Compensatory mechanisms are common in our body’s design. In fact recent evidence confirms compensatory tearing is how most dry eye disease (DED) patients can temporarily lower their tear osmolarity (TO) in a daily cyclical process in response to an unstable tear film secondary to hyperosmolarity. Have you ever wondered if patients with significant meibomian gland dysfunction (MGD) can experience increased tear production through lacrimal gland compensation?
In an Article in Press in the Ophthalmology journal, Arita et al present interesting evidence of this occurring in “Increased Tear Fluid Production as a Compensatory Response to Meibomian Gland Loss”. They compared tear film parameters as well as meibomian gland morphologic features and function among patients with meibomian gland dysfunction (MGD), those with non–Sjögren syndrome aqueous-deficient dry eye (non-SS ADDE), those with non-SS ADDE and MGD, and normal subjects. The tests include: ocular symptom score, lid margin abnormality score, meiboscore (infrared observation), meibum grade, fluorescein score, TBUT, and Schirmer’s test value. They conclude an increase in tear fluid production likely compensates for loss of meibomian glands in individuals with MGD.
Read more here.
Authors: Dr. Reiko Arita et al.