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PurposeSingle center, noninterventional cohort study to assess 10-year visual and anatomical outcomes following initiation of treatment with antivascular endothelial growth factor (anti-VEGF) agents in neovascular age-related macular degeneration (AMD) patients. Neovascular AMD patients initiated on intravitreal anti-VEGF injections in 2008–2009 and continued to be followed up for at least 10 years were included in this study.MethodsThe Moorfields OpenEyes database was searched for all patients who were initiated on anti-VEGF therapy for neovascular AMD in 2008–2009 and the visual acuity (VA) in Early Diabetic Retinopathy Study (ETDRS) letters and injection records were analyzed for those who have had at least 10-year follow-up. The spectral-domain optical coherence tomography (SD-OCT) scans, color fundus photos, and fundus fluorescein angiography (FA) were graded by two retinal physicians. The outcomes were also compared between those with good and poor VA outcomes based on pre-defined criteria. The primary end point was change in VA at 10 years; secondary outcomes included percentage with VA of 20/40 or better, 20/70 or better, VA gains and losses, anatomic outcomes and number of injections.ResultsAfter a mean of 10.04 years after initiation of anti-VEGF therapy, the mean decline in VA from baseline was −2.1 ETDRS letters (SD 19.9, p = 0.65). One hundred eyes (67.1%) achieved a VA threshold of 20/70 or better, 33.5% achieved a VA of 20/40 or better, and 76.5% eyes maintained VA defined as a loss of less than 15 letters. Fourteen percent of study eyes had VA of 20/200 or worse and 23.5% declined by 15 letters or more. 87.5% of eyes were switched from ranibizumab to aflibercept during the course of 10 years and the eyes received a mean of 52.2 (SD 18.1) injections over 10 years. From this cohort, 87 (58.3%) eyes are having on-going treatment. On OCT, 34.9% had persistent fluid at the last visit, 6.7% patients showed new onset atrophy compared to baseline, and 43.7% had increased area of macular atrophy. The mean area of atrophy at the final visit was 4.15 mm2. Comparison between the good and worse visual outcome groups showed lower baseline VA, fovea-involving atrophy and final area of atrophy had a statistically significant negative effect on the final visual outcome (p < 0.05).ConclusionsRegular monitoring and anti-VEGF treatment over 10 years reduce the risk of visual loss of 15 letters or more in patients with neovascular AMD. The most common cause of substantial visual decline was macular atrophy.

Background Diabetic macular edema (DME) and proliferative diabetic retinopathy (PDR) are sight-threatening complications of diabetes mellitus and leading causes of adult-onset blindness worldwide. Genetic risk factors for diabetic retinopathy (DR) have been described previously, but have been difficult to replicate between studies, which have often used composite phenotypes and been conducted in different populations. This study aims to identify genetic risk factors for DME and PDR as separate complications in Australians of European descent with type 2 diabetes. Methods Caucasian Australians with type 2 diabetes were evaluated in a genome-wide association study (GWAS) to compare 270 DME cases and 176 PDR cases with 435 non-retinopathy controls. All participants were genotyped by SNP array and after data cleaning, cases were compared to controls using logistic regression adjusting for relevant covariates. Results The top ranked SNP for DME was rs1990145 ( p  = 4.10 × 10 − 6 , OR = 2.02 95%CI [1.50, 2.72]) on chromosome 2. The top-ranked SNP for PDR was rs918519 ( p  = 3.87 × 10 − 6 , OR = 0.35 95%CI [0.22, 0.54]) on chromosome 5. A trend towards association was also detected at two SNPs reported in the only other reported GWAS of DR in Caucasians; rs12267418 near MALRD1 ( p  = 0.008) in the DME cohort and rs16999051 in the diabetes gene PCSK2 ( p  = 0.007) in the PDR cohort. Conclusion This study has identified loci of interest for DME and PDR, two common ocular complications of diabetes. These findings require replication in other Caucasian cohorts with type 2 diabetes and larger cohorts will be required to identify genetic loci with statistical confidence. There is considerable overlap in the patient cohorts with each retinopathy subtype, complicating the search for genes that contribute to PDR and DME biology.

