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R. Sharma, T. Jackson, A. A. Hussain, J. Marshall; Scleral Permeability and Suprachoroidal Albumin Concentration: Understanding the Pathogenesis of Uveal Effusion Syndrome. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6003.
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To test the the hypothesis that uveal effusion syndrome (UES) is caused by reduced scleral permeability to protein, resulting in raised suprachoroidal protein concentration and osmotic fluid retention.
Surgical scleral specimens were obtained from 11 patients undergoing sclerectomy. Sclera was clamped in a modified Ussing chamber and the rate of transscleral FITC-dextran (n 5) and FITC-albumin (n 1) diffusion was determined using a spectrophotometer and predetermined standard curves. Scleral hydraulic conductivity was measured (n 10) using a modified Ussing chamber connected to a water column set at intraocular pressure. Suprachoroidal fluid was sampled for albumin and total protein concentration, and compared to systemic serum concentration (n 1). Clinical data were obtained using postal questionnaires sent to the treating ophthalmologist. Results were compared to age-matched controls (n 10 albumin; n 6 dextran; n 18 hydraulic conductivity). Tissue was processed for light and transmission electron microscopy (TEM).
Histological staining with Alcian blue showed interfibrillary acid mucin deposits. TEM showed deposits measuring 1-10 microns and collections of expanded, degenerate collagen fibrils. The mean albumin diffusion coefficient was 12% of that in controls, and below the lower 95% confidence limit of the control group. Three of six patients had dextran diffusion (20 kDa) below the 95% confidence limit. Hydraulic conductivity tended to be higher than controls. Suprachoroidal albumin and protein concentration were five times greater than serum levels and at least 13 times greater than physiological levels.
These results suggest that UES is associated with a reduction in the normal transscleral diffusion of protein, with resulting osmotic fluid retention in the suprachoroidal space.
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