J Refract Surg. 2020 Feb 1;36(2):124-130. doi: 10.3928/1081597X-20200114-01.
To review cytokine- and chemokine-mediated mechanisms of diffuse lamellar keratitis (DLK) after lamellar corneal surgical procedures.
Review of the basic science and clinical literature.
DLK can occur early or late (months to decades) after all lamellar corneal surgeries, including laser in situ keratomileusis, small incision lenticule extraction, anterior lamellar keratoplasty, and Descemet's stripping automated endothelial keratoplasty. It is most commonly triggered by epithelial injury during or after lamellar surgery, which leads to the release of interleukin (IL)-1α, IL-1β, and tumor necrosis factor (TNF)-α from the epithelium and into the stroma. These chemokines directly attract inflammatory cells into the cornea from the limbal blood vessels and also bind to receptors on keratocytes and corneal fibroblasts where myriad chemokines are upregulated that also chemotactically attract monocytes, macrophages, granulocytes, lymphocytes, and other bone marrow-derived cells into the corneal stroma. Other factors that can trigger DLK include retained blood in the interface, endotoxins and other toxins, and excessive keratocyte necrosis caused by femtosecond lasers. Infiltrating cells show a preference to enter any lamellar interface in the cornea, regardless of the time since surgery, because of the ease of movement toward the chemotactic attractants relative to the surrounding stroma with intact collagen lamellae and stromal cells that serve as relative barriers impeding motility. The mainstay of treatment is topical corticosteroids, but severe cases may also be treated with flap lift irrigation and systemic corticosteroids.
DLK can occur early or late after any lamellar corneal surgical procedure and is most commonly triggered by epithelial-stromal-bone marrow-derived cellular interactions mediated by corneal cytokines and chemokines. [J Refract Surg. 2020;36(2):124-130.].
综述板层角膜手术后弥漫性层状角膜炎（DLK）的细胞因子和趋化因子介导机制。
对基础科学和临床文献进行综述。
DLK 可在所有板层角膜手术后的早期或晚期（数月至数十年）发生，包括激光原位角膜磨镶术、微切口透镜提取术、前板层角膜移植术和 Descemet 膜撕除自动内皮角膜移植术。它最常由板层手术后的上皮损伤引发，导致白细胞介素（IL）-1α、IL-1β 和肿瘤坏死因子（TNF）-α从上皮释放到基质中。这些趋化因子直接将炎症细胞从缘血管吸引到角膜中，并与角膜成纤维细胞上的受体结合，在那里无数趋化因子被上调，也趋化性地吸引单核细胞、巨噬细胞、粒细胞、淋巴细胞和其他骨髓来源的细胞进入角膜基质。其他可能引发 DLK 的因素包括界面中残留的血液、内毒素和其他毒素以及飞秒激光引起的成纤维细胞过度坏死。浸润细胞表现出进入角膜任何板层界面的偏好，无论手术后时间长短，这是因为相对于胶原板层和基质细胞完整的基质，向趋化吸引剂移动更容易，而这些细胞作为相对的屏障阻碍了其运动。治疗的主要方法是局部皮质类固醇，但严重病例也可能需要进行瓣掀起冲洗和全身皮质类固醇治疗。
DLK 可在任何板层角膜手术后的早期或晚期发生，最常由角膜细胞因子和趋化因子介导的上皮-基质-骨髓源性细胞相互作用引发。[J Refract Surg. 2020;36(2):124-130.]。
