Abstract
Background
Corneal inflammation has long been associated with contact lens wear and the use of extended‐wear lenses enhances the risk of corneal injury. Elucidation of the molecular mediators of contact lens‐associated inflammation has the potential to provide injury‐identifying markers early in the inflammatory process, as well as determine potential therapeutic targets.
Methods
This cross‐over study investigated a potential correlation between overnight contact lens wear and the concentrations of two markers of inflammation, α1‐antitrypsin and C‐reactive protein, in tear fluid. To obtain baseline measurements, 17 subjects adapted to wearing silicone hydrogel contact lenses wore their prescribed eye glasses for one week, after which tears were collected and ocular health assessed by a licensed optometrist. Subjects then returned to wearing their prescribed silicone hydrogel lenses continuously for one week. A second tear sample was collected and ocular inflammation was again assessed. Enzyme‐linked immunosorbent assays were performed on all tear samples for both α1‐antitrypsin and C‐reactive protein.
Results
α1‐antitrypsin was significantly (p = 0.01) elevated after continuous contact lens wear, with increases above baseline concentrations averaging 2.48‐fold. Optometric assessment of inflammation loosely correlated with levels of this inflammatory marker. C‐reactive protein was detected in the tears of subjects at both times and levels were also slightly elevated after extended lens wear, but not significantly (p > 0.5) and not consistently in all subjects.
Conclusion
The results of this study suggest that α1‐antitrypsin in tear fluid may be useful as an early marker of contact lens‐associated ocular irritation and inflammation. The presence of C‐reactive protein in the tears of contact lens wearers is a novel finding which, while not correlative with either α1‐antitrypsin concentrations or clinically observable inflammation, may warrant further study.
Acknowledgements
The authors would like to thank Dr Mark Taylor for his expertise in clinically evaluating optic inflammation, the study subjects for their participation and Dr Leonard Gary Nielsen for his contributions to the study design.
This study was funded by the Weber State University Office of Undergraduate Research and by the George S. & Delores Dore Eccles foundation.