Sodium hyaluronate decreases ocular surface toxicity induced by benzalkonium chloride-preserved latanoprost: an in vivo study.

PURPOSE To investigate the effects of sodium hyaluronate (SH) on ocular surface toxicity induced by benzalkonium chloride (BAC)-preserved latanoprost. METHODS Twenty-one white rabbits (42 eyes) were randomly divided into three groups. The control group was untreated. The two experimental groups were treated with 0.02% BAC-containing latanoprost once a day combined with unpreserved 0.3% SH or PBS three times daily for 60 days. Schirmer test, fluorescein and rose bengal staining, and conjunctiva impression cytology were performed on days 0, 31, and 61. Apoptosis of conjunctival epithelium was detected by TUNEL assay on day 61. Conjunctival inflammation was evaluated with light microscopy. Cornea and conjunctiva ultrastructure were observed by electron microscopy. RESULTS Compared with the control group, the PBS-treated latanoprost group showed increases in fluorescein and rose bengal scores, decreases in Schirmer scores, and goblet cell density (GCD) on days 31 and 61. Increases in inflammatory and apoptotic cells in conjunctiva, and ultrastructural disorders of the cornea and conjunctiva were also observed on day 61. Compared with the PBS-treated latanoprost group, the SH-treated latanoprost group showed decreases in fluorescein and rose bengal scores, and increases in Schirmer scores and GCD on days 31 and 61. Decreases in inflammatory and apoptotic cells in conjunctiva and amelioration of ultrastructural disorders were also observed. CONCLUSIONS Topical application of SH significantly decreased the ocular surface toxicity induced by BAC-preserved latanoprost. As a vehicle or neutralizing material, SH could be proposed to reduce ocular toxicity and protect the ocular surface in long-term BAK-preserved antiglaucoma medication treatment.