading causes of blindness in the working-aged population of most developed countries. The increasing number of persons with diabetes worldwide suggests that DR/DME will continue to be major contributors to vision loss and associated functional impairment for years to come. Early detection of retinopathy in persons with diabetes is critical in preventing visual loss, but current methods of screening fail to identify a sizable number of high-risk patients. The control of diabetes-associated metabolic abnormalities (ie, hyperglycemia, hyperlipidemia, and hypertension) is also important in preserving visual function, as these conditions have been identified as risk factors for both the development and progression of DR/DME. The non-pharmacologic interventions for DR/DME, laser photocoagulation and vitrectomy, only target advanced stages of disease. Several biochemical mechanisms, including increased vascular endothelial growth factor production, protein kinase C β activation, oxidative stress, and accumulation of intracellular sorbitol and advanced glycosylation end products, may contribute to the vascular disruptions that characterize DR/DME. The inhibition of these pathways holds the promise of the intervention for diabetic retinopathy with higher success rate and also at earlier, non-sight-threatening stages.








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