Fast Five Quiz: Dry Eye Disease (Keratoconjunctivitis Sicca) Etiology and Pathophysiology

Christina R. Prescott, MD, PhD


November 10, 2022

Androgens are believed to be trophic for the lacrimal and meibomian glands. They exert potent anti-inflammatory activity via production of TGF-β, which suppresses lymphocytic infiltration. In meibomian gland dysfunction, androgen deficiency results in loss of the lipid layer (specifically loss of triglycerides, cholesterol, monounsaturated essential fatty acids such as oleic acid, and polar lipids including phosphatidylethanolamine and sphingomyelin). Loss of polar lipids, which are present at the aqueous-tear interface, exacerbates evaporative tear loss. Loss of unsaturated fatty acids raises the melting point of meibomian gland secretions, or meibum. This leads to thicker, more viscous secretions that obstruct ductules and cause stagnation of secretions.

Both androgen and estrogen receptors are located in the lacrimal and meibomian glands. At menopause, a decrease in circulating sex hormones occurs, possibly affecting the functional and secretory aspect of the lacrimal gland. This may explain the prevalence of DED in women (the sex discrepancy increases with age). According to a 2019 study of 46 androgen-deficient patients, those treated with androgen replacement had statistically significant improvements in tear breakup time, corneal staining, Schirmer scores, and Ocular Surface Disease Index scores at 4 weeks compared with those receiving placebo.

Learn more about sex hormone deficiency in DED.


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