Prospective Study to Determine the Effect of Subconjunctival Bevacizumab (AVASTIN) in Corneal Neovascularization

To determine the effect of subconjunctival Bevacizumab in corneal neovascularization

Corneal transplantation is the most commonly performed transplant surgery in the world today. Immunologic rejection is the leading cause of graft failure, with about 25% of graft recipients experiencing at least one episode of rejection. Of these episodes, about 20% are irreversible. The rate of corneal graft rejection in high-risk eyes, such as corneal neovascularization, has been reported to be 50% to 70%. Vascularized corneas have a much higher rate of graft rejection than avascular corneas. Whereas the normal cornea is devoid of blood and lymphatic vessels, both can invade the cornea secondary to a variety of corneal diseases and after surgery. This not only reduces visual acuity, but also renders such a cornea high-risk, if subsequent corneal transplantation is performed.Anti-angiogenesis, the pharmacologic inhibition of new blood vessel growth and formation, is a new treatment strategy under active and vigorous investigation. Multiple growth factors have been shown to contribute to the molecular events involved in the regulation of blood vessel growth Similarly, it is assumed that angiogenic growth factors such as vascular endothelial growth factor (VEGF), considered a major pro-angiogenic factor, could play a role in the pathogenesis of neovascularization. Several approaches can be taken to neutralize VEGF. Bevacizumab (Avastin) is a full-length humanized murine monoclonal antibody against the VEGF molecule.It binds to and inhibits the biologic activity of human VEGF preventing the interaction of this molecule to its receptors on the surface of endothelial cells. The interaction of VEGF with its receptors leads to endothelial cell proliferation and new vessel formation. There is evidence that triamcinolone acetonide (TA) inhibits vasogenic edema and inflammation, decreases vascular leakage, reduces the secretion of VEGF by pigment epithelial cells during oxidative stress and, down-regulates the expression of the VEGF gene in vascular smooth muscle cells Furthermore, TA decreases the paracellular permeability of cultured epithelial cells and down-regulates the inflammatory expression of endothelial adhesion molecules.