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Preservative, not the antiglaucoma agent, is cause of CME
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 Kensaku Miyake, MD, gave the Binkhorst Medal Lecture at ESCRS. |
NICE, France — The preserved vehicle, not the antiglaucoma agent, is the cause of cystoid macular edema in pseudophakic patients, according to research presented here.
The acceleration of blood-aqueous barrier disruption and the heightened incidence of cystoid macular edema (CME) in early postoperative pseudophakes is induced by the preservative benzalkonium chloride, not the glaucoma medication itself, said Kensaku Miyake, MD.
“From the results of our studies, we believe the addition of the preservative contributes significantly to CME produced by antiglaucoma eye drops rather than the main agents, such as latanoprost and timolol,” Dr. Miyake said. He presented his research on the cause of postop CME in his 2002 Binkhorst Medal Lecture, “Pseudophakic preservation maculopathy,” here at the European Society of Cataract and Refractive Surgeons meeting.
Citing multiple studies, Dr. Miyake noted that it has been well documented that antiglaucoma drugs — specifically epinephrine, dipivefrin, latanoprost and timolol — have been reported to induce CME in postoperative aphakic and pseudophakic eyes.
“This is very remarkable and is an interesting phenomenon,” he said.
The purpose of Dr. Miyake’s study was to investigate the influence of antiglaucoma eye drops on the blood-aqueous barrier and CME.
In 1977, Dr. Miyake developed the hypothesis that the addition of a preservative to glaucoma drugs may contribute to the incidence of CME. Citing published studies and his own multiple prospective, randomized controlled trials, he illustrated that a preservative may indeed be impetus for CME formation.
To confirm the clinical results, Dr. Miyake investigated the effects of latanoprost, timolol and benzalkonium chloride on cell morphological damage and expression of prostaglandin-E2.
“The results of our study indicate that benzalkonium chloride, as a preservative in eye drops of latanoprost and timolol maleate, damages lens epithelial cells and stimulates the expression of chemical mediators,” Dr. Miyake said.
In a phenomenon he termed preservation maculopathy, the preservative accelerates biosynthesis of prostaglandins by intraocular cells during the wound-healing process.
Dr. Miyake noted that these results correspond well to his 1977 hypothesis. He said further study is needed relative to the reaction induced by other postoperative eye drops.