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Geographic atrophy (GA) is currently an untreatable condition. Emerging evidence from recent clinical trials show that anti-complement therapy may be a successful treatment option. However, several trials in this therapy area have failed as well. This raises several questions. Firstly, does complement therapy work for all patients with GA? Secondly, is GA one disease? Can we assume that these failed clinical trials are due to ineffective interventions or are they due to flawed clinical trial designs, heterogeneity in GA progression rates or differences in study cohorts? In this article we try to answer these questions by providing an overview of the challenges of designing and interpreting outcomes of randomised controlled trials (RCTs) in GA. These include differing inclusion-exclusion criteria, heterogeneous progression rates of the disease, outcome choices and confounders.摘要: 地图样萎缩 (Geographic atrophy, GA) 是一种目前尚无法治愈的疾病。最近来自临床试验的新兴证据表明, 抗补体治疗可能成为一种有效的治疗方式。然而, 基于该治疗方式的几项试验都失败了。这就提出了几个问题。首先, 补体治疗是否适用于所有GA患者? 其次, GA是一种疾病吗? 我们是否可以提出几个假设: 这些临床试验失败是因为干预措施无效还是因为临床试验设计有缺陷? GA进展率是否具有异质性或研究队列内是否存在差异? 在本文中, 我们总结了这些GA随机对照试验 (RCT) 在试验设计和结果解读中面临的挑战, 其中包括不同的纳入-排除标准、疾病的异质性进展率、结局选择和混杂因素, 并试图以此来回答这些问题。.

Aims To estimate the incidence of early treatment diabetic retinopathy study (ETDRS) level 47 and 53 and progression to treatment with panretinal photocoagulation (PRP) for proliferative DR (PDR). Methods Log-linear regression was used to estimate the incidence of level 47–53 or worse for 33,009 people with diabetes (PWD) in Gloucestershire during 2013–2016 by calendar year and diabetes type, based on the first recording. Progression was analysed in Gloucestershire and Bristol with a parametric survival analysis examining the association of baseline and time-varying demographic and clinical factors on time to PRP after the first recording of level 47–53. Results Incidence decreased from 0.57 (95% confidence intervals (CI) 0.48–0.67) per 100 PWD in 2013 to 0.35 (95% CI 0.29–0.43) in 2016 (p 1c were associated with an increase in the risk of initiating PRP (hazard ratio 3.14 (95% CI: 1.60–6.15) and 1.21 (95% CI: 1.06–1.38 per 10 mmol/mol) respectively). Conclusion This study provides additional understanding of this population and shows that a high proportion of patients with ETDRS levels 47–53 need to be monitored as they are at high risk of progressing to PDR.

PurposeTo compare the efficacy and safety of subthreshold micropulse laser (SML) with threshold conventional laser (TCL) in central serous chorioretinopathy (CSC).MethodsProspective, randomized, double-masked, non-inferiority, 12-week clinical trial. Patients were randomly assigned 1:1 to SML group or TCL group. Patients in the SML group were treated with 577 nm micropulse laser. The spot size was 160 µm, the duty cycle was 5% and exposure time was 0.2 s. The power was 50% threshold tested. Patients in the TCL group were treated with 577 nm continuous laser. The power was 100% threshold tested. The primary outcome was the mean change in best-corrected visual acuity (BCVA) at week 12, with a non-inferiority limit of five letters on the Early Treatment Diabetic Retinopathy Study (ETDRS) visual acuity charts.ResultsEighty-eight patients were enroled. Seventy-seven patients were male. Forty-four patients were in SML group and 44 in TCL group. At week 12, SML was equivalent to TCL with a gain of 6.23 ± 8.59 and 6.61 ± 6.35 letters, respectively, (SML–TCL difference: −0.38 letters; 95% confidence interval (CI):−3.58–2.81;Pnon-inferiority = 0.0026). There was no statistically significant difference between the two groups (t = 0.240,P = 0.811). At week 12, the proportion of patients whose SRF had been totally absorbed was 63.63 and 81.82% respectively for SML and TCL groups. There was no statistically significant difference between the two groups (χ2 = 3.67,P = 0.056).ConclusionsBoth SML and TCL can improve visual acuity in CSC. SML was non-inferior to TCL in the improvement of BCVA.

Background: Diabetic macular oedema (DMO) is effectively treated with ranibizumab but multiple injections are required. Where there is also peripheral ischaemia, it has been promoted that targeted panretinal photocoagulation (PRP) may reduce the number of injections. Method: Patients with optical coherence tomography confirmed DMO and Ultra-widefield Fundus Fluorescein Angiography confirmed peripheral retinal ischaemia were randomised to PRP plus ranibizumab or ranibizumab monotherapy. After three injections, repeat injections were given until the visual acuity was stable and the macula was dry. Re-treatment was given if there was a drop of visual acuity and/or a recurrence of intra-retinal fluid. The primary outcome was the number of repeat injections required after the first 6 months up until 1 year. Results: There were 49 patients, 25 in the ranibizumab only group and 24 in the ranibizumab + PRP group recruited at seven UK sites. The average number of injections in the ranibizumab-only arm was 6.84 over 1 year and 2.52 between months 6 and 12. The average number of injections in the combined arm was 6.67, with the number of injections in the second 6 months 1.92. For the primary outcome, comparing the number of 6- to 12-month injections, the result was not statistically significant (p = 0.33). Conclusion: The addition of targeted PRP to areas of non-perfusion in a patient with DMO does not reduce the number of injections required in the first year. It seems most likely that local VEGF at the macula is the main cause of DMO.

Age-related macular degeneration (AMD) is a common condition in older adults. Since publication of the last guidelines in 2009, new data have emerged on the management of AMD and novel solutions have been tested to meet the ongoing challenge of AMD service demands. Thus, there are compelling reasons to update the College guidelines on AMD. This is a summary of the guidelines. The full guidelines are available at http://www.rcophth.ac.uk/page.asp?section=451&sectionTitle=Clinical+Guidelines The purposes of the guidelines are to set the standards for best practice, to educate medical trainees, to inform patients, carers, and consumer organisations, to act as a benchmark for service planning by providers, to guide commissioners, and to set national standards for audit.

Photoreceptor cell death is the final, irreversible event in many blinding diseases including retinitis pigmentosa, age-related macular disease and retinal detachment. This paper examines the potential strategies for preventing photoreceptor cell death in the context of current understanding of the mechanisms of cell death. There is evidence to suggest that photoreceptor cells are inherently vulnerable, apoptosis is the final common pathway of photoreceptor cell loss, and other retinal cells play an important role in the survival of rods and cones. Furthermore, the rationale of using neurotrophic factors as therapeutic agents in retinal degeneration is discussed in detail. Photoreceptor rescue by manipulation of genes involved in apoptosis and some pharmacological agents is also described.