Mitochondrial haplogroups H1, H2 and UK have previously been reported to be associated with proliferative diabetic retinopathy (PDR) in Caucasian patients with diabetes. We aimed to replicate this finding with a larger sample and expand the analysis to include different severities of DR, and diabetic macular edema (DME). Caucasian participants (n = 2935) with either type 1 or type 2 diabetes from the Australian Registry of Advanced Diabetic Retinopathy were enrolled in this study. Twenty-two mitochondrial single nucleotide polymorphisms were genotyped by MassArray and haplogroups reconstructed using Haplogrep. Chi square tests and logistic regressions were used to test associations between haplogroup and DR phenotypes including any DR, non-proliferative DR (NPDR), proliferative DR (PDR) and DME. After stratifying the samples in type 1 and type 2 diabetes groups, and adjusting for sex, age, diabetes duration, concurrent HbA1c and hypertension, neither haplogroups H1, H2, UK, K or JT were associated with any DR, NPDR, PDR or DME.

Purpose: To describe the possible association between central serous chorioretinopathy (CSCR) and desmopressin use. Methods: The case histories of 2 middle-aged men with CSCR using desmopressin nasal spray were studied. Results: The diagnosis of CSCR was made on the basis of clinical features and ancillary testing (fluorescein angiography and optical coherence tomography). Both patients were using desmopressin nasal spray for polyuria when they developed the first ocular symptoms. Both of them also had an independent risk factor for developing CSCR. Conclusion: We suggest that desmopressin-induced hypercortisolism might implicate the development of CSCR in some patients. A larger study on patients using desmopressin nasal spray would be beneficial to confirm the possible association between this form of therapy and the development of CSCR.

Purpose To study associations of optical coherence tomography (OCT) features with presenting visual acuity (VA) in treatment naive neovascular age-related macular degeneration (nAMD). Methods Patients with nAMD initiated on aflibercept therapy were recruited from December 2019 to August 2021. Demographic and OCT (Spectralis, Heidelberg Engineering) features associated with good VA (VA ≥ 68 ETDRS letters, Snellen ≥ 6/12) and poor VA (VA < 54 letters, Snellen < 6/18) were analysed using Generalised Estimating Equations to account for inter-eye correlation. Results Of 2274 eyes of 2128 patients enrolled, 2039 eyes of 1901 patients with complete data were analysed. Mean age was 79.4 (SD 7.8) years, female:male 3:2 and mean VA 58.0 (SD 14.5) letters. On multivariable analysis VA < 54 letters was associated with increased central subfield thickness (CST) (OR 1.40 per 100 µm; P  < 0.001), foveal intraretinal fluid (OR 2.14; P  < 0.001), polypoidal vasculopathy (PCV) relative to Type 1 macular neovascularisation (MNV) (OR 1.66; P  = 0.049), presence of foveal subretinal hyperreflective material (SHRM) (OR 1.73; P  = 0.002), foveal fibrosis (OR 3.85; P  < 0.001), foveal atrophy (OR 5.54; P  < 0.001), loss of integrity of the foveal ellipsoid zone (EZ) or external limiting membrane (ELM) relative to their preservation (OR 3.83; P  < 0.001) and absence of subretinal drusenoid deposits (SDD) (presence vs absence; OR 0.75; P  = 0.04). These features were associated with reduced odds of VA ≥ 68 letters except MNV subtypes and SDD. Conclusion Presence of baseline fovea-involving atrophy, fibrosis, intraretinal fluid, SHRM, PCV EZ/ELM loss and increased CST determine poor presenting VA. This highlights the need for early detection and treatment prior to structural changes that worsen baseline VA.

Aims/hypothesis Diabetic retinopathy is a serious complication of diabetes mellitus and can lead to blindness. A genetic component, in addition to traditional risk factors, has been well described although strong genetic factors have not yet been identified. Here, we aimed to identify novel genetic risk factors for sight-threatening diabetic retinopathy using a genome-wide association study. Methods Retinopathy was assessed in white Australians with type 2 diabetes mellitus. Genome-wide association analysis was conducted for comparison of cases of sight-threatening diabetic retinopathy ( n  = 336) with diabetic controls with no retinopathy ( n  = 508). Top ranking single nucleotide polymorphisms were typed in a type 2 diabetes replication cohort, a type 1 diabetes cohort and an Indian type 2 cohort. A mouse model of proliferative retinopathy was used to assess differential expression of the nearby candidate gene GRB2 by immunohistochemistry and quantitative western blot. Results The top ranked variant was rs3805931 with p  = 2.66 × 10 −7 , but no association was found in the replication cohort. Only rs9896052 ( p  = 6.55 × 10 −5 ) was associated with sight-threatening diabetic retinopathy in both the type 2 (p  = 0.035) and the type 1 ( p =  0.041) replication cohorts, as well as in the Indian cohort ( p  = 0.016). The study-wide meta-analysis reached genome-wide significance ( p  = 4.15 × 10 −8 ). The GRB2 gene is located downstream of this variant and a mouse model of retinopathy showed increased GRB2 expression in the retina. Conclusions/interpretation Genetic variation near GRB2 on chromosome 17q25.1 is associated with sight-threatening diabetic retinopathy. Several genes in this region are promising candidates and in particular GRB2 is upregulated during retinal stress and neovascularisation.

