Meibomian gland dysfunction (MGD) is believed to be the leading cause of dry eye disease (DED), which afflicts tens of millions Americans (1). Of particular interest, the most common pharmaceutical treatment for the management of MGD in the United Statesis the off-label use of topical azithromycin (2). This macrolide antibiotic is presumed to be effective because of its anti-inflammatory and anti-bacterial actions, which may suppress the MGD-associated posterior blepharitis and growth of lid bacteria (3). However, there are no published, peer-reviewed data demonstrating that azithromycin has the ability to act directly on the human meibomian gland to enhance this tissue’s function, and to ameliorate the pathophysiology of MGD. We hypothesize that azithromycin can act directly on human meibomian gland epithelial cells to stimulate their differentiation, enhance the quality and quantity of their lipid production, and promote their holocrine secretion. Our purpose was to begin to test our hypothesis.
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Liu et al. (2013) studied this question.
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