PURPOSE To evaluate extracellular matrix regulators and inflammatory factors in a patient who developed ectasia after small incision lenticule extraction (SMILE) despite normal preoperative tomographic and biomechanical evaluation. METHODS The SMILE lenticules from both eyes of the patient with ectasia and three control patients (5 eyes) matched for age, sex, and duration of follow-up were used for gene expression analysis of lysyl oxidase (LOX), matrix metalloproteinase 9 (MMP9), collagen types I alpha 1 (COLIA1) and IV alpha 1 chain (COLIVA1), transforming growth factor-beta (TGF-beta), bone morphogenetic protein 7 (BMP7), interleukin-6 (IL-6), cathepsin K, cluster of differentiation 68, integrin beta-1, and tissue inhibitor of metalloproteinase-1 (TIMP1). Furthermore, the functional role of LOX was assessed in vitro by studying the collagen gel contraction efficiency of LOX overexpressing in primary human corneal fibroblast cells. RESULTS Preoperatively, manifest refraction was -9.25 diopters (D) in the right eye and -10.00 D in the left eye. Corneal thickness, Pentacam (OCULUS Optikgeräte GmbH, Wetzlar, Germany) tomography, and Corvis biomechanical indices (OCULUS Optikgeräte GmbH) were normal. The ectatic eye lenticule (left) had reduced expression of LOX and COLIA1 compared to controls without ectasia. Increased mRNA fold change expression of TGF-beta, BMP7, IL-6, cathepsin K, and integrin beta-1 was noted in the ectatic left eye compared to controls; however, MMP9 and TIMP1 levels were not altered. Ectopic LOX expression in human corneal fibroblast induced significantly more collagen gel contraction, confirming the role of LOX in strengthening the corneal stroma. CONCLUSIONS Reduced preexisting LOX and collagen levels may predispose clinically healthy eyes undergoing refractive surgery to ectasia, presumably by corneal stromal weakening via inadequately cross-linked collagen. Preoperative molecular testing may reveal ectasia susceptibility in the absence of tomographic or biomechanical risk factors. [J Refract Surg. 2019;35(1):6-14.].

中文翻译：

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具有不对称减少的基质分子标记的SMILE后的双侧不对称角膜蜕膜病变。

目的评估尽管术前X线断层扫描和生物力学评估正常的小切口小孔镜摘除术（SMILE）后发展为水肿的患者的细胞外基质调节剂和炎性因子。方法采用年龄，性别和随访时间相匹配的双眼扩张病患者和三名对照患者（5只眼）的SMILE晶状体进行赖氨酰氧化酶（LOX），基质金属蛋白酶9（MMP9）的基因表达分析。 ），I型胶原蛋白I alpha 1（COLIA1）和IV型胶原蛋白alpha 1链（COLIVA1），转化生长因子β（TGF-beta），骨形态发生蛋白7（BMP7），白介素6（IL-6），组织蛋白酶K， 68，整合素β-1和金属蛋白酶1（TIMP1）的组织抑制剂组成的簇。此外，通过研究LOX在原代人角膜成纤维细胞中过度表达的胶原蛋白凝胶收缩效率来评估LOX的功能作用。结果术前，右眼的明显屈光度为-9.25屈光度（D），左眼的屈光度为-10.00D。角膜厚度，Pentacam（OCULUSOptikgeräteGmbH，德国韦茨拉尔）的断层扫描和Corvis生物力学指标（OCULUSOptikgeräteGmbH）是正常的。与无扩张的对照组相比，扩张的眼小透镜（左）的LOX和COLIA1表达降低。与对照组相比，直肠左眼的TGF-β，BMP7，IL-6，组织蛋白酶K和整联蛋白β-1的mRNA倍数变化表达增加。但是，MMP9和TIMP1的水平没有改变。人角膜成纤维细胞中异位LOX的表达明显诱导更多的胶原蛋白凝胶收缩，证实了LOX在增强角膜基质中的作用。结论降低的既往LOX和胶原蛋白水平可能使接受屈光手术的临床健康的眼睛易患扩张症，可能是由于交联胶原蛋白不足导致角膜基质变弱。术前进行的分子检测可能会在没有断层扫描或生物力学危险因素的情况下显示出扩张性敏感性。[J Refract Surg。2019; 35（1）：6-14。]。[J Refract Surg。2019; 35（1）：6-14。]。[J Refract Surg。2019; 35（1）：6-14。]。