Background: Cataract surgery is the most common operative procedure performed in Canada, and how patients are affected by wait times for this surgery has important clinical, public health and health policy considerations. We conducted a systematic review to understand the relation between wait time for cataract surgery and patient outcomes and the variables that modify this relation. Methods:We performed an electronic search of 11 databases and the proceedings of 4 conferences. The search was restricted to studies published after the transition to phacoemulsification (1990). We assessed the quality of the included studies using the Jadad Scale for randomized controlled trials and the Newcastle-Ottawa Scale for cohort and case-control studies. The data were found to be inappropriate for meta-analysis, thus we performed a qualitative synthesis. Results:We found a total of 27 studies that met our inclusion criteria. When these studies were reviewed, a dichotomy was observed for the wait time-outcome relation: outcomes associated with wait times of ≤ 6 weeks were better than outcomes associated with wait times of ≥ 6 months. Patients who waited more than 6 months to receive cataract surgery experienced more vision loss, a reduced quality of life and had an increased rate of falls compared with patients who had wait times of less than 6 weeks. The outcomes associated with wait times between 6 weeks and 6 months remain unclear. Interpretation:Patients who wait more than 6 months for cataract surgery may experience negative outcomes during the wait period, including vision loss, a reduced quality of life and an increased rate of falls. CMAJ 2007;176(9):1285-90 Abstract

PTK is an important treatment of RCES refractory to other therapies. Long-term data suggest that most patients treated with PTK do not develop recurrences, and side effects from PTK are minimal.

Purpose Benzalkonium chloride (BAK) is the most commonly found preservative in eye drops, and has been shown to cause ocular surface inflammation and toxicity. Lacritin is a human tear glycoprotein secreted from the lacrimal glands that has been found to be cytoprotective. This study was designed to determine if the presence of lacritin confers protection to a cultured human corneal epithelial (HCE) cell line, CRL-11515, and primary HCE cells after exposure to the ocular preservative agent BAK. Materials and Methods Recombinant human lacritin was cloned into intein fusion vectors, expressed in E. coli, and purified on chitin beads and DEAE Sepharose. Metabolic curves were established using the MTT assay after exposure of subconfluent CRL-11515 cells to BAK or lacritin. Western blot analysis of lipidated LC3 (LC3-II) provided a measure of autophagy in CRL-11515 cells exposed to lacritin and/or BAK. Results BAK reduced CRL-11515 cellular metabolic activity in a time and dose dependent manner. BAK-induced cellular stress was evident by elevated autophagy that increased with rising concentrations of BAK compared to control (P < 0.05). Lacritin increased HCE cell proliferation at an optimal dose of 1 nM. Preconditioning HCE cells with 1 nM lacritin for 24 hours prior to BAK exposure significantly dampened levels of LC3-II (P < 0.05) and promoted a significant increase in cellular metabolic activity (P < 0.01) compared to BAK alone. Conclusions These results suggest lacritin protects cultured HCE cells stressed with BAK. Lacritin may have the potential to be used as a topical adjunctive therapy in eyes chronically exposed to BAK.

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