Topical aminocaproic acid facilitates reepithelialization of persistent epithelial defects

After corneal injury, persistent epithelial defects (PED's) may occur due to the chronic failure of the regenerating epithelium to adhere to the underlying stroma. The aim of this study was to examine the potential of epsilonaminocaproic acid (EACA) as a topical treatment for PED's. EACA inhibits the activation of plasmin, which metabolizes fibronectin. Fibronectin, a glycoprotein, anchors corneal epithelium to the basement membrane and the underlying stroma.

In anesthetized rabbits, PED's were induced with sodium hydroxide (1 N). Seven days later, during the late healing phase, treatment began with administration of EACA (30%) to the right eye and administration of vehicle alone to the left eye three times daily. A control group received neither EACA nor vehicle. Rabbits were treated for 19 days. PED's were visualized by fluorescein staining. Their size was mapped using digital planimetry.

After 11 days of treatment with EACA, treated PED's were 50% smaller than in corneas treated with vehicle alone. Following treatment for 15 days, corneas treated with EACA had significantly greater re-epithelialization than vehicle-treated or control corneas. Frozen sections stained immunofluorescently for fibronectin appeared to qualitatively contain more adherent fibronectin in treated corneas. Transmission and scanning electron microscopy indicated that the epithelium was more polymorphic, thinner and vacuolated in untreated controls compared to EACA treated eyes. Light microscopy demonstrated more continuous adherent epithelium after EACA treatment.

Topically administered EACA decreases both the severity and incidence of persistent epithelial defects produced by alkali bums to the cornea. EACA appears to promote adherence of the regenerating epithelium to the underlying stroma. Thus, topically administered EACA may be an effective treatment for this chronic condition.