discovering dry eye
to Severe Dry Eye
BY BARBARA CAFFERY, OD, MS, FAAO
When examining dry eye disease, it's often interesting to take a closer look at the driest of dry eyes to learn more about the end stage of the disease. Many of these patients have Sjögren's Syndrome.
Some, however, experience comparably bad symptoms and appear to have equally bad ocular surfaces but no autoimmune disease. Let's look at how the two groups differ.
Sjögren's Syndrome patients have documented autoantibodies in their blood. By definition they have Schirmer scores of less than 5mm or they have a high degree of rose bengal staining and have suffered dry eye symptoms for more than three months. Their documented salivary gland inflammation likely reflects the inflammatory response of the lacrimal gland.
The Sjögren's disease process seems understandable. As in all autoimmune diseases, the cells of the secretory glands change their surfaces in such a way that the lymphocytes perceive them as foreign and attack. The attack destroys the acinar cells or prevents them from secreting, whereby the lacrimal gland becomes dysfunctional. This reduced secretion causes a breakdown of the surface cells of the cornea and conjunctiva that appears as staining.
The epithelial cells that normally secrete mucins onto the surface of the eye stop performing this task and goblet cells become fewer in number and do not secrete their particular mucins to the ocular surface. We then observe these uncomfortable eyes as severe dry eyes.
What about the other severe dry eyes that we see? Who are these patients and what is their
pathophysiology? Their blood does not contain the autoantibodies rho and la, so the autoimmune process that causes Sjögren's cannot occur. Proof is that their salivary and lacrimal glands do not hold the inflammatory lymphocytes present in Sjögren's Syndrome.
The clinical measures of their disease vary somewhat in severity. Their symptoms are the same but they tend to exhibit a lesser degree of staining and higher Schirmer results.
A Mystery to Solve
What is the process of severe dry eye disease if autoantibodies are not present? Perhaps unknown factors break down the neurological stimulus to the lacrimal gland. Or the neurology is fine but the gland is unwilling to accept the stimulus. Have the acinar cells undergone a change that prevents them from secreting? Is the final common pathway of the disease the same no matter what the
Finally, how does this thought process apply to our everyday mild to moderate dry eye patients? Are some of them early Sjögren's patients whose disease has not progressed to the level of clinical diagnosis? If we analyzed their lacrimal glands would we see the beginnings of lymphocyte infiltration? If we could analyze their cell walls would we find changes in proteins on the cellular surfaces that will eventually result in autoimmune processes? Or do these patients represent an entirely separate group who have extraordinarily sensitive ocular surfaces? Is another inflammatory process happening that defies analysis because of our crude methods?
In Search of an Answer
The amazing reality is that we don't know. This pervasive disease remains a mystery. Clinicians are working to solve the problem, but more are needed to lend insight into dry eye. We must continue asking, looking and
thinking. Many keys exist that can help unlock the mysteries of this disease. We will continue to search until we find them.
Dr. Caffery has practiced optometry in Toronto, Canada, in a group setting dedicated to contact lens and tear film research since
Contact Lens Spectrum, Issue: November 2003