Study Suggests Majority of Dry-Eye Patients Have No Eye Surface Inflammation
In a new study published this month in Investigative Ophthalmology (2006:47:2445-2450), Narayanan and co-workers report the results of a study of patients with moderate dry eye. This is an important group because according to a paper by Lemp and referenced by the authors, "nearly two thirds of persons with dry eye have a moderate form of the disease, NS KCS (non-Sjögren's dry eye)." In other words, the authors are reporting on the type of dry eye most people with dry eye have.
They found that although these patients had a significant level of dry-eye irritation, increased tear film osmolarity (increased salt concentration in their tears), definite eye surface damage as evidenced by flourescein and lissamine green vital dye staining, shorter tear-film breakup times (instability of their tear film) and delayed tear clearance (with decreased tear production the tears stay in the eye longer), there was no increase in inflammatory cytokine expression on the eye surface.
They conclude, ""Even though this small amount of ocular surface damage was adequate to cause significant dry eye symptoms in our study, it might not have been enough to up regulate IL-1b and the other inflammatory cytokines to a detectable level...In summary, the results of the present study indicate that the role of IL-1b inflammation in the pathogenesis of ocular surface damage in moderate dry eye is questionable."
This paper provides yet more evidence that inflammation of the eye surface does not cause symptoms of dry eye, and continues to support the theory that elevated tear film osmolarity causes the symptoms of dry eye, and drives the changes that subsequently develop on the ocular surface. Earlier studies that had found increased expression of inflammatory cytokines on the ocular surface had studied a rarer group of patients with more severe disease. We can hypothesize that in these patients the inflammatory process represents part of the ocular surface healing response.
In addition the paper decreases the rationale for the broad use of topical anti-inflammatory treatments in the majority of dry-eye patients. To read the paper, click HERE.
They found that although these patients had a significant level of dry-eye irritation, increased tear film osmolarity (increased salt concentration in their tears), definite eye surface damage as evidenced by flourescein and lissamine green vital dye staining, shorter tear-film breakup times (instability of their tear film) and delayed tear clearance (with decreased tear production the tears stay in the eye longer), there was no increase in inflammatory cytokine expression on the eye surface.
They conclude, ""Even though this small amount of ocular surface damage was adequate to cause significant dry eye symptoms in our study, it might not have been enough to up regulate IL-1b and the other inflammatory cytokines to a detectable level...In summary, the results of the present study indicate that the role of IL-1b inflammation in the pathogenesis of ocular surface damage in moderate dry eye is questionable."
This paper provides yet more evidence that inflammation of the eye surface does not cause symptoms of dry eye, and continues to support the theory that elevated tear film osmolarity causes the symptoms of dry eye, and drives the changes that subsequently develop on the ocular surface. Earlier studies that had found increased expression of inflammatory cytokines on the ocular surface had studied a rarer group of patients with more severe disease. We can hypothesize that in these patients the inflammatory process represents part of the ocular surface healing response.
In addition the paper decreases the rationale for the broad use of topical anti-inflammatory treatments in the majority of dry-eye patients. To read the paper, click HERE.
posted by Jeffrey P. Gilbard, MD at 2:43 PM
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