Factors assoсiated with ocular structural changes inherent to pseudoexfoliation syndrome among Ukrainian patients.

Abstract

Objective: Aim: To identify factors associated with ocular structural changes inherent to PEX among Ukrainian patients.

Patients and methods: Materials and Мethods: The study was based on a clinical examination of 56 patients (112 eyes) aged 14 to 88 years. The main group included 39 patients (78 eyes) with ocular structural changes confirming the diagnosis of PEX: 14 patients (28 eyes) and 25 patients (50 eyes) with uni- and bilateral lateral involvement, respectively. The control group consisted of 17 patients (34 eyes) without any signs of PEX. The follow-up period was 5 years.

Results: Results: The findings of the study support the concept of PEX as a systemic fibrillopathy, accompanied by a significant association with chronic coronary syndrome (64%), joint pathology (72%), diabetes mellitus (40%), and central nervous system (56%) disorders compared with the control group. Environmental factors, particularly urbanization (52%) and increased radiation background (64%), are likely additional contributors to disease development. The study demonstrated that bilateral PEX is accompanied by changes in eye structures: pronounced trabecular pigmentation (48%), a critical decrease in corneal endothelial cell density (80%), progression of age-related macular degeneration (40-44%), and the development of posterior subcapsular cataract (96%). In contrast, patients with unilateral PEX demonstrated a significantly higher long-term risk of nuclear cataract progression.

Conclusion: Conclusions: Managing patients with PEX necessitates a comprehensive multidisciplinary approach in view of the associated comorbidities and contributing factors. The clinical course of unilateral PEX is strongly linked to exposure to exogenous triggers (urbanization, increased background radiation, and tobacco smoking). The absolute majority of eyes with bilateral PEX showed biomechanical weakness of the sclera and cornea.