Intravitreal Aflibercept for Macular Edema Following Branch Retinal Vein Occlusion

Clark, W. Lloyd; Boyer, David S.; Heier, Jeffrey S.; Brown, David M.; Haller, Julia A.; Vitti, Robert; Kazmi, Husain; Berliner, Alyson J.; Erickson, Kristine; Chu, Karen; Soo, Yuhwen; Cheng, Yenchieh; Campochiaro, Peter A.

doi:10.1016/j.ophtha.2015.09.035

Cited by 225 publications

(205 citation statements)

References 25 publications

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“…11 Macrophages are a major source of many cytokines, such as TNF, IL-1, IL-6, IL-8, and IL-12, and central in the regulation of inflammatory processes. 12 As the inflammatory responses may be influenced at different stages of RVO by therapeutic agents such as intravitreal steroids 13,14 or anti-VEGF agents, [15][16][17] a better understanding of the cascade of inflammation following RVO may help guide treatment decisions.…”

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confidence: 99%

Microglia Activation and Recruitment of Circulating Macrophages During Ischemic Experimental Branch Retinal Vein Occlusion

Ebneter

Kokona

Schneider

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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METHODS. Experimental BRVO was induced in Balb/c mice and histologic changes were studied. Tissue hypoxia was visualized using pimonidazole hydrochloride. Monocyte-derived retinal cells were quantified using histology and flow cytometry. To investigate the dynamics of invading blood-borne macrophages, chimera mice were generated using bone marrow grafts from Cx3cr1 (gfp/gfp) mice to rescue lethally irradiated wild-type BALB/c mice. Longitudinal in vivo imaging was performed to monitor cell invasion. The levels of proinflammatory cytokines in the retina were quantified by quantitative real-time PCR.RESULTS. Histology showed disruption of tissue architecture and temporary swelling with marked hypoxia coinciding with increased VEGF-A and hypoxia inducible factor-1a (HIF-1a) expression and elevation of proinflammatory cytokines within 3 days after experimental BRVO, followed by thinning of the inner retinal layers at later time points. Proinflammatory cytokine levels were elevated. Activation of resident retinal microglia and recruitment of circulating macrophages in areas of hypoxic retina were evident early after the insult and peaked at day 7, remaining elevated for up to 28 days. Flow cytometry showed upregulation of CD68 and major histocompatibility complex class-II (MHC-II) expression at day 3, culminating at day 7.CONCLUSIONS. Experimental BRVO causes hypoxia and breakdown of the inner blood-retina barrier, followed by activation of microglia and invasion of macrophages from the systemic circulation. Consequently, treatments targeting microglia activation or macrophage recruitment might potentially mitigate the sequelae and attenuate degenerative changes induced by retinal vein occlusion.

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confidence: 99%

Microglia Activation and Recruitment of Circulating Macrophages During Ischemic Experimental Branch Retinal Vein Occlusion

Ebneter

Kokona

Schneider

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…Mean number of scheduled injections was similar in both groups: 2.8 in IVR group, and 2.4 in IVAfl group, which were both lower than seen in prospective multicenter studies (9)(10)(11)(12)(13). In pivotal studies that evaluated IVR and IVAfl in cases of ME secondary to RVO, 6 initial monthly injections were performed (9)(10)(11)(12).…”

Section: Discussionmentioning

confidence: 69%

“…In pivotal studies that evaluated IVR and IVAfl in cases of ME secondary to RVO, 6 initial monthly injections were performed (9)(10)(11)(12). Subsequently, various treatment regimens were pursued (9)(10)(11)(12)(13).Loading phase of anti-VEGF drugs has been investigated in some studies, and low-frequency ranibizumab treatment was found to be effective (15). It is worth recalling here that in real-life setting, it is not always possible to conform to strict follow-up and treatment criteria (14)(15)(16)(17)(18)(19)(20).…”

Section: Discussionmentioning

confidence: 99%

“…The first drug is used off-label; the others are approved for this purpose (2,8,(9)(10)(11)(12). In pivotal multicenter studies in which strict follow-up and treatment criteria were observed, successful treatment outcomes have been reported (9)(10)(11)(12)(13). However, it is usually not possible to replicate these strict criteria in real-life practice (14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

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Ranibizumab versus Aflibercept in Macular Edema Secondary to Retinal Vein Occlusion in Real Life: A Retrospective Case Control Study

Özkaya¹

2017

Beyoglu Eye J

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Objectives:The present study is comparison of efficacy of ranibizumab and aflibercept in the treatment of macular edema (ME) secondary to retinal vein occlusion (RVO) in real life. Methods: Design was retrospective, case-control study. Treatment naïve RVO patients with ME who were treated with ranibizumab or aflibercept and had minimum follow-up time of 6 months were included. Primary outcome measures were changes in best corrected visual acuity (BCVA) and central retinal thickness (CRT). Secondary outcome measure was number of injections administered. Results: Mean baseline, month 3, and month 6 BCVA in ranibizumab group was 0.95±0.61-, 0.50±0.30-, and 0.66±0.58 logarithm of the minimum angle of resolution (LogMAR), respectively. Mean baseline, month 3, and month 6 BCVA in aflibercept group was 0.85±0.65-, 0.61±0.58-, and 0.65±0.55 LogMAR, respectively. Mean baseline, month 3, and month 6 CRT in ranibizumab group was 598±189-, 473±162-, and 359±134 μm, respectively. Mean baseline, month 3, and month 6 CRT in aflibercept group was 512±141-, 345±154-, and 374±172 μm, respectively. Mean number of injections was 2.7±0.8 for ranibizumab group, and 2.2±1.0 for aflibercept group (p=0.08). Conclusion: Ranibizumab and aflibercept are both effective agents in the treatment of ME secondary to RVO. Visit and injection figures were lower than those reported in prospective, multicenter studies, as expected, but functional and anatomical outcomes were comparable.

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“…Three different anti-VEGF agents are available for intravitreal administration: bevacizumab (off-label), ranibizumab and aflibercept. Given the impressive results of major clinical trials, 12,13 anti-VEGF drugs rapidly became the gold-standard therapy for BRVO associated ME. Further pharmacotherapeutic options include intravitreal corticosteroids (triamcinolone/off-label; dexamethasone).…”

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confidence: 99%

Branch Retinal Vein Occlusion – Update on Treatment Options

Michels¹,

Wirth²

2016

European Ophthalmic Review

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The advent of new pharmacotherapeutic options and diagnostic methods have led to a revolution in the management of branch retinal vein occlusion over the past few years. Despite the variety of treatment options, we are confronted with several questions: which drug should we use? Is switching between or combining treatment options beneficial? What is the recommended treatment regimen? When should we start treatment and for how long should we continue it? Should we still use retinal laser therapy? The wide range of possibilities and emerging treatment choices not only aids, but also challenges clinicians striving for evidence-based management. KeywordsBranch retinal vein occlusion, macular oedema, anti-vascular endothelial growth factor (VEGF)

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Intravitreal Aflibercept for Macular Edema Following Branch Retinal Vein Occlusion

Cited by 225 publications

References 25 publications

Microglia Activation and Recruitment of Circulating Macrophages During Ischemic Experimental Branch Retinal Vein Occlusion

Microglia Activation and Recruitment of Circulating Macrophages During Ischemic Experimental Branch Retinal Vein Occlusion

Ranibizumab versus Aflibercept in Macular Edema Secondary to Retinal Vein Occlusion in Real Life: A Retrospective Case Control Study

Branch Retinal Vein Occlusion – Update on Treatment Options

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