Faculty Bibliography

PURPOSE: To report the short term anatomic and visual acuity response after intravitreal injection of bevacizumab (Avastin, Genentech) in patients with macular edema due to central retinal vein occlusion (CRVO). METHODS: The authors conducted a retrospective study of patients with macular edema due to CRVO who were treated with at least one intravitreal injection of bevacizumab 1.25 mg in 0.05 mL. Patients underwent Snellen visual acuity testing, optical coherence tomography (OCT) imaging, and ophthalmoscopic examination at baseline and follow-up visits. RESULTS: There were 16 eyes of 15 consecutive patients with a mean age of 76.1 years (SD 9.8 years). Intravitreal triamcinolone had been previously administered to 9 patients, but all of these patients either had no improvement or had excessive intraocular pressure caused by the triamcinolone. The patients received a mean of 2.8 injections of bevacizumab per eye. No adverse events were observed, including endophthalmitis, clinically evident inflammation, increased intraocular pressure, retinal tears, retinal detachment, or thromboembolic events in any patient. The mean central macular thickness at baseline was 887 microm and decreased to a mean of 372 microm at month 1 (P < 0.001). The mean baseline acuity was 20/600 (logMAR = 1.48) and the mean acuity at month 1 was 20/200 (logMAR = 1.05), a difference that was highly significant (P = 0.001). At last follow-up, a mean of 3 months after the first injection, the mean visual acuity was 20/138 (logMAR = 0.84), which was significantly better than baseline (P < 0.001). Visual acuity improvement, defined as a halving of the visual angle, was seen in 14 of the 16 eyes. CONCLUSION: Initial treatment results of patients with macular edema secondary to CRVO did not reveal any short-term safety concerns. Intravitreal bevacizumab resulted in a significant decrease in macular edema and improvement in visual acuity. The number of patients in this pilot study was limited and the follow-up is too short to make any specific treatment recommendations, but the favorable short-term results suggest further study is needed

PURPOSE: To report the short-term anatomic and visual acuity response after intravitreal injection of bevacizumab (Avastin, Genentech) in patients with proliferative diabetic retinopathy complicated by vitreous hemorrhage. METHODS: Two patients with vitreous hemorrhage due to proliferative diabetic retinopathy were treated with at least one intravitreal injection of bevacizumab 1.25 mg in 0.05 mL. The patients underwent Snellen visual acuity testing, ophthalmoscopic examination, and fluorescein angiography at baseline and follow-up visits. RESULTS: Both patients had proliferative diabetic retinopathy with vitreous hemorrhage extensive enough to preclude panretinal photocoagulation. Following intravitreal injection of bevacizumab both patients experienced improvement in visual acuity starting within the first week. At 1 month of follow-up one patient had 2 lines of improvement in visual acuity and the other 5 lines. Each patient had regression of retinal neovascularization at 1 month of follow-up. Repeat injection was given to one patient at the 1-month follow-up because of slight leakage from neovascularization on the nerve, and to the other patient at 3 months because the retinal neovascularization showed early signs of reperfusion. The vitreous hemorrhage in each patient showed partial resolution at 1 week and nearly complete regression at 1 month. No adverse events were observed in either patient. CONCLUSIONS: Initial treatment results of patients with vitreous hemorrhage and proliferative diabetic retinopathy did not reveal any short-term safety concerns. Intravitreal bevacizumab resulted in marked regression of neovascularization and rapid resolution of vitreous hemorrhage. The favorable short-term results suggest further study is needed in a larger group of patients

PURPOSE: To provide a conceptual framework for the development and use of combination therapies for choroidal neovascularization secondary to age-related macular degeneration. DESIGN: Literature review, integration of data, and creation of hypothesis. METHODS: An assessment of angiogenesis, cancer therapy, and inflammation was performed as they may pertain to choroidal neovascularization. A conceptual framework was created in which therapies for choroidal neovascularization could be evaluated alone or in combination. RESULTS: Angiogenesis occurs because cells produce angiogenic stimuli to encourage blood vessels to develop. This growth of vessels involves an orchestrated interaction among many mediators offering opportunity to modulate or inhibit the entire process. A two-component model for choroidal neovascularization is proposed. The vascular component of choroidal neovascularization is comprised of vascular endothelial cells, endothelial cell precursors, and pericytes. The extravascular component, which by histopathology appears to be both the source of angiogenic stimuli and often the largest component volumetrically, is comprised of inflammatory, glial and retinal pigment epithelial cells, and fibroblasts. Tissue damage can be caused by either component. Each component can be targeted through as variety of monotherapies. Combination therapies offer the possibility of attacking one component in more than one way or by attacking both components simultaneously. CONCLUSIONS: The two-component model of choroidal neovascularization can be used to evaluate the mechanism of action and possible interactions of these agents in a conceptual framework. Extension of these ideas can help guide development of new treatment agents and approaches