الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Diabetic macular edema (DME) is the main cause of vision loss in diabetic retinopathy. Recent studies have demonstrated that VEGF is an important mediator of blood–retinal-barrier breakdown, leads to fluid leakage and induces the development of DME; anti-VEGF agents have been proven to offer effective treatment.
Anti-VEGF agents interfere with receptor binding, thus inhibiting VEGF’s signal, which results in inhibition of abnormal blood vessel formation and decreased vascular permeability . Intravitreal Anti-VEGF agents like ranibizumab and bevacuimab is now widely used in treatment of DME .
Ranibizumab are frequently used to treat vascular pathologies in cases of DR; however, little consideration has been given to treatment modalities to prevent neurodegeneration.
This cross-sectional study included 45 eyes of 45 diabetic with DME patients attending Ophthalmology clinic at Suez Canal University Hospital, Ismailia, Egypt. It included 45 eyes scanned before IVI Ranibizumab for DME and after one month of IVI of Ranibizumab for DME. Measurement of RNFL and GCC layer (GCC) thickness using OCT scans was done using DRI OCT Triton plus (Topcon Co., Tokyo, Japan) - Swept source with implemented SMART Track TM system©.
This study found that macular retinal nerve fiber layer was thinner after one month of IVI of Ranibimuzab for DME(46.4±9.34) than before IVI of Ranibimuzab for DME (48.3±10.01) with statistically highly significant difference (p<0.001).
Also, macular ganglion cell layer was thinner after one month of IVI of Ranibimuzab for DME (68.9±11.36) than before IVI of Ranibimuzab for DME (70.5±12.29) with statistically significant difference (p0.033).