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Editors Selection IGR 18-1
Basic Science: Source of VEGF in neovascular glaucoma
Comment by Tina Wong on:
58858 Human ciliary epithelium as a source of synthesis and secretion of vascular endothelial growth factor in neovascular glaucoma, Chalam KV; Brar VS; Murthy RK, JAMA ophthalmology, 2014; 132: 1350-1354
The effective treatment of neovascular glaucoma lies in the cause and site of elevated VEGF secretion. Most commonly the retinal pigment epithelium to secrete VEGF into the vitreous humor, and diffusing into the aqueous humor, in response to a hypoxic or ischaemic event. Appropriate treatment with pan retinal photocoagulation reduces the local tissue hypoxia by destroying the retinal cells responsible for secreting VEGF as well as stimulating angiogenic inhibitors. The authors observed though that despite extensive PRP, iris neovascularisation and therefore elevated IOP persisted in some individuals. Through the application of Nd:YAG laser cyclophotocoagulation or cyclocryotherapy, complete regression of iris neovacularization was noted in these eyes. This prompted Chalam et al. to investigate the ciliary epithelium as another source of VEGF and explain the angiogenic response following treatment from the two laser types.
The authors evaluated the expression of VEGF in human enucleated eyes with intractable neovascular glaucoma with no light perception previously treated with standard PRP, using in situ hybridization and immunohistochemical staining. Positive staining for VEGF expression was found in all affected eyes compared to healthy control cadaver eyes. The authors conclude that the ciliary epithelium to be an important source of VEGF and proposed that cyclophotocoagulation should be considered in highrisk eyes to prevent the secretion of VEGF from the ciliary epithelium which can lead to a poorer prognosis in eyes that are already sick. The results of the study prove to be an important step to improving current clinical management of neovascular glaucoma. It also provides an insight into greater understanding of the cellular events that occur in response to global ischaemia or hypoxia. It would be most interesting to further evaluate this idea with a prospective study.
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