Purpose: A retrospective clinical and a genetic study was carried out of severe subepithelial corneal haze occurring after photorefractive keratectomy (PRK). Since this clinical condition resembles the lumican-null mouse phenotype, mutation analysis of lumican and keratocan was carried out to investigate whether germline genetic alterations have an effect on development of severe corneal haze in humans. Corneal thickness, photoablation depth, and severity of persistent corneal haze were also analyzed. In vivo confocal microscopy examination was also performed to study corneal structure and endothelial cells. Methods: Severity of corneal haze was evaluated by slit-lamp biomicroscopy according to Hanna's scale. Corneal structure and endothelial cell shapes and density were viewed with a scanning confocal microscope. PCR-based mutational analysis was performed using temperature gradient gel electrophoresis (TGGE) and direct sequencing. Results: Preoperative corneal thickness was normal (539±23.13 μm, mean±SD),and the photoablation depth was 88.94±18.64 μm (mean±SD). The most severe corneal haze was grade 2.0 on Hanna's scale one year after PRK. In vivo confocal microscopy also showed normal endothelial cell density and morphology. Aside from an intronic polymorphism in a control, no genetic alterations were found in the lumican and keratocan genes. Conclusions: There was no evidence that endothelial dysfunction and germline mutation of lumican and keratocan genes participate in the etiology of subepithelial corneal haze. Our findings suggest that the mechanisms of the development of severe corneal opacity are different in humans after PRK compared to the lumican deficient knockout mouse model.
|Number of pages||9|
|Publication status||Published - May 25 2006|
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