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Contact lens-associated corneal infiltrates
Authors:Robboy Marc W  Comstock Timothy L  Kalsow Carolyn M
Affiliation:Bausch & Lomb, Inc., Rochester, NY, USA. mrobboy@bausch.com
Abstract:PURPOSE This review article examines recent studies pertaining to contact lens-associated corneal infiltrates (CLACI) that occur in the absence of culture-proven microbial infection. METHODS The literature was reviewed in regard to the clinical appearance, incidence and risk, etiology, pathophysiology, differential diagnosis, and management of CLACI. Recent insights are presented in the context of future directions for prevention of CLACI. RESULTS Contact lens-associated corneal infiltrates may manifest in various forms that require careful observational skills to ensure proper diagnosis. Although the reported incidence of CLACI varies widely, even a low percentage of contact lens wearers would constitute a substantial number of affected individuals. Any one or a combination of multiple mechanical, hypoxic, or toxic stimuli associated with contact lens use can induce proinflammatory responses that lead to infiltration of inflammatory cells into the cornea. A number of candidate cytokines, chemokines, adhesion molecules, and so forth have been identified. In addition to differentiation from microbial keratitis, CLACI also should be differentiated from ocular disorders not associated with contact lenses but involving corneal infiltrates and from contact lens-associated disorders that may resemble infiltrates. Management of CLACI can range from simple monitoring of the patient to the use of pharmacologic intervention. CONCLUSIONS The small percentage of affected lens wearers translates into a notable number of individuals who, although not experiencing a vision-threatening event, are inconvenienced by the development of infiltrates. Design of preventive measures for CLACI should focus on the elimination of various mechanical, hypoxic, and toxic stimuli that can induce infiltrates and on the approaches for molecular intervention of the inflammatory cascade initiated by the stimuli.
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