Abstract

Citation: Qiu TG (2014) Ocriplasmin and Muller Glia. Adv Ophthalmol Vis Syst 1(1): 00002. DOI: 10.15406/ aovs.2014.01.00002 Stalsmans et al. [1] published an article entitled of “Enzymatic Vitreolysis with Ocriplasmin for Vitreomacular Traction and Macular Holes” based on the two pivotal Phase-III clinical safety and efficacy studies of ocriplasmin. The overall clinical efficacy was encouraging and marked 40%-60% anatomic closures of macular holes without further surgery. Whilst taking a close look at the safety profile noted on FDA Ophthalmic Drug Advisory Committee Meeting Debriefing [2], 5.6% patients experienced a vision decrease (2-3 line loss) during the first week post injection and slowly recovered over a six-month period, accordingly, a transit reduction of Electroretinogram (ERG) on both aand b-wave amplitudes was remarkable [2]. By far, there seems no sound biological explanation to such adverse event. This letter is to shed light on Muller glia as the primary biologic interface between ocriplasmin and neurosensory retina.

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