الفهرس 
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Abstract
Diabetic retinopathy (DR) remains one of the leading causes of visual morbidity. Worldwide, there are approximately 194 million people with diabetes, and this number is likely to increase to 334 million by 2025. DR is divided into two major forms: non-proliferative and proliferative.
After 20 years with the disease, 60% of type-2 diabetics and virtually 100% of type-1 diabetics will manifest some form of retinopathy. Generally, the prevalence of retinopathy at diagnosis of type-1 diabetes is reportedly low, between 0% and 3% while a higher proportion of those with newly diagnosed type-2 diabetes have evidence of DR 6.7–30.2%.
Eyes with obvious foveal involvement by edema or lipid are categorized as ”severe DME”. Eyes with edema and/or lipid relatively distant from the macula are graded as ”mild DME”, ”Moderate DME” was used to identify cases in which retinal thickening and/or lipid are close to the fovea.
The exact mechanism by which diabetes causes retinopathy remains unclear, but several theories have been postulated to explain the typical course and history of the disease. The role of vascular endothelial growth factor appears to be central in the pathogenesis of proliferative diabetic retinopathy.
The fundus fluorescein angiography and optical coherence tomography are indicated and extremely useful in confirming the diagnosis, helping guide the treatment pattern, measuring macular thickness and detecting presence of vitreomacular traction.
Strict metabolic control, tight blood pressure control, laser photocoagulation, and vitrectomy remain the conventional management of diabetic retinopathy. Treatment does not cure diabetic retinopathy but it is effective in preventing further vision loss.
Laser treatment of diabetic retinopathy is still the gold standard of treatment for focal and diffuse diabetic macular edema and proliferative diabetic retinopathy. Laser treatment reduced the risk of vision loss due to diabetic macular edema by 50–70%. However, the limited efficacy of laser treatment has put the need for other lines of treatment in order to control cases with persistent or recurrent diabetic macular edema which do not respond well to laser photocoagulation.
Steroids are currently gaining attention with the growing use of intravitreal triamcinolone (IVTA). Corticosteroids may work through multiple mechanisms of action. In addition to their well-known anti-inflammatory effects, corticosteroids may cause down-regulation of VEGF. They also block the release of arachidonic acid from cell membranes and thus reduce the synthesis of prostaglandins. Furthermore, they inhibit the migration of leukocytes and the release of pro-inflammatory mediators such as VEGF.
There is a strong direct positive correlation between VEGF concentration and grade of DR. There are statistically high VEGF concentrations (of vitreous and serum samples) in both diabetic groups (NPDR and PDR) compared to control group. The highest level is in PDR patients. The vitreous is a more powerful indicator of severity of DR than serum levels. VEGF concentrations increased progressively with the progression of DR. The lowest concentration is in patients with very mild DR and the highest level is found in patients with tractional retinal detachment.
The role of VEGF in ocular angiogenesis has been established. So, interruption of the angiogenic casecade through inhibition of VEGF action has been proved. Bevacizumab (Avastin) which is the most common one and offer many advantages than steroid injection.
PKC-beta inhibitors inhibit more than 95% of the edema formation in the retina of diabetic animal models and may eventually offer a new treatment option for patients with diabetes.
Experimental studies for systemic drugs as antioxidants, somatostatin analogues, angiotensin II receptor blockers, and other potential therapies may lead to the introduction of additional treatments and a corresponding reduction in the frequency of visual loss due to DR.
Vitrectomy including removal of the ILM leads to resolution of diffuse DME and improvement in VA without subsequent ERM formation. Thus, complete release of tractional forces and inhibition of re-proliferation of fibrous astrocytes seem to be prudent in the eyes of patients with diabetes and advanced vitreo-retinal interface disease of the macula. A careful selection of eyes with favorable preoperative clinical characteristics may be necessary to improve surgical outcomes.