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Fabiano Cade, Eleftherios Paschalis, Caio V. Regatieri, Reza Dana, Claes H. Dohlman; Retinal Damage in Severe Chemical Burn and the Use of Infliximab Therapy. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6272.
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Severe alkali burns can lead not only to corneal opacity, but also to hard-to-treat glaucoma and/or traction retinal detachment. The aim of this study was to identify the mechanisms of damage to the retina, and its prevention by reducing the inflammatory response after chemical injury.
A 20 second burn was performed by applying a 3mm filter paper soaked with 1N NaOH to the central cornea of anesthetized Balb/c mice, followed by continuous irrigation for 15 minutes. The animals were randomly divided into two groups. Group 1 received an intra-peritoneal (i.p.) injection of (anti-TNFα) infliximab, and Group 2 received the same amount of isotype-matched IgG control i.p.. The mice were clinically evaluated at days 1, 3, 5, 7, 10, and 14. Neovascularization of the cornea was measured and compared between groups. TUNEL assay was performed to assess retina damage.
TUNEL assay showed damage to the ganglion cell layer in Group 2, but not in the infliximab-treated Group 1. Although no statistically significant difference was found at days 1 and 3, subsequently corneal neovascularization invasion into the cornea was significantly less in the infliximab group 1 compared to the control group 2. There was no difference in terms of opacification of the cornea.
This study demonstrates damage to the ganglion cell layer early after severe alkali burn. Additionally, the data suggest suppression of TNFα can drastically reduce both corneal and retinal damage.
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