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Editors Selection IGR 12-2

Medical Therapy: OH after VEGF

Comment by Malik Kahook on:

25833 Persistent ocular hypertension following intravitreal bevacizumab and ranibizumab injections, Adelman RA; Zheng Q; Mayer HR, Journal of Ocular Pharmacology and Therapeutics, 2010; 26: 105-110

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The intravitreal injection of anti-vascular endothelial growth factors (VEGF), such as bevacizumab and ranibizumab (Genentech Inc., South San Francisco, CA), has been linked with persistent elevation in intraocular pressure (IOP).^1-3This phenomenon has been noted after single or multiple injections of these agents and the exact cause of the IOP spikes is still under investigation.⁴ Adelman et al. (901) recently reported four cases of persistent elevation in IOP after multiple injections of anti-VEGF agents in patients who were treated for wet age-related macular degeneration. This represented 3.45% (4/116) of the patients who were included in their retrospective review. The authors also noted that the IOP spikes occurred after a mean of 13.3 injections (range 3-19) and that a disruption of the posterior capsule (from YAG capsulotomy), present in two of the four patients, may predispose to elevation in pressure. The authors did note that none of the four patients had a history of glaucoma or ocular hypertension (OHT). On review of their report, however, it does appear that three of the patients had an increase in cup-todisc ratio and/or history of long-term steroid use at the time of the diagnosis of OHT. The authors provide some possible causes of the IOP spikes including the possibility of anti-VEGF agents causing an obstruction in the aqueous outflow system of the eye due to their large molecular weights. Others have published similar cases to those reported by Adelman et al. and have agreed that this phenomenon is likely linked to intravitreal anti-VEGF injections and not merely a chance occurrence in a susceptible patient population.^1-3 It is unlikely, however, that the IOP spikes are due to a mechanical obstruction from the bevacizumab monomers or the ranibizumab fab fragments alone. If this were the case, there likely would be many more cases reported in the literature. Recent work indicates that repackaging of bevacizumab in plastic syringes and the mishandling of ranibizumab vials can sometimes lead to aggregation of proteins as well as to the formation of leachable contaminants (silicone) within the injected solution that may then lead to obstruction of the aqueous outflow system when injected into the eye.⁴ This problem is more likely to arise with improper handling of the protein based therapeutic agents and would be a much more plausible explanation for the low number of OHT cases noted after intravitreal anti-VEGF therapy in clinics around the world. The cases noted by Adelman et al as well as prior publications have shed light on this potentially sight threatening phenomenon. More studies will be needed to better understand the cause of these IOP spikes and how to decrease the incidence of OHT caused by intravitreal anti-VEGF therapy.

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