PurposeThe aim of this study was to investigate the factors associated with decreases in corneal endothelial cell density (ECD) resulting from cataract surgery in eyes with pseudoexfoliation syndrome (PEX).MethodsThe clinical records of 78 eyes of 78 patients with PEX who had undergone cataract surgery were reviewed. ECD was measured preoperatively and at 3 months postoperatively with specular microscopy. Multiple regression analysis was used to assess the factors that were significantly related to the rate of ECD loss. Explanatory variables included age, preoperative ECD, pupil diameter, cataract grade, concomitance of glaucoma or diabetes mellitus, preoperative anterior chamber depth, surgery time, total time and power of ultrasound, performance of intraoperative pupillary enlargement manipulation, and postoperative aqueous flare intensity at 1 week and 1 month.ResultsECD before and after surgery was 2,464±337 cells/mm2 and 2,400±347 cells/mm2, respectively, with an ECD loss rate of 2.6%±5.1% (mean ± SD). Multiple regression analysis revealed that ECD loss was significantly associated with the cataract grade (P=0.019) and preoperative anterior chamber depth (P=0.023).ConclusionWith modern small incision cataract surgery, the ECD loss varied with surgical invasions due to severe cataract and shallow anterior chamber, and the presence of PEX was least affected.

UMIN000009372.

Granular corneal dystrophy (GCD) is an autosomal dominant hereditary disease in which multiple discrete and irregularly shaped granular opacities are deposited in the corneal stroma. GCD is caused by a point mutation in the transforming growth factor-β-induced (TGFBI) gene, located on chromosome 5q31. Here, we report the first successful application of CRISPR-Cas9-mediated genome editing for the correction of a TGFBI mutation in GCD patient-derived primary corneal keratocytes via homology-directed repair (HDR). To correct genetic defects in GCD patient cells, we designed a disease-specific guide RNA (gRNA) targeting the R124H mutation of TGFBI, which causes GCD type 2 (GCD2). An R124H mutation in primary human corneal keratocytes derived from a GCD2 patient was corrected by delivering a CRISPR plasmid expressing Cas9/gRNA and a single-stranded oligodeoxynucleotide HDR donor template in vitro. The gene correction efficiency was 20.6% in heterozygous cells and 41.3% in homozygous cells. No off-target effects were detected. These results reveal a new therapeutic strategy for GCD2; this method may also be applicable to other heredity corneal diseases.

Long-term evaluation indicated that the reduction in ECD after argon-Nd:YAG laser LPI was present but small during the initial year and was negligible after 1 year.

The use of NSAID ophthalmic solution had almost no impact on PG analog-related conjunctival hyperemia. This partly suggests that the action mechanism of endogenous PG after administrating PG analog might be no correlation with conjunctival hyperemia.