Intraocular pressure after intravitreal injection of dexamethasone implant for macular edema resulting from retinal vein occlusion.

PURPOSE: A recognized side effect of corticosteroids intravitreal injections (IVT) is the onset of ocular hypertension. The aim of our study was to analyze changes in short-term intraocular pressure (IOP) after IVT of sustained-release dexamethasone implant in order to provide an appropriate monitoring scheme. METHODS: In this retrospective study, the charts of 44 eyes of 42 patients treated by IVT of dexamethasone implant for macular edema resulting from retinal vein occlusion were reviewed. The IOP measurements were performed at baseline and at 15 minutes, 7 days (D7), 1 month (M1), 2 months (M2), and 4 months (M4) after IVT. RESULTS: Mean IOP was 13.4 ± 2.5 mm Hg at baseline. Twelve eyes out of 44 (27.3%) were treated with antihypertensive eyedrops for a well-controlled glaucoma at baseline. Following IVT, mean IOP was 11.5 ± 3.6 mm Hg at 15 minutes, 14.7 ± 3.1 mm Hg at D7, 16.4 ± 7.0 mm Hg at M1, 19.3 ± 7.9 mm Hg at M2, and 13.5 ± 3.1 mm Hg at M4. An IOP ≥25 mm Hg or increased by 10 mm Hg or more was not observed in any eye at 15 minutes, D7, or M4 after IVT, but in 8.6% of cases at M1 and in 25% at M2. CONCLUSIONS: It seems reasonable to perform the first IOP monitoring 1 month after IVT of dexamethasone implant and at each efficacy assessment visit (M2, M4). Special attention should be given to patients at risk, such as glaucoma patients. An IOP measurement immediately after IVT and in the following days (1 week) does not seem to be appropriate on a routine basis.

Apolipoprotein E-promoter single-nucleotide polymorphisms affect the phenotype of primary open-angle glaucoma and demonstrate interaction with the myocilin gene.

Primary open-angle glaucoma (POAG) is an optic neuropathy that has a high worldwide prevalence and that shows strong evidence of complex inheritance. The myocilin (MYOC) gene is the only one that has thus far been shown to have mutations in patients with POAG. Apolipoprotein E (APOE) plays an essential role in lipid metabolism, and the APOE gene has been involved in neuronal degeneration that occurs in Alzheimer disease (AD). Here, we report that two APOE-promoter single-nucleotide polymorphisms (SNPs) previously associated with AD also modify the POAG phenotype. APOE(-219G) is associated with increased optic nerve damage, as reflected by increased cup:disk ratio and visual field alteration. In addition, APOE(-491T), interacting at a highly significant level with an SNP in the MYOC promoter, MYOC(-1000G), is associated with increased intraocular pressure (IOP) and with limited effectiveness of IOP-lowering treatments in patients with POAG. Together, these findings establish APOE as a potent modifier for POAG, which could explain the linkage to chromosome 19q previously observed by use of a genome scan for this condition and an increased frequency of glaucoma in patients with AD. The findings also shed new light on potential mechanisms of optic nerve damage and of IOP regulation in POAG.