Anonic Silicon Hydrogels Affect the Concentration of Proteins in Tears during Wear.

PURPOSE: The objective of this study was to quantitatively assess the concentration of human tear proteins in patients wearing contact lenses of various ionicities and determine whether differences were related to the incidence of corneal infiltrative events (CIE). METHODS: 24 subjects (samples) were randomly selected for spectral count analysis to obtain protein concentrations using LCMS analysis. The subjects were neophyte and ametropic with ages between 18 and 40; 6 wore control lenses, 8 wore TestLens1, and 10 wore TestLens2. 16 subjects experienced CIEs during the study. RESULTS: A pairwise multiple hypothesis test identified 7 proteins that significantly differed in concentration between TestLens1 and control, and 11 proteins that differed between TestLens2 and control. Of the 12 unique proteins, 9 were at increased concentration and 3 were at lower concentration in the tears of test lens wearers compared to the control lens group. Bootstrap clustering confirmed these findings, showing 3 similar clusters to the original sample groups which separated people wearing control lenses from those wearing TestLens1 or TestLens2 with 83% accuracy and between TestLens1 and TestLens2 with 45% accuracy. Permutation testing identified 5 proteins that had significantly changed in concentration between people wearing TestLens2 and Control lenses. There was no difference in protein concentrations between those subjects who experienced a CIE and those who did not. CONCLUSION: Wearing contact lenses of different ionicities can affect the concentration of proteins in the tear film. The current study did not find any associations of the concentration of proteins with CIEs. Future tests with increased sample size are needed to establish any relations between these changes and clinical performance.

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

CLINICAL RELEVANCE: A leading reason for patients to abandon their contact lenses is discomfort. Mechanisms and biomarkers for lens discomfort remain to be elucidated. BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.