Moilanen Jukka A O, Holopainen Juha M, Helintö Maaret, Vesaluoma Minna H, Tervo Timo M T
Department of Ophthalmology, University of Helsinki, Helsinki, Finland.
J Cataract Refract Surg. 2004 Feb;30(2):341-9. doi: 10.1016/j.jcrs.2003.09.057.
To examine the inflammatory reaction in acute or late-onset post-laser in situ keratomileusis (LASIK) diffuse lamellar keratitis (DLK) associated with an epithelial defect.
Department of Ophthalmology, Helsinki University Central Hospital, Helsinki, Finland.
Six consecutive LASIK patients presented with stage 2 to 3 unilateral DLK 1 to 4 days after formation of an epithelial detachment (intraoperatively or up to 19 months postoperatively). Five corneas of 5 DLK patients, 1 eye twice, were examined by corneal in vivo confocal microscopy 1 to 8 days after the appearance of the epithelial defect. Confocal microscopy of conjunctival venules was performed in 2 of 6 DLK patients to quantify leukocyte rolling and extravasation. Corneas of 5 patients and conjunctival venules of 4 patients who had uneventful LASIK served as controls.
Two of the 4 patients examined 0 to 1 day after the onset of DLK presented with small objects, presumably inflammatory cells (diameter 6.0 to 10.0 microm), in the LASIK flap interface. A third patient examined 1 day after the onset of DLK had larger objects (approximately 13.0 microm in diameter) in the interface. Three other cases (1 to 7 days after the onset of DLK) showed changes typical of keratocyte activation and altered extracellular matrix. All cases healed completely following treatment with steroids. Control LASIK subjects showed some keratocyte activation on day 5.
Neither uneventful LASIK nor DLK induced an inflammatory reaction displaying leukocyte rolling in conjunctival venules or extravasation into the conjunctival stroma. Diffuse lamellar keratitis related to an epithelial defect does not always lead to the appearance of inflammatory cells in the flap interface. The corneal manifestations of epithelial defect-related DLK may originate from sterile epithelial-stromal or inflammatory cell-stromal cell interactions, leading to alteration of the keratocyte phenotype.
研究急性或迟发性准分子激光原位角膜磨镶术（LASIK）后弥漫性板层角膜炎（DLK）合并上皮缺损时的炎症反应。
芬兰赫尔辛基大学中心医院眼科。
6例连续的LASIK患者在出现上皮脱离后1至4天（术中或术后长达19个月）出现2至3期单侧DLK。5例DLK患者的5只角膜（1只眼检查2次）在出现上皮缺损后1至8天接受角膜共聚焦显微镜检查。6例DLK患者中的2例进行结膜微静脉共聚焦显微镜检查以量化白细胞滚动和渗出。5例LASIK手术顺利患者的角膜和4例患者的结膜微静脉作为对照。
4例在DLK发病后0至1天接受检查的患者中有2例在LASIK瓣界面出现小物体，推测为炎性细胞（直径6.0至10.0微米）。第3例在DLK发病后1天接受检查的患者在界面有较大物体（直径约13.0微米）。其他3例（DLK发病后1至7天）显示出典型的角膜细胞活化和细胞外基质改变。所有病例经类固醇治疗后均完全愈合。对照LASIK受试者在第5天显示出一些角膜细胞活化。
无论是手术顺利的LASIK还是DLK均未引起结膜微静脉中白细胞滚动或渗入结膜基质的炎症反应。与上皮缺损相关的弥漫性板层角膜炎并不总是导致瓣界面出现炎性细胞。与上皮缺损相关的DLK的角膜表现可能源于无菌的上皮-基质或炎性细胞-基质细胞相互作用，导致角膜细胞表型改变。
