ObjectiveAge-related macular degeneration (ARMD) is a leading cause of visual impairment. Intravitreal injections of anti-vascular endothelial growth factor (VEGF) are the standard treatment for wet ARMD. There is however, variability in patient responses, suggesting patient-specific factors influencing drug efficacy. We tested whether single nucleotide polymorphisms (SNPs) in genes encoding VEGF pathway members contribute to therapy response.Methods and analysisA retrospective cohort of 281 European wet ARMD patients treated with anti-VEGF was genotyped for 138 tagging SNPs in the VEGF pathway. Per patient, we collected best corrected visual acuity at baseline, after three loading injections and at 12 months. We also registered the injection number and changes in retinal morphology after three loading injections (central foveal thickness (CFT), intraretinal cysts and serous neuroepithelium detachment). Changes in CFT after 3 months were our primary outcome measure. Association of SNPs to response was assessed by binomial logistic regression. Replication was attempted by associating visual acuity changes to genotypes in an independent Japanese cohort.ResultsAssociation with treatment response was detected for seven SNPs, including in FLT4 (rs55667289: OR=0.746, 95% CI 0.63 to 0.88, p=0.0005) and KDR (rs7691507: OR=1.056, 95% CI 1.02 to 1.10, p=0.005; and rs2305945: OR=0.963, 95% CI 0.93 to 1.00, p=0.0472). Only association with rs55667289 in FLT4 survived multiple testing correction. This SNP was unavailable for testing in the replication cohort. Of six SNPs tested for replication, one was significant although not after multiple testing correction.ConclusionIdentifying genetic variants that define treatment response can help to develop individualised therapeutic approaches for wet ARMD patients and may point towards new targets in non-responders.

Background and Objective: Several cases of central serous chorioretinopathy (CSC) in divers have been reported in our medical retina center over the past few years. This study was designed to evaluate possible changes induced by SCUBA diving in ophthalmic parameters and especially subfoveal choroidal thickness (SFCT), since the choroid seems to play a crucial role in physiopathology of CSC. Materials and Methods: Intraocular pressure (IOP), SFCT, pachymetry, flow-mediated dilation (FMD), blood pressure, and heart rate were measured in 15 healthy volunteer divers before diving, 30 and 60 min after a standard deep dive of 25 m depth for 25 min in a dedicated diving pool (NEMO 33). Results: SFCT reduces significantly to 96.63 ± 13.89% of pre-dive values (p = 0.016) 30 min after diving. It recovers after 60 min reaching control values. IOP decreases to 88.05 ± 10.04% of pre-dive value at 30 min, then increases to 91.42 ± 10.35% of its pre-dive value (both p < 0.0001). Pachymetry shows a slight variation, but is significantly increased to 101.63 ± 1.01% (p = 0.0159) of the pre-dive value, and returns to control level after 60 min. FMD pre-dive was 107 ± 6.7% (p < 0.0001), but post-dive showed a diminished increase to 103 ± 6.5% (p = 0.0132). The pre-post difference was significant (p = 0.03). Conclusion: Endothelial dysfunction leading to arterial stiffness after diving may explain the reduced SFCT observed, but SCUBA diving seems to have miscellaneous consequences on eye parameters. Despite this clear influence on SFCT, no clear relationship between CSC and SCUBA diving can be drawn.

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In patients with angioid streaks, diving headfirst can lead to subretinal hemorrhages and traumatic ruptures in Bruch membrane and increase the risk of maculopathy. Ophthalmologists should caution patients with angioid streaks against diving headfirst.