炎性黄斑水肿的生理病理观察。

Developments in ophthalmology Pub Date : 2017-01-01 Epub Date: 2017-03-28 DOI:10.1159/000455279
Marc D de Smet
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引用次数: 17

摘要

黄斑水肿是葡萄膜炎患者永久性视力丧失的最常见原因之一。目前对视网膜内水分平衡和代谢的了解,使我们对急性和慢性炎症引起的黄斑水肿的机制有了更好的了解。当水的流入和流出失去平衡时,更重要的是当代偿机制被淹没时,会发生葡萄膜性黄斑水肿(UME)。而在急性环境下,控制炎症可以重建体内平衡,慢性炎症可以导致替代途径来建立水平衡。要了解UME,必须了解炎症在组织水平上的调节和后果。炎症和视网膜之间存在着良好的相互作用,充满了代偿机制、旁观者效应和炎症消退后的结构性后遗症。这一认识可能使我们开发出治疗炎性黄斑水肿的新治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insights into the Physiopathology of Inflammatory Macular Edema.

Macular edema is one of the most common causes of permanent vision loss in patients with uveitis. The current understanding of water balance and metabolism within the retina has given us better insight into the mechanisms underlying macular edema arising from both acute and chronic inflammation. Uveitic macular edema (UME) occurs when the equilibrium between water influx and efflux is lost, and more importantly when compensatory mechanisms are overwhelmed. While in the acute setting, control of inflammation can reestablish homeostasis, chronic inflammation can lead to alternate pathways to establish a water balance. To understand UME, one must understand the regulation and consequences of inflammation at the tissular level. A fine interplay exists between inflammation and the retina replete with compensatory mechanisms, bystander effects, and structural sequelae once inflammation subsides. This understanding may allow us to develop new therapeutic strategies for the treatment of inflammatory macular edema.

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