## 4 Discussion  
SAS is characterized by recurrent episodes of total or partial collapse of the upper airways. It is associated with daytime drowsiness that cannot be explained by other factors, or the patients \"experience two or more of the following factors: episodes of suffocation during sleep, recurrent episodes of awakening during sleep, fatigue during the day, impaired ability to focus, restless sleep\" [1,2,8]. Known as one of the characteristic mechanisms of SAS, hypoxia can progress with cardiovascular, neurological, ophthalmic complications [9]. Current evidence suggests that the inflammatory processes, oxidative stress, and endothelial dysfunction play a role in the pathogenesis of sleep apnea complications. Most ophthalmic connections with SAS show a vascular potential etiology [6]. Among the ocular manifestations, the most significantly evaluated ones by our study are the damage to the ocular surface (dry-eye syndrome and changes in corneal biomechanics) and lesions in the optic nerve (glaucoma, ischemic optic neuropathy), etc. In SAS, the levels of pro-inflammatory cytokines (TNF-alpha, IL-1, IL-6) are increased based on chronic intermittent hypoxia. As AHI increases, the mechanical stress of tissues, the hypoxia and inflammation of the ocular surface increase, which in turn lead to loss of meibomian and goblet cells function, and a decrease of corneal sensitivity and of tear production as a response to the stimulation of the lacimal glands. The loss of these cells is clinically reflected as deterioration in the tear film quality [5]. An early complication of SAS is the dry-eye syndrome, especially the one associated with floppy eye syndrome, highlighted by the Schirmer 1 test and the Break-up time test. In 2019, [PERSON] et al. [9] conducted their first study aiming at evaluating the ocular surface and the morphological changes of meibominus glands by specific tests: the breaking of the tear film (break-up time), Schirmer 1 test and objectively by meibography in patients diagnosed with SAS to highlight the connection between SAS and dry-eye syndrome. The meibography showed significant loss of the meibominus glands, their morphological alterations including shortening of the ducts, dilation, and distortion. As a result, the hypothesis was validated, while in the case of patients with severe SAS a particularity was observed, namely: the association of SAS with a dry-eye syndrome by evaporation. In 2020 [PERSON] et al. conducted a cohort study where they confirmed the connection between the dry-eye syndrome and other factors, including ocular disease surface. High blood pressure and high BMI were strongly associated with fewer dry-eye symptoms or current smoking, while former smokers had drier eyes [10]. In our study, the Schirmer I test was performed, and according to statistical analysis the results were similar to [PERSON]'s study, i.e., it was significantly statistical lower in patients with glaucoma and SAS vs. those without SAS, thus demonstrating the effects of sleep apnea on the ocular surface. [PERSON] et al. [9] claim that the damage to the meibominus gland in the upper eyelids in patients with SAS is much more visible compared to healthy subjects, especially those with severe SAS. The connection between SAS and glaucoma has been confirmed over time by several studies, which investigated several glaucoma-specific ocular parameters, including increased IOP, thinning of RNFL peripapillary, visual field impairment, glaucomatous changes of the optic nerve [3]. The prevalence of glaucoma in SAS patients has been investigated by numerous studies, the results ranging from 5.9% [3], 12.9%--[PERSON] et al.