Cornea · 2018
Chemical Burns of the Eye: The Role of Retinal Injury and New Therapeutic Possibilities.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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История · было → стало
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Dohlman Claes H, Cade Fabiano, Regatieri Caio V, Zhou Chengxin, Lei Fengyang, Crnej Alja, Harissi-Dagher Mona, Robert Marie-Claude, Papaliodis George N, Chen Dongfeng, Aquavella James V, Akpek Esen K, Aldave Anthony J, Sippel Kimberly C, DʼAmico Donald J, Dohlman Jan G, Fagerholm Per, Wang Liqiang, Shen Lucy Q, González-Andrades Miguel, Chodosh James, Kenyon Kenneth R, Foster C Stephen, Pineda Roberto, Melki Samir, Colby Kathryn A, Ciolino Joseph B, Vavvas Demetrios G, Kinoshita Shigeru, Dana Reza, Paschalis Eleftherios I
Аннотация
PURPOSE: To propose a new treatment paradigm for chemical burns to the eye - in the acute and chronic phases.
METHODS: Recent laboratory and clinical data on the biology and treatment of chemical burns are analyzed.
RESULTS: Corneal blindness from chemical burns can now be successfully treated with a keratoprosthesis, on immediate and intermediate bases. Long term outcomes, however, are hampered by early retinal damage causing glaucoma. New data suggest that rapid diffusion of inflammatory cytokines posteriorly (TNF-α, etc) can severely damage the ganglion cells. Prompt anti-TNF-α treatment is markedly neuroprotective. Long term profound reduction of the intraocular pressure is also vital.
CONCLUSION: A new regimen, in addition to standard treatment, for severe chemical burns is proposed. This involves tumor necrosis factor alpha (TNF-α) inhibition promptly after the accident (primarily for retinal neuroprotection), prophylactic maximal lowering of the intraocular pressure (starting immediately), and keratoprosthesis implantation in a later quiet state.
METHODS: Recent laboratory and clinical data on the biology and treatment of chemical burns are analyzed.
RESULTS: Corneal blindness from chemical burns can now be successfully treated with a keratoprosthesis, on immediate and intermediate bases. Long term outcomes, however, are hampered by early retinal damage causing glaucoma. New data suggest that rapid diffusion of inflammatory cytokines posteriorly (TNF-α, etc) can severely damage the ganglion cells. Prompt anti-TNF-α treatment is markedly neuroprotective. Long term profound reduction of the intraocular pressure is also vital.
CONCLUSION: A new regimen, in addition to standard treatment, for severe chemical burns is proposed. This involves tumor necrosis factor alpha (TNF-α) inhibition promptly after the accident (primarily for retinal neuroprotection), prophylactic maximal lowering of the intraocular pressure (starting immediately), and keratoprosthesis implantation in a later quiet state.