Relationship between in vitro toxicity of benzalkonium chloride (BAC) and preservative-induced dry eye.

Abstract

The term “dry eye syndrome” encompasses various ocular surface defects with a common element: deterioration in quantity and/or quality of lacrymal film. A constant step in the evolution of dry eye is an increase in tear osmolarity, leading in turn to other anomalies of the ocular surface. These include decreased conjunctival goblet cell density, increased corneal epithelial desquamation and destabilization of the cornea-tear interface. Iatrogenically induced dry eye is commonly encountered in clinical practice, especially while long-term treatments are employed for chronic ophthalmic affections such as glaucoma or allergy.1–4 On the cellular level, long-term use of topical, preserved drugs is associated with conjunctival metaplasia, stromal infiltrates, and epithelial expression of inflammation-dependent molecules (HLA DR), as well as apoptotic markers.5,6 The toxic and pro-inflammatory actions of preservatives on surface epithelia, as well as their detergent effect on the lipid phase of lacrymal film, seem to be responsible for these alterations.7,8 The role of active compounds of topical drugs in these pathological processes is not well established, although some in vivo and in vitro studies have demonstrated the lack of any noxious, tissue or cellular side effects.9,10 The aim of the present study was to investigate the relationship between the possible in vitro toxic effects of benzalkonium chloride (BAC), the most commonly used ophthalmic preservative, and the pathology of dry eye.