Silicone hydrogel contact lenses retain and document ocular surface lipid mediator profiles.

A leading reason for patients to abandon their contact lenses is discomfort. Mechanisms and biomarkers for lens discomfort remain to be elucidated. Physical stress and tear film interaction are likely factors for lens discomfort. Lipid mediators are generated from polyunsaturated fatty acids. They regulate ocular surface physiology and pathophysiology, are constituents of human tears and may interact with contact lenses. This study set out to determine if hydrogel lenses and silicone hydrogel lenses interact with tear film polyunsaturated fatty acids and polyunsaturated fatty acids-derived mediators. In vitro incubations, rat experiments and analysis of worn human lenses assessed polyunsaturated fatty acids and lipid mediator interactions with lenses. Silicone hydrogel and hydrogel lenses were incubated with lipid mediators and polyunsaturated fatty acids up to 24 hours. Rats were fitted with custom silicone hydrogel lenses and basal tears collected. Silicone hydrogel lenses worn for 2 weeks were obtained from 57 human subjects. Tear and lens lipidomes were quantified by mass spectrometry. Silicone hydrogel lenses retained polyunsaturated fatty acids and lipid mediators within 15 minutes in vitro. Lenses contained 90% of total polyunsaturated fatty acids and 83–89% of total monohydroxy fatty acids by 12 hours. Retention correlated with polarity of lipid mediators and lipophilic properties of silicone hydrogel lenses. Polyunsaturated fatty acids and lipid mediators such as lipoxygenase- and cyclooxygenase-derived eicosanoids were present in tears and worn lenses from rats. Worn silicone hydrogel lenses from human subjects established robust and lens-type specific lipidomes with high levels of polyunsaturated fatty acids, lipoxygenase-pathway markers and subject-specific differences in lipoxin A4 and leukotriene B4. Worn silicone hydrogel lenses rapidly retain and accumulate tear polyunsaturated fatty acids and lipid mediators. Marked subject and lens type differences in the lipidome may document changes in ocular surface physiology, cell activation or infection that are associated with lens wear. If contact lens discomfort and adverse events induce specific tear and lens fatty acid and lipid mediator profiles warrants further studies. [ABSTRACT FROM AUTHOR]