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BackgroundTo describe 10-year trends in visual outcomes, anatomical outcomes and treatment burden of patients receiving antivascular endothelial growth factor (anti-VEGF) therapy for neovascular age-related macular degeneration (nAMD).MethodsRetrospective cohort study of treatment-naïve, first-affected eyes with nAMD started on ranibizumab before January 1, 2009. The primary outcome was time to best-corrected visual acuity (BCVA) falling ≤35 ETDRS letters after initiating anti-VEGF therapy. Secondary outcomes included time to BCVA reaching ≥70 letters, proportion of eyes with BCVA ≥70 and ≤35 letters in 10 years, mean trend of BCVA and central retinal thickness over 10 years, and mean number of injections.ResultsFor our cohort of 103 patients, Kaplan-Meier analyses demonstrated median time to BCVA reaching ≤35 and ≥70 letters were 37.8 (95% CI 22.2 to 65.1) and 8.3 (95% CI 4.8 to 20.9) months after commencing anti-VEGF therapy, respectively. At the final follow-up, BCVA was ≤35 letters and ≥70 letters in 41.1% and 21%, respectively, in first-affected eyes, while this was the case for 5.4% and 48.2%, respectively, in a patient’s better-seeing eye. Mean injection number was 37.0±24.2 per eye and 53.6±30.1 at patient level (63.1% of patients required injections in both eyes).ConclusionsThe chronicity of nAMD disease and its management highlights the importance of long-term visual prognosis. Our analyses suggest that one in five patients will retain good vision (BCVA ≥70 ETDRS letters) in the first-affected eye at 10 years after starting anti-VEGF treatment; yet, one in two patients will have good vision in their better-seeing eye. Moreover, our data suggest that early treatment of nAMD is associated with better visual outcomes.

Aflibercept (aflibercept) is a novel anti-vascular endothelial growth factor drug indicated for wet age-related macular degeneration and macular oedema secondary to retinal vein occlusion and diabetic macular oedema. While only newly introduced on the market, it is growing in popularity and over 5.5 million doses have been prescribed worldwide. Due to its versatile mechanism, it is indicated for numerous eye pathologies, and in particular, has been adapted to treat various types of retinopathy. To our knowledge, this is the first case report of solely using aflibercept to treat cystoid macular oedema in radiation retinopathy.

Background: Previous in vitro experiments have demonstrated that PGF2α reduced proliferation and adipogenesis in a murine cell line and human orbital fibroblasts derived from subjects with inactive Graves' orbitopathy (GO). The objective of this study was to determine if the PGF2α analogue Bimatoprost is effective at reducing proptosis in this population.Methods: A randomized controlled double-masked crossover trial was conducted in a single tertiary care academic medical center. Patients with longstanding, inactive GO but persistent proptosis (> 20 mm in at least one eye) were recruited. Allowing for a 15% dropout rate, 31 patients (26 females) were randomized in order to identify a treatment effect of 2.0 mm (p=0.05, two-sided paired t-test, power 0.88). Following informed consent, participants were randomized to receive Bimatoprost or placebo for three months after which they underwent a two-month washout, before switching to the opposite treatment. The primary outcome was the change in exophthalmometry readings over the two 3-month treatment periods.Results: The mean exophthalmometer at baseline was 23.6 (range 20.0-30.5) mm and the mean age was 55 (range 28-74) years. The median duration of GO was 7.6 (IQR 3.6-12.3) years. The majority were still suffering from diplopia (61.3%) with bilateral involvement (61.3%). Using multilevel modeling adjusted for baseline, period and carryover, Bimatoprost resulted in a -0.17 mm (reduction) exophthalmometry change (95% CI -0.67 to +0.32) p=0.490. Intraocular pressure was reduced -2.7 mmHg (95% CI -4.0 to -1.4) p=0.0070. One patient showed periorbital fat atrophy (PAP) on treatment which resolved on stopping treatment. Independent analysis of proptosis by