I think back to 1996 when I was a resident. PRK and LASIK were just coming into their own as predominant refractive surgical procedures. At the time, we didn’t know whether the variability in the outcomes of these procedures was due to broad beam technology, flap interface abnormalities or something else. Ultimately, we figured it was due largely to this little known, rarely mentioned thing — dry eye disease. Seriously, we knew nothing about DED. We only knew that these patients had issues, and we had no earthly idea of how to really “fix” them.
Fast forward 20 years. We grapple with the complexity and variability of the disease. We have seen blockbuster drugs and devices. Through it all, we have barely scratched the surface of truly solving the mystery. In my opinion, this is largely because we are “stuck” thinking of dry eye as an ocular disease because, well… that is what we look at. But maybe, just maybe, we are missing something.
BACK TO THE FUTURE
Only in the future will we be able to look back and know what is missing with certainty. I think we will finally “see” that DED is an ocular manifestation of a much larger array of interconnected systemic diseases. We will likely find that MGD is largely linked to multiple different endocrine dysfunctions. Some components will be alterations in testosterone, while others will be directly related to certain DNA-linked lipid production abnormalities. We will likely find that the production abnormalities influence not just ocular lipid issues but also various dermatological conditions, gastroenterological diseases and notably hemodynamics, as blood pH has a much greater role in disease status than we give it credit for. We will likely find that aqueous issues are largely an inflammatory reaction that start with androgenic changes and are exacerbated by certain medications that affect both gut biome and overall nutritional deficiencies.
More important, we will begin to understand that the most efficient and productive treatments are systemic in nature and that diagnosis is only partially found in a slit lamp. We will likely diagnose through hormone profiles, serum inflammatory markers and DNA testing.
Treatments will also likely look radically different. I am not saying the way we currently treat is wrong, just early in the life cycle of treatment as we will come to know it. Circa 1996 glaucoma therapy consisted of a beta blocker and pilocarpine, but I am guessing that much as we look at that as “primitive” now, we will see drops, drugs and plugs in the same way in the future. I believe we will find that localized treatment is temporary and that if we really want to “fix” these disease states, we need to look much deeper than the lids, ocular surface epithelium and that 5 um thick tear prism. Treatments will likely target adjusting hormone levels, correcting nutritional deficiencies and altering anti-inflammatory markers at a systemic level.
HELPING THE WHOLE PERSON
I think that future researchers and astute clinicians will find that most “inflammatory ocular surface conditions” are really manifestations of something much grander than that two-inch stripe between our nose and forehead. Maybe we will look back and wonder why we were so focused on such a small area, when helping the “dry eye” patient is about helping the whole person from head to toe. OM