Evaluation of offset of conjunctival hyperemia induced by a Rho-kinase inhibitor; 0.4% Ripasudil ophthalmic solution clinical trial.

Glaucoma leads to irreversible blindness. Numerous anti-glaucoma eye drops have been developed. Unfortunately, many patients with glaucoma still suffer from progressive visual disorders. Recently, ripasudil hydrochloride hydrate, a selective Rho-associated protein kinase inhibitor, was launched for the treatment of glaucoma. However, adverse events, such as conjunctival hyperemia, are often noted in clinical trials using healthy subjects. Therefore, we investigated the onset, offset, and kinetic changes of conjunctival hyperemia induced by ripasudil ophthalmic solution in patients with open-angle glaucoma or ocular hypertension who had already been treated with anti-glaucoma eye drops other than ripasudil. Conjunctival hyperemia was evaluated by both clinical grading by 3 ophthalmic physicians and pixel coverage of conjunctival blood vessels determined by conjunctival hyperemia-analyzing software. Conjunctival hyperemia appeared within 10 min post-instillation in most of the participants. Clinical grade and pixel coverage increased significantly 10 min post-instillation and then decreased. In most of the participants, hyperemia resolved within 2 h. Median conjunctival hyperemia offset was 90 min. A tendency of monotonic increase was observed between clinical grade and pixel coverage. Taken altogether, hyperemia induced by ripasudil was transient in glaucoma patients who had already been treated with anti-glaucoma eye drops other than ripasudil.

Requirement of longer term antiviral therapy in patients with cytomegalovirus anterior uveitis with corneal endothelial cell damage.

BACKGROUND: The aim of the study was to investigate the efficacy of therapy in patients with cytomegalovirus (CMV) anterior uveitis. PATIENTS AND METHODS: We reviewed the records of patients with CMV anterior uveitis who attended our institution between October 2010 and December 2015 and who were confirmed to have CMV DNA in the aqueous humor by polymerase chain reaction analysis. RESULTS: Fourteen immunocompetent patients (10 men and 4 women, total of 17 eyes) were enrolled. The mean ± SD age at the onset of antiviral therapy was 63.1 ± 11.3 years (range, 44-87 years). CMV DNA was not detected in the aqueous humor of 3 patients on initial testing, but it was detected on subsequent analysis. All patients underwent systemic antiviral therapy. Among the patients who were followed up for more than 6 months after starting systemic antiviral therapy, systemic antiviral therapy was successfully terminated in all 4 patients without corneal endothelial loss but had to be continued because of disease recurrence on its termination in 5 of 8 patients (62.5%) with corneal endothelial damage (P = 0.038). CONCLUSIONS: Patients with corneal endothelial cell loss are likely to require longer term antiviral therapy than those without endothelial damage. In addition, whereas definitive diagnosis of CMV anterior uveitis requires the detection of CMV DNA in aqueous humor by polymerase chain reaction, one-fifth of patients in the present study tested negative on initial examination.