ABSTRACT
Bevacizumab has demonstrated an ability to have a profound biologic effect on ocular neovascularization and macular edema. Intravitreal administration seems to provide a similar biologic effect to intravenous administration, at lower cost and with less risk of systemic side-effects. The discovery and cloning of vascular endothelial growth factor (VEGF) in the 1980s and the subsequent development of antibodies to it allowed identification of the key role of VEGF in the development of retinal neovascularization. Injection of VEGF in primates can produce a retinopathy similar to diabetic retinopathy and can even produce iris neovascularization. Inhibition of VEGF can prevent iris neovascularization in primates, and inhibit the development of choroidal neovascularization in animal models. Bevacizumab is a humanized monoclonal antibody to VEGF designed for intravenous administration and approved for the treatment of colorectal cancer. VEGF levels are often elevated following significant retinal vascular occlusive disease, and this can lead to retinal and anterior segment neovascularization, neovascular glaucoma, and retinal edema.
