Dry eye: pharmacological approaches, effects, and progress.
OBJECTIVE
The effects of available pharmaceuticals on the tear film and ocular surface in dry eye are reviewed and the progress that has been made in dry eye treatment is discussed.


METHODS
Pharmaceuticals are examined with regard to their effect on physical and morphological events or milestones in the natural history of dry eye disease.


RESULTS
Dry eye disease evolves cumulatively over time through a sequence of four events: 1) decreased tear production or increased tear film evaporation (increased tear osmolarity); 2) decreased conjunctival goblet-cell density; 3) increased corneal epithelial desquamation; and, finally, 4) destabilization of the cornea-tear interface. In the 1970s, demulcents were introduced to decrease tear film instability. More recently, preservative-free solutions have been shown to decrease corneal desquamation. The newest pharmaceutical available today is known as TheraTears (ATF); in pre-clinical studies it restores conjunctival goblet cells. On the horizon are medications such as 3-isobutyl-1-methylxanthine (IBMX), which directly stimulate tear production.


CONCLUSIONS
As our understanding of the pathogenesis and natural history of dry eye disease has improved, pharmaceuticals have been designed to act at earlier and more crucial points in the disease process. We are now entering a new era in dry eye treatment with the introduction of the first agent that can reverse the basic events of dry eye surface disease.
Gilbard
J P
JP
Cornea Research Unit, Schepens Eye Research Institute, Harvard Medical School Boston, MA, USA.
D003315:Cornea / Q000378:metabolism / Q000473:pathology; D015352:Dry Eye Syndromes / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D009885:Ophthalmology / Q000639:trends*; D013666:Tears / Q000378:metabolism
D006003:Glycogen