February 21, 2017
One of the neat things about being on the Rubber Chicken Dinner Circuit of industry-sponsored talks is that you get to hear firsthand what it is that your peers are thinking about and talking about in their practice lives. You also get a sense of how much (or how little) of what you understand as basic knowledge in your own practice is in place out in the wild. It’s especially enlightening when you learn how confusing much of the information that supports the use of our various medicines can be made in the name of marketing.
Take, for example, the importance of goblet cell function in inflammatory dry eye disease (DED). That is to say, in pretty much all of DED. It doesn’t matter what incited the initial inflammation; all of it is going to cause goblet cells to throw up their collective hands and quit doing their job. Your patient, the unsuspecting goblet cell landlord, is then going to suffer the symptoms of DED. Meibomian gland dysfunction, high osmolarity, reduced aqueous production, true allergy or adenoviral infection — it just doesn’t matter. Inflammation rocks goblet cells in a non-“Rock on, dude” way.