OBJECTIVE: To explore the mechanism by which diclofenac sodium eyedrops exert an adverse effect on the cornea. METHODS: In 10 healthy Japanese volunteers, 0.1% diclofenac sodium solution was instilled into one eye 3 times daily for 2 weeks. Only vehicle was applied to the other eye. Tear samples were taken before drug treatment, at 2 weeks (on the final day of treatment), and at 4 weeks. Prostaglandin E(2) and substance P concentrations in tears were measured using enzyme immunoassays. RESULTS: After treatment for 2 weeks, concentrations of both prostaglandin E(2) and substance P in tears from diclofenac sodium-treated eyes had decreased significantly, and both had returned to baseline levels by 4 weeks. No significant changes were seen in prostaglandin E(2) and substance P levels in vehicle-treated eyes at any time points. CONCLUSIONS: Diclofenac sodium eyedrops concurrently reduced concentrations of prostaglandin E(2) and substance P in tears. Depletion of substance P (a pain-associated neurotransmitter) by diclofenac sodium may promote development of corneal complications.
OBJECTIVE: To explore the mechanism by which diclofenac sodium eyedrops exert an adverse effect on the cornea. METHODS: In 10 healthy Japanese volunteers, 0.1% diclofenac sodium solution was instilled into one eye 3 times daily for 2 weeks. Only vehicle was applied to the other eye. Tear samples were taken before drug treatment, at 2 weeks (on the final day of treatment), and at 4 weeks. Prostaglandin E(2) and substance P concentrations in tears were measured using enzyme immunoassays. RESULTS: After treatment for 2 weeks, concentrations of both prostaglandin E(2) and substance P in tears from diclofenac sodium-treated eyes had decreased significantly, and both had returned to baseline levels by 4 weeks. No significant changes were seen in prostaglandin E(2) and substance P levels in vehicle-treated eyes at any time points. CONCLUSIONS:Diclofenac sodium eyedrops concurrently reduced concentrations of prostaglandin E(2) and substance P in tears. Depletion of substance P (a pain-associated neurotransmitter) by diclofenac sodium may promote development of corneal complications.