Introduction
The aim of this study was to comparatively analyze the effects of topical intraocular pressure (IOP)-lowering drugs on the ocular surface and to elucidate whether the main causative factor of toxicity is associated with benzalkonium chloride (BAK) or an active compound.
Methods
The medical records of 300 eyes in 187 glaucoma patients that had instilled IOP-lowering drugs were cross-sectionally reviewed. Corneal epithelial punctuate erosion and tear break-up time (BUT) were quantitatively assessed. Durations of glaucoma, sums of concentrations of BAK in current medication (BAK%sum), and the presence of beta-blockers were investigated as risk factors (Institutional Review Board of Seoul National University Hospital, Seoul - IRB number: H-1007-103-324).
Results
Age-adjusted BAK%sum was found to be significantly and positively correlated with corneal epithelial punctate erosion (P = 0.001, r = 0.208) and negatively correlated with BUT (P = 0.042, r = 0.131). BAK%sum adjusted corneal epithelial erosion was found to be significantly greater in beta-blocker containing eyedrop-instilled eyes (P = 0.016). No difference in ocular toxicity was found between carbonic anhydrase inhibitor and prostaglandin analog or between latanoprost- and travoprost-treated eyes.
Conclusion
Long-term treatment with BAK-containing antiglaucoma medication appears to be the main contributor to corneal toxicity and to do so in a dose-dependent manner. Formulations containing beta-blockers also appear to contribute to corneal toxicity.