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S.S. Samudre, F.A. Lattanzio, Jr., P.G. Loose-Thurman, J.D. Sheppard, Jr.; Does Confocal Microscopy Effectively Predict Cellular Effects of Steroid-treated Acute Uveitis? . Invest. Ophthalmol. Vis. Sci. 2003;44(13):727.
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Purpose: Protein concentration, glucocorticoid receptor internalization (GCR), corneal thickness and intraocular pressure (IOP) all reflect the response to treatment of acute uveitis. GCR internalization and protein concentration are surrogate markers for uveitis, but these highly invasive measurements are clinically impractical. This study explores the ability of noninvasive in vivo confocal microscopy (CFM) to effectively and accurately predict trends during treatment of acute uveitis with topical steroids. Methods: Acute uveitis was induced in New Zealand white rabbits by endotoxin injection into the vitreous humor. After 24 hours, all were randomly assigned to topical steroids or saline treatment 4 times a day for 2d or 4d. Corneal thickness was measured daily by CFM. IOP was measured and slit lamp examination was performed daily. Internalization of the glucocorticoid receptor in iris was assayed by Western blot, and protein by Bradford assay. Correlation assessment was performed using Pearson product moment correlation analysis test. Results: Following 2 day treatment, GCR internalization positively correlated with protein concentration (p=0.038). Also, corneal thickness and IOP were inversely correlated (p=0.024). Following 4 day treatment, the positive correlation between GCR internalization and protein concentration and the inverse correlation between corneal thickness and IOP were sustained but not significant. In addition, there was a non-significant inverse trend between corneal thickness and GCR internalization, and IOP and protein concentration. Also, GCR internalization and IOP showed positive but non-significant trend. Less than 10% of the rabbits did not develop uveitis and were not included in the study. Conclusions: The reduction in IOP measurement in this model of uveitis is associated with ciliary body compromise, and in part from changes in permeability of the corneal endothelium and leukocyte infiltration into the cornea. These changes in permeability and the release of cytokines by leukocytes also cause corneal edema. This infiltration and thickening are measurable through in vivo CFM. In those cases where IOP did not decline, the corneal endothelium remained anatomically normal with little leukocyte infiltration. Local increase of glucocorticoids or administration of topical steroids promoted GCR internalization. Increased protein was related to leukocyte infiltration and fibrin production. Thus, noninvasive CFM is a suitable surrogate marker to document clinical progression of acute uveitis.
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