The role of lumican and keratocan genes in persistentsubepithelial corneal haze following excimer laser photorefractivekeratectomy

摘要

Purpose: A retrospective clinical and a genetic study was carriedout of severe subepithelial corneal haze occurring after photorefractivekeratectomy (PRK). Since this clinical condition resembles thelumican-null mouse phenotype, mutation analysis of lumican and keratocanwas carried out to investigate whether germline genetic alterations havean effect on development of severe corneal haze in humans. Cornealthickness, photoablation depth, and severity of persistent corneal hazewere also analyzed. In vivo confocal microscopy examination was alsoperformed to study corneal structure and endothelial cells.Methods: Severity of corneal haze was evaluated by slit-lampbiomicroscopy according to Hanna's scale. Corneal structure andendothelial cell shapes and density were viewed with a scanning confocalmicroscope. PCR-based mutational analysis was performed usingtemperature gradient gel electrophoresis (TGGE) and direct sequencing.Results: Preoperative corneal thickness was normal (539±23.13μm, 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'sscale one year after PRK. In vivo confocal microscopy also showed normalendothelial cell density and morphology. Aside from an intronicpolymorphism in a control, no genetic alterations were found in thelumican and keratocan genes.Conclusions: There was no evidence that endothelial dysfunction andgermline mutation of lumican and keratocan genes participate in theetiology of subepithelial corneal haze. Our findings suggest that themechanisms of the development of severe corneal opacity are different inhumans after PRK compared to the lumican deficient knockout mousemodel.