Особенности клинической картины, визуализации и лечения инфильтративного кератита после ускоренного кросслинкинга роговичного коллагена

Insights into the clinical presentation, imaging, and management of infiltrative keratitis following accelerated corneal collagen cross-linking.

CXL offers solution to a wide range of patients with progressive keratoconus.[¹] However, it carries certain risks associated with procedural complications. The conventional and accelerated CXL begin with epithelial debridement and impregnation of corneal stroma with riboflavin. This is followed by exposure to ultraviolet-A light for induction of biochemical reaction. The corneal epithelium is a major anatomical barrier and one of the first defence mechanisms of the eye. The corneal epithelium features four types of junctions: tight junctions (zonula occludens), desmosomes (macula adherens), adherens junctions (zonula adherens), and gap junctions. These junctions create a robust barrier, further strengthened by the secretion of heavily O-glycosylated transmembrane mucins like MUC1, MUC4, and MUC16. Additionally, the corneal epithelium plays a role in regulating the immune response. When the epithelium is compromised, cell surface glycosylation is disrupted and galectin-3 expression increases, which can increase susceptibility to infections. In response, corneal epithelial cells produce antimicrobial peptides, such as β-defensins, to help protect against potential pathogens.[²] Thus, any disruption of corneal epithelium, inadvertently multiplies the risks of infection.