Intravitreal Bevacizumab for Treatment of Diabetic Macular Oedema

Abstract

Abstractdiabetic macular oedema (dMo) is a leading cause of vision loss in the working-age population worldwide. Numerous early studies suggest an important role for intravitreal anti-VEGF agents such as bevacizumab in the management of dMo. We reviewed manuscripts that had investigated pharmacokinetic, efficacy, safety, dose and frequency of intravitreal bevacizumab (iVB) injections as well as effect of macular ischaemia, initial macular thickness and optical coherence tomography (ocT) patterns of dMo on the final results of treatment with iVB. in summery literature searches disclosed that almost all studies published up to now provided evidence supporting use of iVB for treatment of either naïve or persistent dMo in short and long term up to 2 years. KeywordsBevacizumab, clinically significant diabetic macular oedema, diabetic retinopathy, macular laser photocoagulation, triamcinolone acetonide Pathophysiology of Diabetic Macular OedemaSeveral physiological mechanisms have been proposed to contribute to the pathogenesis of dMo. The exact mechanisms by which elevated glucose initiates the vascular disruption and results in the ultimate blood retinal barrier (BRB) breakdown in diabetic retinopathy remain poorly defined. There are several hypotheses that contribute to dMo formation including:1. increase in hydrostatic pressure that was described by Starling.Similar to congestive heart failure, dMo can be considered as a congestive macular oedema. Based on Starling law hydrostatic and oncotic pressure counteract each other; pressure differences are responsible for the movement of fluid between tissue beds and intravascular spaces. changes in vessel diameter together with increased hydrostatic pressure can contribute to oedema formation. Furthermore the above mentioned mechanism can increase in shear stress which may cause damage to endothelial cells and cause endothelial decoupling over time. [9][10][11] 2. ischaemia secondary to hypoxia can lead to decrease in oxygen tension in retina which results in vasodilation of the retinal vessels that can increase macular oedema by increasing hydrostatic pressure. increased in oxygen tension may decrease macular oedema by reversing the earlier described mechanism.3. hyperglycaemia per se or together with other mechanisms may induce endothelial dysfunction and cause more vascular damage. [12][13][14] 4. increased VEGF production: VEGF mediates angiogenesis by promoting endothelial cell migration, proliferation and survival.amongst the various VEGF family members, VEGF-a, is a critical regulator of ocular angiogenesis and vascular permeability. 15VEGF can cause rapid post-translational modifications to tight junctions by stimulating occluding phosphorylation and inducing tyrosine phosphorylation of zonula occludence that result in