There are many capillary occlusions by leukocytes and capillary dropout or degeneration associated with leukocytes in the diabetic retina ( 27). A recent study showed that diabetic vascular leakage and nonperfusion are temporally and spatially associated with retinal leukostasis in streptozotocin-induced diabetic rats ( 28). In particular, leukocytes in diabetes are less deformable, a higher proportion are activated, and they may be involved in capillary nonperfusion, endothelial cell damage, and vascular leakage in the retinal microcirculation ( 27). In diabetes, there is increased retinal leukostasis, which affects retinal endothelial function, retinal perfusion, angiogenesis, and vascular permeability. Leukocytes possess large cell volume, high cytoplasmic rigidity, a natural tendency to adhere to the vascular endothelium, and a capacity to generate toxic superoxide radicals and proteolytic enzymes ( 27). There is evidence that retinal leukostasis may also play an important role in the pathogenesis of DR. This review will focus on the current understanding of the epidemiology and pathophysiology of DR/DME, the updated clinical diagnostic grading system, screening and management, and the rationale behind the potential for pharmacological treatments. Several pharmacological therapies are being developed to treat early stages of DR/DME, but will require a renewed emphasis on early detection. Current treatments for DR/DME, such as laser photocoagulation, only target advanced stages of disease. Adherence to these recommendations is hampered by the fact that the condition is generally asymptomatic at early stages. The current management strategy for DR/DME requires early detection and optimal glycemic control to slow the progression of disease. DME occurs after breakdown of the blood-retinal barrier because of leakage of dilated hyperpermeable capillaries and microaneurysms. At any time during the progression of DR, patients with diabetes can also develop DME, which involves retinal thickening in the macular area. These blood vessels grow in an attempt to supply oxygenated blood to the hypoxic retina. Advanced stages of DR are characterized by the growth of abnormal retinal blood vessels secondary to ischemia. To implement new therapies effectively, more individuals will need to be screened for DR/DME at earlier stages-a process requiring both improved technology and interdisciplinary cooperation among physicians caring for patients with diabetes.ĭiabetic retinopathy (DR) and diabetic macular edema (DME) are common microvascular complications in patients with diabetes and may have a sudden and debilitating impact on visual acuity (VA), eventually leading to blindness. The inhibition of these pathways holds the promise of intervention for DR at earlier non–sight-threatening stages. Several biochemical mechanisms, including protein kinase C–β activation, increased vascular endothelial growth factor production, oxidative stress, and accumulation of intracellular sorbitol and advanced glycosylation end products, may contribute to the vascular disruptions that characterize DR/DME. The currently available interventions for DR/DME, laser photocoagulation and vitrectomy, only target advanced stages of disease. The control of diabetes-associated metabolic abnormalities (i.e., hyperglycemia, hyperlipidemia, and hypertension) is also important in preserving visual function because these conditions have been identified as risk factors for both the development and progression of DR/DME. Early detection of retinopathy in individuals with diabetes is critical in preventing visual loss, but current methods of screening fail to identify a sizable number of high-risk patients. The increasing number of individuals with diabetes worldwide suggests that DR and DME will continue to be major contributors to vision loss and associated functional impairment for years to come. Diabetic retinopathy (DR) and diabetic macular edema (DME) are leading causes of blindness in the working-age population of most developed countries.
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