Evaluation of dry eye syndrome in patients with obstructive sleep apnea syndrome based on serum hypoxia-inducible factor 1 alpha (HIF-1α), matrix metalloproteinase 2 (MMP-2), and desmosine levels

To determine changes in dry eye parameters and serum HIF-1α, MMP-2, and desmosine levels in obstructive sleep apnea syndrome (OSAS) and their correlation. This prospective case-control study included 125 patients divided into mild-to-moderate OSAS (n = 40), severe OSAS (n = 46), and control groups (n = 39). Meibomian gland dropout was evaluated with a tomograph and corneal topographer, apnea-hypopnea index (AHI) with polysomnography, and serum HIF-1α, MMP2, and desmosine levels were analyzed using an enzyme-linked immunosorbent assay. Serum HIF-1α and MMP2 levels of the participants in the mild-to-moderate and severe OSAS groups were significantly higher, and serum desmosine levels were significantly lower than those in the control group (all p = 0.001). The upper eyelid meibomian gland dropout values were higher in the severe OSAS group than those in the control group (p = 0.001) (Table 1). Lower and total eyelid meibomian gland dropout values of the participants in the severe and mild-to-moderate OSAS groups were higher than those in the control group (all, p = 0,001). The NIKBUT-first, NIKBUT-average, total eyelid abnormality score, FES, and Oxford scores were not significantly different. The SPEED questionnaire scores of the participants in the severe and mild-to-moderate OSAS groups were higher than those in the control group, and the SPEED questionnaire values of the participants in the severe OSAS group were higher than those in the mild-to-moderate OSAS group (all, p = 0,001). The serum HIF-1α and MMP-2 levels of the participants were positively correlated with the total eyelid meibomian gland dropout values (r = 0,208, p < 0,05 and r = 0,227, p < 0,05, respectively). There was a negative correlation between inflammatory mediators (HIF-1α and MMP-2) and meibomian gland dropout in OSAS. This indicates that there are systemic factors involved in the etiopathogenesis of OSAS damage on the ocular surface. Further research on developing treatment strategies to modulate HIF-1α and MMP-2 may help reduce ocular surface morbidity in patients with OSAS.