Hypotheses on the role of prostaglandins in the pathogenesis of epinephrine maculopathy and aphakic cystoid macular edema.

Abstract

This article presents hypotheses regarding pathogenesis of epinephrine maculopathy. According to these hypotheses, two points are the most essential in the development of epinephrine-induced CME: one is the stimulation of PG synthesis by some tissues, presumably, the anterior uvea by the applied epinephrine, the other is the dysfunction, in some aphakic eyes, of the active transport system (Bito's pump) which is responsible for the removal of PGs from intraocular fluids. To test these hypotheses, the authors and their group conducted several experimental studies. The results of these studies, which have been reviewed in this article, strongly suggest that epinephrine maculopathy is induced by a mechanism involving PGs or possibly, other related eicosanoids and not simply by epinephrine per se, as has previously been suggested. This in turn suggest the existence of some common factors in the pathogenesis of epinephrine maculopathy and aphakic or pseudophakic CME.