Obstructive sleep apnea-hypopnea syndrome (OSAHS) is sometimes accompanied by posterior and anterior segment diseases, the latter of which can cause ocular surface damage. Knowing this, it’s important to take a closer look at the meibomian glands, which protect the ocular surface and prevent ocular morbidity.

Researchers recently found that OSAHS yielded a loss in meibomian glands and a shortened first noninvasive tear break-up time (f-NTBUT), indicating that there could be a predisposition for evaporative dry eye originating from meibomian gland damage.

The study evaluated the right eye of 59 participants (32 OSAHS patients and 27 controls). The team measured f-NTBUT and average noninvasive TBUT and collected Schirmer scores, meibography and conjunctival impression cytology.

In the study and control groups, the investigators observed median f-NTBUTs of 2.1 seconds and 5.7 seconds and median average noninvasive TBUTs of 5.6 seconds and 7.2 seconds, respectively. They noted that the mean Schirmer values were 16.3±5.9mm and 17.3±6.6mm in the study and control groups, respectively.

In upper eyelid meibography, they discovered that the median losses in the meibomian glands were 20.10% in the study group and 14.70% in the control group; whereas, they were 19.00% in the study group and 12.40% in the control group in lower eyelid meibography. They added that the median Nelson grades in conjunctival impression cytology were one in both groups.

“Damage occurs in the meibomian glands of patients with OSAHS, and the meibomian gland loss causing this damage can be objectively determined with meibography,” the study authors concluded in their paper. “Therefore, it can be considered that in patients presenting with meibomian gland damage of unknown cause, OSAHS should be kept in mind.”