June 14, 2018
5 min read
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Who has dry eye in 2018: an update

Over the years, the DED population exploded as the disease definition expanded.

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It is 2018. Who has dry eye disease today? One-half of all eye care tweets are about dry eye. Tiny organizations and journals that have microscopic readership hashtag dry eye treatments as if they invented them. You could simply declare that everyone who comes to your clinic has dry eye, drop the mic and walk off the stage to a standing ovation. While that is probably not entirely true, it is actually pretty close to reality.

When I started my own ophthalmology odyssey at NYU in the mid-1980s, dry eye (all lowercase, not even a syndrome let alone a disease) was pretty much universally considered the crabgrass that grew on the lawn of eye care. Neither ophthalmologists nor optometrists had any interest at all in the care of patients with dry eye for the simple reason that neither ophthalmologists nor optometrists had any idea what to do for those patients.

Was that a problem? As I recall, dry eye was largely confined to an elderly population in general, and specifically to those elderly patients who did lots of reading. Mind you, this was reading of a different sort than what we will get to here in a minute. The printed word was really just that, words printed in ink on paper that was variously consolidated in things called books, newspapers and magazines. Whether it was decreased blink frequency (the near vision effect), low tear volume or an early tear film breakup time (nearly never measured, by the way), you addressed every case in precisely the same way.

“Go to the pharmacy and pick up some artificial tears. Put them in when you feel like you need them. No, it doesn’t matter which one you get.”

To be sure, this elderly patient who is otherwise devoid of any other problem still exists. However, our ability to more finely parse the nuances of dry eye has increased in parallel with the explosive increase in options to treat what we now call Dry Eye Disease (all caps). Is DED actually more common now, or is it simply this increase in our dual capabilities (and with them an increase in doctors treating DED) that makes it appear more common? The answer is an unqualified “yes.”

More patients

Allergan rightly gets credit for the first effort to crack the DED code. Research done just before the launch of Restasis (cyclosporine ophthalmic emulsion 0.05%) identified another cohort of patients we still see to this day: young women on their way to entering mid-life. The archetype of a DED patient in the early aughts was a woman between the ages of 35 and 55 years who lived what we would all consider a regular life. She had reduced tear volume, usually had some punctate staining and was often very, very unhappy. There really is something about being female that makes DED both more common and often more severe. This patient is still very common; there is no excuse to miss the diagnosis of DED in a young woman who has DED symptoms.

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Here it stood for a good solid 10 years when we gave thought to who it was who came to our offices with DED. All of those older patients were still there, joined by their daughters and daughters-in-law. Estimates of the prevalence of DED were generally in the single-digit millions in the U.S. What happened in the late 2000s that produced the second bump in the number of patients diagnosed with DED? Mike Lemp gave compelling evidence that elevated tear osmolarity was diagnostic of DED, and Bill Trattler showed how DED was a frequent cause of poor vision. Dr. Trattler alerted us to think DED in cases of blurred vision, and Dr. Lemp was instrumental in developing a test that helped us diagnose DED in non-classic settings.

For several years, DED was seen primarily in elderly patients, women in mid-life and adults who came to the office complaining of blurred vision. Surveys and studies now suggested that 10 million to 12 million Americans suffered from DED enough to require at least one visit to an eye doctor. Of these, at least 1 million were actively treated with some sort of professionally directed care. It was around 2008 that we started to see more cornea docs talking about DED as a subspecialty of anterior segment care. Still, with only one medication available with an on-label dry eye indication, our limited ability to treat DED put the brakes on our efforts to diagnose it more frequently.

Symptomatic DED

There we may very well have stayed had it not been for another brilliant doctor supported by some of the most bold and imaginative industry executives in our midst. Gary Foulkes showed us that evaporative DED was associated with very specific abnormalities in meibomian gland secretions. An early tear film breakup could be tracked back to carbon chain structural changes in tear film lipid that produced an increased melting point and thick, sludge-like secretions. Foulkes pointed out that topical azithromycin normalized the carbon chain structure, reduced the melting point of meibum and effectively treated many cases of evaporative DED.

Much to the chagrin of the FDA, in 2010 Inspire launched the “Metal Man” campaign, which changed our focus from the lacrimal glands and goblet cells and directed our attention to the lid margin. Good thing, that, because meibomian gland dysfunction is the reason why it seems like every single patient you see has DED. We now think that there are 50 million to 60 million Americans who have symptomatic DED. Although we still have patients with aqueous deficient DED, most of these patients have evaporative DED. Why so many and why now?

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In 2010, Apple introduced the iPhone 4, the first real smartphone and the progenitor of the multi-screen lifestyle.

Remember the beginning of my story, those elderly patients who did not blink as frequently when they read? Every computer screen, including a smartphone, induces that near vision effect of reduced blink frequency. They also reduce the blink amplitude, how completely one blinks. Since the introduction of the iPhone 4, everyone you see now spends hours every day looking at a computer screen. The industrialization of food production in the U.S. (corn-based sweeteners, corn as feed for livestock and farmed fish) is partly responsible over the long course for less healthy meibomian glands. Inadequate blinking leads to greater degrees of evaporation from the ocular surface, and both produces and propagates surface inflammation. Xiidra’s (lifitegrast ophthalmic solution 5%, Shire) arrival allowed us to effectively treat a greater percentage of these inflamed eyes, giving eye doctors more incentive to make the diagnosis.

Why do people come to see you? Ocular discomfort of some sort? The No. 1 cause is DED. Blurred or altered vision of some sort? The No. 2 cause is DED (No. 1 is spectacle need). Face it, 95% of your patients eat a regular American diet with food they purchase at a grocery store; 95% of your patients have at least one computer screen that they look at for hours every single day. Even kids have DED! A Korean study of grade school children found that 9% of kids younger than 10 years have DED. Preeya Gupta’s group recently found similar stats at Duke. Unless you are a subspecialist with a very narrow scope of practice, every single patient you see has DED.

Drops mic.

Disclosure: White reports he is a consultant to Allergan, Shire, Sun, Kala, Ocular Science, Rendia, TearLab, Eyevance and Omeros; is a speaker for Shire, Allergan, Omeros and Sun; and has an ownership interest in Ocular Science and Eyevance.