T. M. Zhmud, G. I. Drozhzhyna, L. M. Velychko

It is known that chronic hyperglycemia contributes to defective wound regeneration in the external layers of the cornea, abnormalities in sub-basal nerve fiber plexus, and loss of endothelial pump function. Pathological alterations are observed in the functioning of the Meibomian glands (MGs) in individuals with type 2 diabetes. Dysfunction of the MGs leads to increased viscosity of secretions, stasis of secretions in the ducts, and gradual loss of MGs, resulting in qualitative and quantitative changes in the lipid layer of the tear film.

The ocular surface is a unique environment due to its immune properties. In addition to its typical barrier function, it provides protection against self-immune cells and potential damage resulting from their excessive activation in response to infectious, mechanical, or chemical agents. Neutrophil granulocytes (CD45, CD15) are representative of innate cellular immunity, primarily due to their phagocytic properties and direct migration to the site of inflammatory processes and infiltration of adjacent tissues.

In the study, the prognostic value of the neutrophil activation marker CD15+ was evaluated as a predictive factor for ocular surface damage in patients with type 2 diabetes.

Results: For the first time, the prognostic role of the relative level of CD15+ neutrophil activation marker was assessed in ocular surface damage associated with type 2 diabetes. A sufficiently high sensitivity index for the CD15+ biomarker (88.3%) allows its use as a screening method for detecting ocular surface impairment in patients with type 2 diabetes. The relative expression level of CD15+ neutrophils in the blood of patients with type 2 diabetes (>27%) increases the risk of ocular surface damage by 10.52 times.