Antagonism of Vascular Endothelial Growth Factor for Macular Edema Caused by Retinal Vein Occlusions: Two-Year Outcomes

Campochiaro, Peter A.; Hafiz, Gulnar; Channa, Roomasa; Shah, Syed Mahmood; Nguyen, Quan Dong; Ying, Howard S.; Diana, V.; Zimmer-Galler, Ingrid; Solomon, Sharon D.; Sung, Jennifer; Syed, Beena

doi:10.1016/j.ophtha.2010.03.060

Cited by 69 publications

(45 citation statements)

References 12 publications

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“…VEGF has a role in the complex and intriguing pathophysiological mechanisms causing ME via the effects on blood-retinal barrier breakdown and vascular permeability (19). Several clinical studies evaluated the role of anti-VEGF therapy among patients with retinal vascular diseases with ME and found a beneficial effect of this treatment on the progression of ME (6,(25)(26)(27)(28)(29)(30). A multicenter randomized study, BRAVO, evaluated the role of 6-month ranibizumab therapy in BRVO, which revealed a decrease in CRT and improvement in visual acuity compared to the control group (25).…”

Section: Discussionmentioning

confidence: 99%

Intravitreal PRN ranibizumab treatment for macular edemadue to branch retinal vein occlusion

et al. 2017

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Background/aim: To evaluate the effect of intravitreal pro re nata (PRN) ranibizumab treatment from the start on the best-corrected visual acuity (BCVA) and the central retinal thickness (CRT) in macular edema (ME) due to branch retinal vein occlusion (BRVO). Materials and methods:Patients with ME secondary to BRVO, who were treated on a PRN basis after a single intravitreal ranibizumab injection, were retrospectively evaluated. The main outcome measures were changes in BCVA and CRT as measured by optical coherence tomography. Results:The number of injections over 6 months was 2.43 ± 1.16. The mean BCVA of the patients was 0.84 ± 0.10 logMAR at baseline and 0.41 ± 0.06 at the 6th month (P < 0.001). Mean BCVA of the ischemic BRVO group was 1.06 ± 0.68 logMAR at baseline and 0.44 ± 0.30 logMAR at the 6th month (P < 0.05). Similarly, the mean BCVA of the nonischemic BRVO group was 0.77 ± 0.53 logMAR at baseline and 0.41 ± 0.36 logMAR at the 6th month (P < 0.05). Between groups, there was no significant difference in mean BCVA at any examination. Conclusion:Intravitreal ranibizumab is a safe and effective treatment option for ME due to ischemic and nonischemic BRVO using PRN from the start.

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Section: Discussionmentioning

confidence: 99%

Intravitreal PRN ranibizumab treatment for macular edemadue to branch retinal vein occlusion

et al. 2017

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“…Although several prognostic factors (e.g., hypertension, macular ischemia) are reported in BRVO, 2,18,19 it was poorly defined what kinds of pathogenesis determine visual prognosis. Recent publications demonstrated that the disrupted IS/OS or ELM delineated by OCT, suggesting foveal photoreceptor damage and their significant association with poor visual function in resolved ME associated with retinal vascular diseases including BRVO.…”

Section: Discussionmentioning

confidence: 99%

“…18,19 Ischemia hinders the efficient exchange of nutrients, gases, and wastes, in addition to exacerbating the dysfunction and degeneration of retinal neuronal components. Macular ischemia might be similar to C + S (+), in which foveal neuroglial components are exposed to nutritional deficiency.…”

Section: Discussionmentioning

confidence: 99%

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Disrupted Foveal Photoreceptors After Combined Cystoid Spaces and Retinal Detachment in Branch Vein Occlusion Treated With Bevacizumab

Murakami

Tsujikawa

Miyamoto

et al. 2012

Retina

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“…Recent studies have implicated VEGF as the major stimulus for diabetic macular edema [19][20][21][22] and macular edema due to retinal vein occlusions. [23][24][25][26] Therefore, VEGF blockade provides benefit for two major causes of vision loss in patients with ischemic retinopathy, retinal NV and macular edema.…”

Section: Ischemic Retinopathiesmentioning

confidence: 99%

Gene transfer for ocular neovascularization and macular edema

Campochiaro

2011

Gene Ther

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Diseases complicated by abnormal growth of vessels or excessive leakage are the most prevalent cause of moderate or severe vision loss in developed countries. Recent progress unraveling the molecular pathogenesis of several of these disease processes has led to new drug therapies that have provided major benefits to patients. However, those treatments often require frequent intraocular injections, and despite monthly injections, some patients have a suboptimal response. Gene transfer of antiangiogenic proteins is an alternative approach that has the potential to provide long-term suppression of neovascularization (NV) and/or excessive vascular leakage in the eye. Studies in animal models of ocular NV have demonstrated impressive results with a number of transgenes, and a clinical trial in patients with advanced neovascular age-related macular degeneration has provided proof-of-concept. Two ongoing clinical trials, one using an adeno-associated viral (AAV) vector to express a vascular endothelial growth factor-binding protein and another using a lentiviral vector to express endostatin and angiostatin, will provide valuable information that should help to inform future trials and provide a foundation on which to build.

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Antagonism of Vascular Endothelial Growth Factor for Macular Edema Caused by Retinal Vein Occlusions: Two-Year Outcomes

Cited by 69 publications

References 12 publications

Intravitreal PRN ranibizumab treatment for macular edemadue to branch retinal vein occlusion

Intravitreal PRN ranibizumab treatment for macular edemadue to branch retinal vein occlusion

Disrupted Foveal Photoreceptors After Combined Cystoid Spaces and Retinal Detachment in Branch Vein Occlusion Treated With Bevacizumab

Gene transfer for ocular neovascularization and macular edema

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