[Meibomian gland dysfunction in Salzmann's nodular degeneration]

Salzmann's nodular degeneration (SND) is a corneal disease characterized by superficial subepithelial fibrosis. The exact pathophysiological mechanism of corneal damage in SND is unclear. It is likely related to the disruption of the structural integrity of corneal epithelial cells due to chronic inflammation and impaired homeostasis of the ocular surface.

This study aimed to evaluate tear film (TF) status and meibomian gland (MG) function in SND.

The study included 196 patients (386 eyes) with typical clinical features of SND (the main group) and 50 nominally healthy individuals (100 eyes) who underwent routine ophthalmic screening (the control group). The mean age in the study group was 48.0±12.7 years, with women comprising 85% of participants. Keratotopography and the dry eye disease (DED) diagnostic system were used to assess the first tear film break-up time (FTBUT) and the average tear film break-up time (ATBUT), tear meniscus height, lipid layer thickness, degree of MG loss (atrophy), eyelid margin condition, and conjunctival/limbal hyperemia.

All patients in the study group exhibited DED and grade 2-3 meibomian gland dysfunction (MGD); FTBUT and ATBUT were 5.2±1.5 s and 6.4±1.7 s, respectively. In the control group, mean FTBUT (11.4±3.7 s) and ATBUT (12.2±4.1 s) values were within normal limits, and MG atrophy corresponded to grade 1 MGD, showing statistically significant differences from the study group. No significant intergroup differences were found in tear meniscus height (21.2±4.3 mm vs. 22.4±3.6 mm), lipid layer thickness (41.3±1.6 nm vs. 56.6±1.4 nm), eyelid margin and conjunctival/limbal hyperemia.

SND predominantly affects women aged 45-50 years. The main risk factor for the disease is stage II-III MGD (MG atrophy of more than ⅓), accompanied by DED. Significant irregularity of the corneal surface in SND further exacerbates the course of DED.