March 2013
Volume 54, Issue 3
Research Highlight  |   March 2013
Anti-VEGF in Retinopathy of Prematurity, Need to Titrate
Investigative Ophthalmology & Visual Science March 2013, Vol.54, 2027. doi:10.1167/iovs.13-11948
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      Demetrios G. Vavvas; Anti-VEGF in Retinopathy of Prematurity, Need to Titrate. Invest. Ophthalmol. Vis. Sci. 2013;54(3):2027. doi: 10.1167/iovs.13-11948.

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      © ARVO (1962-2015); The Authors (2016-present)

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Retinopathy of prematurity (ROP) is a major cause of blindness in children in the Western World. Premature birth disturbs normal vascular development. Children with more avascular retina have higher risk of developing pathologic neovascularization (NV) and severe ROP. The present standard of care has been laser or cryoablation of the peripheral avascular retina in order to control the pathologic neovascularization. Despite the undeniable benefit of these primitive yet time tested interventions, there is incomplete effectiveness and significant morbidity. Molecular understanding of normal and abnormal vascular development has highlighted the role of VEGF and suggested a role of anti-VEGF therapy. 1 The effectiveness of anti-VEGF therapy in AMD and other neovascular diseases has generated excitement about application of “gentler” anti-VEGF therapies for ROP. The Bevacizumab Eliminates the Angiogenic Threat of Retinopathy of Prematurity study gave us excitement, but also caution about delayed normal vascular development and NV formation. 2  
It is natural to think that in a developing organ, the exact level of VEGF inhibition will be important in order to control pathologic NV, while at the same time allowing normal vascular development to proceed. Lutty et al. 3 has demonstrated this principle in a dog model of ROP using an agent that blocks simultaneously VEGF-A, VEGF-B, and placental growth factor. In this issue, McCloskey et al. 4 show similar findings using VEGF blockade alone. In a well controlled study in rodents, they show that more anti-VEGF blockade is not better but worse, leading to increased avascular retina and delayed atypical NV formation with activation of compensatory angiogenic signals that may not respond to subsequent VEGF blockade. They also showed that anti-VEGF therapy was associated with reduced weight gain. Their study highlights the need for more systematic research regarding the appropriate dose and monitoring of anti-VEGF in ROP babies in order to have a safer and more effective therapy than the current primitive ablative approaches. 
Smith LE. Through the eyes of a child: understanding retinopathy through ROP the Friedenwald lecture. Invest Ophthalmol Vis Sci . 2008; 49: 5177–5182. [CrossRef] [PubMed]
Mintz-Hittner HA Kennedy KA Chuang AZ BEAT-ROP Cooperative Group. Efficacy of intravitreal bevacizumab for stage 3+ retinopathy of prematurity. N Engl J Med . 2011; 364: 603–615. [CrossRef] [PubMed]
Lutty GA McLeod DS Bhutto I Wiegand SJ. Effect of VEGF trap on normal retinal vascular development and oxygen-induced retinopathy in the dog. Invest Ophthalmol Vis Sci . 2011; 52: 4039–4047. [CrossRef] [PubMed]
McCloskey M Wang H Jiang Y Smith GW Strange J Hartnett ME. Anti-VEGF antibody leads to later atypical intravitreous neovascularization and activation of angiogenic pathways in a rat model of ROP. Invest Ophthalmol Vis Sci . 2013; 54: 2020–2026. [CrossRef] [PubMed]

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