Abstract

This paper demonstrates three different types of corneal epithelial barrier dysfunction: mechanically and/or immunologically oriented (as in superficial punctate kera- topathy); genetically regulated (as in corneal dystrophy); and biologically based (as in conjunctival epithelial invasion of the cornea). Corneal epithelial barrier function was examined by measuring fluorescein uptake using a newly-designed fluorophotometer, after instillation of 3 μl of 0.5% fluorescein. Fluorescein uptake (mean ± standard error, ng/ml) in the central cornea 30 minutes later was 21.4 ± 1.6, 81.9 ± 8.9, 269.0 ± 26.9, and 1400.9 ± 197.2 in normal controls (Grade 0), Grade 1, Grade 2, and Grade 3 superficial punctate keratopathies, respectively, showing significant progression of epithelial barrier dysfunction with severity of clinical manifestation. Among the corneal dystrophies, gelatinous drop-like dystrophy (2584.6 ± 791.7, p = 0.0001), granular dystrophy (351.6 ± 157.5, p = 0.0001) and lattice dystrophy (599.7 ± 222.0, p = 0.001), but not macular dystrophy (51.2 ± 0.3, p = 0.011), showed markedly increased fluorescein uptake in comparison to normal corneas. Extremely high fluorescein uptake in gelatinous droplike dystrophy is speculative of corneal epithelial cell membrane abnormality. The corneas covered by conjunctival epithelium, as proved by impression cytology, showed increased fluorescein uptake (472.1 ± 144.6, p = 0.0001) in comparison to normal controls.

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