Effect of 0.1% diclofenac ophthalmic solution on inflammatory response and macular thickness following phacoemulsification cataract surgery. / [Wplyw 0,1% kropli diklofenaku na odczyn zapalny w komorze przedniej oka i stan plamki po operacji fakoemulsyfikacji zacmy].

Purpose: To evaluate 0.1% diclofenac sodium as an adjunctive therapy with loteprednol etabonate on postoperative inflammation in the anterior chamber and on foveal and parafoveal retinal thickness. Material and methods: Eighty eyes eligible for phacoemulsification were enrolled in a randomized clinical trial. Patients in group I (N = 40) received anti-inflammatory treatment consisting of 0.1% diclofenac with 0.5% loteprednol; group II (N = 40) patients received 0.5% loteprednol alone. Best corrected visual acuity and intraocular pressure were measured, and laser flarephotometry was done. Foveal and parafoveal thickness were assessed by optical coherence tomography. Results: Median flare values decreased more rapidly in group I at 7 and 14 days (7.9 and 7.4 ph/ms, respectively) than in group II (13.7 and 11.8 ph/ms, respectively; p < 0.0001). Group II had significantly increased parafoveal thickness at 14 and 42 days (median 285.59 µm, p = 0.001 and 288.38 µm, p < 0.001, respectively). Parafoveal thickness differed significantly between groups at 14 and 42 days (p = 0.0085, p = 0.0004, respectively). Conclusions: Eyes treated with both diclofenac sodium and loteprednol etabonate showed less inflammatory response and were less likely to develop foveal and parafoveal thickening than those treated with steroid only.

DNA damage and repair in Fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD) is a slowly progressive eye disease leading to blindness, mostly affecting people above 40 years old. The only known method of curing FECD is corneal transplantation. The disease is characterized by the presence of extracellular deposits called "cornea guttata", apoptosis of corneal endothelial cells, dysfunction of Descement's membrane and corneal edema. Oxidative stress is suggested to play a role in FECD pathogenesis. Reactive oxygen species produced during the stress may damage biomolecules, including DNA. In the present study we evaluated the extent of endogenous DNA damage, including oxidatively modified DNA bases, and damage induced by hydrogen peroxide as well as the kinetics of DNA repair in peripheral blood mononuclear cells of 50 patients with FECD and 43 age-matched controls without visual disturbances. To quantify DNA damage and repair we used the alkaline comet assay technique with the enzymes recognizing oxidative DNA damage, hOGG1 and EndoIII. We did not observe differences in the extent of endogenous and hydrogen peroxide-induced DNA damage between FECD patients and controls. However, we found a lower efficacy of DNA repair in FECD patients as compared with control individuals. The results obtained suggest that the lowering of the DNA repair capacity may be one of the mechanisms underlying the role of oxidative stress in the FECD pathology.