Thyroid eye disease (TED) typically manifests as edema, redness in the periorbital tissues in addition to conjunctiva, upper eyelid retraction and proptosis. Dry eye disease (DED) caused by ocular surface damage is also overwhelmingly common for patients with TED (up to 65.2% prevalence rate). This connection may be observed through differences in ocular surface changes during the active and inactive stages of the disease, which were each notably different from the controls in this recent study.

The 60 total study eyes (60 patients) were divided up into three separate groups: Group A, comprised of 20 eyes with active TED, Group B, comprised 20 eyes with inactive TED and Group C, comprised 20 eyes of controls without dry eye manifestations.

The following were assessed and compared between participants: palpebral fissure height, degree of proptosis, degree of lagophthalmos, ocular surface disease index (OSDI), Schirmer test without anesthesia, corneal fluorescein staining, non-invasive tear break-up time, tear meniscus height, lipid layer thickness, meiboscore, meibomian gland dysfunction (MGD) and thyroid antibodies.

Researchers concluded that for patients with TED, the orbital inflammation can trigger DED and ocular surface manifestations in 45% to 85% of patients. MGD was found in 80% of Group A and 55% of Group B. The measured degrees of lagophthalmos and exophthalmos were significantly higher in eyes with active TED. Schirmer’s test values were much lower in Group A compared to those Group B, but both were significantly decreased from that of the controls. They also found that tear film break-up time was shorter and the OSDI and meibography score were higher in those in Group A with active TED. No significant differences were detected between groups for lipid layer thickness.

“The lower Schirmer test values can be explained by the presence of exophthalmos, upper eyelid retraction and lagophthalmos,” the researchers wrote in their paper on the study. “In TED, there was a decrease in both the membranes associated and secretory mucin owing to the inflammatory process that leads to evaporative DED and consequently the other ocular surface parameters including tear film instability.”

The results suggest that DED worsens and is more severe during the active phase of the disease because of mechanical impairment and MGD. Dry eye manifestations were also shown to persist through the inactive phase due to lid retraction and proptosis. Because of the small sample size and other study limitations, further research is needed to determine the role of thyroid antibodies and other possible contributing factors of DED in patients with active or inactive TED.