advertisement
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.
Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Full article11.16 Vehicles, delivery systems, pharmacokinetics, formulation (Part of: 11 Medical treatment)
2.1 Conjunctiva (Part of: 2 Anatomical structures in glaucoma)