Wilson Steven E, Ambrósio Renato
Department of Ophthalmology, University of Washington School of Medicine, Box 356485, Seattle, WA 98195-6485, USA.
Cornea. 2002 Aug;21(6):560-3. doi: 10.1097/00003226-200208000-00005.
To examine the incidence of sporadic diffuse lamellar keratitis (DLK) in a large series of LASIK eyes and to suggest the hypothesis that the etiology of sporadic DLK differs from that of epidemic DLK.
The incidence and severity of DLK was noted in 1352 consecutive eyes that had primary LASIK for myopia or hyperopia and 217 consecutive eyes that had LASIK enhancement.
Twelve of the eyes having primary LASIK had stage 1 DLK and 5 had stage 2 DLK (.9% total). No eyes had stage 3 or stage 4 DLK. Three of the 217 eyes (1.4%) that had LASIK enhancement had stage 1 DLK. The difference in the rate of DLK for primary LASIK compared with LASIK enhancement was not statistically significant (p = 0.69). All eyes responded to intensive corticosteroid therapy, with the addition of flap lifting and irrigation for the eyes with stage 2 DLK. Two of the eyes (one primary LASIK and one LASIK-enhancement) had implanted epithelial nests associated with the DLK. None of the cases of DLK occurred in eyes of patients who had surgery on the same operating day in this series. Two other eyes that had epithelial abrasions more than 3 months after LASIK or LASIK enhancement developed stage 1 DLK.
Many cases of sporadic DLK, including cases associated with epithelial trauma after LASIK, are likely attributable to endogenous factors that trigger inflammation. One trigger is the release of epithelium-derived cytokines such as interleukin-1 that stimulate keratocytes to produce chemokines that are chemotactic to inflammatory cells. Cells likely accumulate at the interface because it is potential space, representing a path of least resistance for cell movement. Some sporadic cases may also be related to exogenous factors such as Betadine. Epidemic DLK is likely associated with exogenous factors that stimulate inflammation, such as endotoxin contaminating sterilizer reservoirs or detergents on instruments.
在大量准分子激光原位角膜磨镶术(LASIK)治疗的眼睛中检查散发性弥漫性板层角膜炎(DLK)的发生率,并提出散发性DLK的病因与流行性DLK不同的假说。
记录1352例因近视或远视接受初次LASIK手术的连续病例以及217例接受LASIK增效手术的连续病例中DLK的发生率和严重程度。
接受初次LASIK手术的眼睛中有12例发生1期DLK,5例发生2期DLK(总计0.9%)。无3期或4期DLK病例。217例接受LASIK增效手术的眼睛中有3例(1.4%)发生1期DLK。初次LASIK与LASIK增效手术的DLK发生率差异无统计学意义(p = 0.69)。所有眼睛对强化皮质类固醇治疗均有反应,对于2期DLK的眼睛还增加了掀开角膜瓣冲洗的操作。其中2只眼睛(1例初次LASIK手术,1例LASIK增效手术)的DLK伴有植入性上皮巢。本系列中,同一天手术的患者眼睛未发生DLK病例。另外2只在LASIK或LASIK增效手术3个月后发生上皮擦伤的眼睛出现了1期DLK。
许多散发性DLK病例,包括LASIK术后与上皮创伤相关的病例,可能归因于触发炎症的内源性因素。其中一个触发因素是上皮衍生的细胞因子如白细胞介素-1的释放,其刺激角膜细胞产生对炎症细胞具有趋化作用的趋化因子。细胞可能在界面处积聚,因为这是一个潜在的间隙,代表了细胞移动阻力最小的路径。一些散发性病例也可能与外源性因素如碘伏有关。流行性DLK可能与刺激炎症的外源性因素有关,如污染消毒器储液器的内毒素或器械上的清洁剂。