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TFOS DEWS二期病理生理学报告 TFOS DEWS II pathophysiology report

期刊名称:The Ocular Surface

卷期:2017年第15卷第3期

摘要

摘要:TFOS DEWS Ⅱ病理生理小组委员会回顾了干眼症起始和延续的机制。其中枢机制是蒸发性水分流失导致的高渗组织损伤。在患者以及动物模型上的研究均表明,无论是直接或通过炎症间接引起,都导致了上皮细胞和杯状细胞的流失。随后的表面湿润度降低导致了早期泪膜破裂并通过恶性循环增加高渗的程度。干眼症的疼痛是由于泪液高渗、润滑减少、以及神经因素导致的,然而视觉症状是由于泪液以及眼球表面不规则引起。摩擦的增加使眼睑和眼球表面受到损伤,导致点状上皮角膜炎、边缘角膜缘结膜炎、丝状角膜炎、睑结膜平行襞以及眼睑刷上皮病变。具有泪液缺乏型和蒸发型两种特性的混合型干眼病很常见,我们应该努力琢磨每种形式对总体图景所起的作用。为了这个目的,需要在临床上采取实际的手段来测量泪液蒸发,同样地,需要在组织学水平测量眼球表面渗透压,这样可以更好的评估干眼症严重程度。未来的研究领域应该包括基因机制在非干燥综合症干眼症中起到的作用,睑板腺疾病中作用于终末导管的靶点,以及凝视动力学和闭眼状态对泪液稳定性和眼球表面炎症的影响。

 

The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjgren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.


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