Glaucoma After Corneal Trauma or Surgery-A Rapid, Inflammatory, IOP-Independent Pathway
Glaucoma After Corneal Trauma or Surgery-A Rapid, Inflammatory, IOP-Independent Pathway
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DOI：
10.1097/ico.0000000000002106
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发表时间：
2019-12-01
期刊：
影响因子：
2.8
通讯作者：
Paschalis, Eleftherios, I
中科院分区：
文献类型：
--
作者：
Dohlman, Claes H.;Zhou, Chengxin;Paschalis, Eleftherios, I
目的：综述角膜手术或急性外伤后发生长期青光眼的临床和细胞分子过程，特别是肿瘤坏死因子α (tnf - α)的关键作用、视网膜神经节细胞继发性损伤的快速性以及早期抗炎干预的临床前景。方法：将一系列损伤后和术后青光眼的实验室研究与临床结果研究进行对比，重点研究碱烧伤对小鼠和家兔角膜视网膜神经节细胞的易损性，并以此为主要实验模型。检测了tnf - α滴度、神经节细胞凋亡和视神经轴突耗竭。抗tnf - α抗体或皮质类固醇已被用于保护视网膜神经节细胞。用测压法记录烧伤后眼压（TOP）。结果：角膜碱烧伤动物视网膜损伤可在24 ~ 72小时内发生。这并不是因为之后pH值的直接变化——碱在虹膜晶状体水平被有效地缓冲了。相反，tnf - α（和其他炎性细胞因子）在前面产生，在后面迅速扩散，导致神经节细胞凋亡。在此期间，TOP仍然远低于引起神经节细胞损伤所需的报告值。如果及时使用tnf - α抗体英夫利昔单抗或皮质类固醇，可显著保护神经节细胞。结论：实验室研究已经确定了急性前段外伤或手术导致的青光眼的快速启动，炎症（tnf - α介导），不依赖于眼压的途径。抗炎药的及时预防性治疗已被证明对视网膜神经节细胞具有显著的神经保护作用，可能能够降低晚期青光眼的风险。
Purpose: To review clinical aspects and cellular and molecular steps in the development of long-term glaucoma after corneal surgery or acute trauma-especially the pivotal role of tumor necrosis factor alpha (TNF-alpha), the rapidity of the secondary damage to the retinal ganglion cells, and the clinical promise of early antiinflammatory intervention.Methods: A series of laboratory studies on post-injury and postsurgery glaucoma have been compared to clinical outcome studies on the subject, focusing particularly on the vulnerability of the retinal ganglion cells Alkali burn to the cornea of mice and rabbits served as the main experimental model. TNF-alpha titer, ganglion cell apoptosis, and depletion of optic nerve axons have been examined. Anti-TNF-alpha antibodies or corticosteroids have been used to protect the retinal ganglion cells. Intraocular pressure (TOP) postburn was recorded by manometric methods.Results: In animals with alkali burn to the cornea, damage to the retina can occur within 24 to 72 hours. This is not because of a direct pH change posteriorly-the alkali is effectively buffered at the iris-lens level. Rather, TNF-alpha (and other inflammatory cytokines), generated anteriorly, rapidly diffuses posteriorly to cause apoptosis of the ganglion cells. During this time, the TOP remains much lower than the reported values required to cause ganglion cell damage. The TNF-alpha antibody infliximab or corticosteroids, if administered promptly, are markedly protective of the ganglion cells.Conclusions: A rapidly initiated, inflammatory (TNF-alpha mediated), IOP-independent pathway to glaucoma, resulting from acute anterior segment trauma or surgery, has been identified in laboratory studies. Prompt prophylactic treatment with antiinflammatory agents has been shown to be markedly neuroprotective of retinal ganglion cells, presumably capable of reducing the risk of late glaucoma.