Aims This study aimed to investigate whether the single-nucleotide polymorphism (SNP) rs2910164 residing within microRNA-146a (miR-146a) is associated with diabetic microvascular complications diabetic nephropathy (DN), proliferative diabetic retinopathy (PDR) or diabetic macular oedema (DME) in either Caucasian patients with type 1 (T1DM) or type 2 (T2DM) diabetes mellitus. Methods Caucasian patients with T1DM ( n  = 733) or T2DM ( n  = 2215) were recruited from ophthalmology, renal and endocrine clinics in Australia and the UK. Patients with T2DM were required to have diabetes mellitus (DM) for at least 5 years and be on treatment with oral hypoglycaemic drugs or insulin. In total, 890 participants had DN (168 with T1DM and 722 with T2DM), 731 had PDR (251 with T1DM and 480 with T2DM) and 1026 had DME (170 with T1DM and 856 with T2DM). Participants were genotyped for SNP rs2910164 in miR-146a. Analyses investigating association were adjusted for relevant clinical covariates including age, sex, DM duration, Hb A1c and hypertension. Results A significant association was found between the C allele of rs2910164 and DN in the T1DM group (OR 1.93; CI 1.23–3.03; P  = 0.004), but no association found in the T2DM group (OR 1.05; CI 0.83–1.32; P  = 0.691). In the subset of T2DM patients, the C allele was specifically associated with DME (OR 1.25; CI 1.03–1.53; P  = 0.025). No association with DME was found in the T1DM group (OR 0.87; CI 0.54–1.42); P  = 0.583), or with PDR for either type of DM. Conclusions Rs2910164 is significantly associated with microvascular complications DN in patients with T1DM and DME in patients with T2DM.

A 31-year-old man presented with acute unilateral visual loss secondary to hand-foot-mouth disease (HFMD). Ophthalmic examination demonstrated best corrected visual acuity (BCVA) of 6/24 and a macular neurosensory detachment. He was diagnosed with unilateral acute idiopathic maculopathy (UAIM), and multimodality imaging was performed. No treatment was warranted. At 3 months, BCVA was 6/5 and funduscopy revealed a juxtafoveal scar. Based on the evidence of the association between HFMD and UAIM, the authors refer to this condition as exudative maculopathy associated with HFMD. Multimodality imaging during acute and convalescent phases is useful to study this disorder and raises questions about choroidal and bilateral involvement. Ophthalmologists should be aware of this and query about systemic signs and symptoms. [Ophthalmic Surg Lasers Imaging Retina. 2014;45:e14–e17.]

AimTo describe the clinical features of a case series of patients with unilateral vitelliform maculopathy and the results of screening BEST1 and PRPH2 for disease-causing mutations.Design/MethodsThis was a retrospective case series study of six patients ascertained over a 2-year period. Ophthalmological examination, fundus photography, autofluorescence imaging, optical coherence tomography and detailed electrophysiological assessment were undertaken. Blood samples were taken for DNA extraction and mutation screening of BEST1 and PRPH2 was performed.ResultsSix patients (3 men and 3 women) with unilateral vitelliform maculopathy were identified, ranging in age from 30 to 68 years. Vision in the affected eye ranged from 20/10 to 20/100. There was no clinical, retinal imaging or electrophysiological evidence of fellow eye involvement. Direct sequencing of BEST1 and PRPH2 did not reveal any disease-causing variants.ConclusionsA case series of patients is reported with an unusual unilateral vitelliform phenotype, often associated with good visual function. The patients do not have the typical characteristics associated with age-related maculopathy or any inherited macular disorders, such as Best vitelliform macular dystrophy. Molecular screening of the candidate genes BEST1 and PRPH2 revealed no mutations.

Thirty per cent of the population aged over 7 5 has some degree of AMD. Ten to 15 per cent of those have the 'wet' form (exudative AMD) which is characterised by choroidal neovascularisation (CNV), retinal pigment epithelial detachments, and their sequelae; while 85-90 per cent have the 'dry' form (atrophic AMD), characterised by intermediate or large drusen, retinal pigment epithelial changes, and slowly progressive chorioretinal atrophy.