الفهرس 
ANTIANGIOGENESISOnly 14 pages are availabe for public view
 |  | from | 124 |  |  |
| | | from | 124 | | |
Abstract
Ocular neovascularization (NV) is the primary cause of blindness in a wide range of ocular diseases, such as diabetic retinopathy (DR), age-related macular degeneration (AMD), retinopathy of prematurity (ROP), central and branch retinal vein occlusion (CRVO and BRVO), infectious keratitis, trauma and various inflammatory ocular diseases. The avascular feature of certain ocular compartments, including the cornea, lens, vitreous and outer retina, is a unique anatomical characteristic to meet the requirement for normal visual function.
In healthy adults, the fully developed ocular vascular system is in quiescent status (also known as homeostasis), which is tightly controlled by the balance between the angiogenic stimulating factors, such as vascular endothelial growth factor (VEGF) and angiogenic inhibitors, such as pigment epithelium-derived factor (PEDF).
Inhibition of VEGF by Avastin and, thereby, inhibiting angiogenesis and decreasing vascular permeability can be an effective treatment for a variety of ocular diseases.
The use of bevacizumab systemically and intravitreally in the treatment of macular degeneration was reported. Intravenous administration of this agent at 5 mg/kg at 2-weeks interval produced a significant reduction in retinal thickening and improvement in VA in a small series.
Intravitreal injection of bevacizumab causes regression of the retinal neovascularization within one month following the injection with no observable morbidity from the injection and the hemorrhage cleared with unexpected rapidity. Intravitreal bevacizumab may prove to be of benefit in a variety of clinical settings, such as when media opacity prevents the placement of panretinal photocoagulation, or in cases of severe PDR with concurrent macular edema, in which injection of bevacizumab in conjunction with panretinal photocoagulation may minimize the exacerbation of macular edema, which can sometimes be caused by panretinal photocoagulation.
Retinal vein occlusion is associated with increased intravitreal levels of VEGF, particularly in cases complicated by neovascularization, so inhibition of VEGF by bevacizumab has been described on an anecdotal basis. Bevacizumab injection is able to improve CME and VA in RVO patients within the first 3 to 9 weeks after injection.
In retinopathy of prematurity with anterior segment ischemia resulting from aggressive posterior laser treatment intravitreal injection of Avastin gives a favorable outcome.
Subconjunctival injection of bevacizumab may offer an additional strategy for the treatment of corneal NV.
Intravitreal injection of bevacizumab is tolerated in patients with diabetes mellitus and might be an emergent treatment of choice for INV that is poorly responsive to conventionally approved treatments. Intravitreal injection of bevacizumab may be an advantageous treatment option rather than laser photocoagulation, especially in the eyes with fundus-obscuring cataract or vitreous hemorrhage.
Avastin also proved efficient in pseudophakic macular edema, idiopathic juxtafoveal retinal telangiectasis, and chronic uveitis with cystoid macular edema.
CONCLUSION
CONCLUSION
• Intravitreal injection of anti-VEGF is a novel and promising treatment that reduces intraocular VEGF concentration and therefore inhibits neovascular proliferation.
• Bevacizumab has a more impressive success rate and lower cost over other members of anti-VEGFs.
• Bevacizumab can be combined with other lines of therapy against ocular neovascularization to enhance the power of therapy and end results.