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Treatment of Proliferative Diabetic Retinopathy

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Diabetic Retinopathy

Abstract

Proliferative diabetic retinopathy (PDR) is an advanced stage of diabetic microangiopathy in which extensive retinal capillary occlusion results in the growth of preretinal fibrovascular tissue. The pathogenesis is not well understood. Underlying pathophysiologic changes in diabetic retinopathy include abnormal shunting of glucose via the aldose reductase pathway, formation of advanced glycation end-products, activation of protein kinase-C beta isoform, induction of vascular endothelial growth factor (VEGF), oxidative damage, and inflammation.1–5 Pathological anatomic changes evolve with abnormal thickening of capillary basement membrane, loss of pericytes, breakdown of the blood–retinal barrier, changes in microvascular caliber, microaneurysm formation, endothelial cell loss associated with capillary occlusion, and neovascularization within the retina (intraretinal microvascular abnormalities) and in the preretinal space with varying degrees of preretinal fibrosis. PDR may cause loss of vision from edema, ischemia, intraocular hemorrhage, premacular membranes, vitreomacular traction, traction retinal detachment, traction–rhegmatogenous retinal detachment, and neovascular glaucoma.6

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Pautler, S.E. (2010). Treatment of Proliferative Diabetic Retinopathy. In: Browning, D. (eds) Diabetic Retinopathy. Springer, New York, NY. https://doi.org/10.1007/978-0-387-85900-2_9

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