Rs2910164 is significantly associated with microvascular complications DN in patients with T1DM and DME in patients with T2DM.

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Diabetic macular oedema is the major cause of visual impairment in type 1 and type 2 diabetes. As type 2 diabetes becomes more prevalent worldwide, the prevalence of diabetic macular oedema is also expected to rise. Current management of diabetic macular oedema is challenging, expensive and not optimal in a subset of patients. Therefore, it is important to increase our understanding of the risk factors involved and develop preventative strategies. While clinical risk factors for diabetic macular oedema have been identified, few studies have addressed potential genetic risk factors. Epidemiology and family studies suggest genetic influences are of importance. In this review, we summarise known clinical risk factors, as well as discuss the small number of genetic studies that have been performed for diabetic macular oedema.

The presence of any DR among those with DM, was associated with a 75% greater 10-y all-cause mortality rate and were more likely to die from renal failure or stroke. We recommend that whenever DR is noted among Indigenous Australians with DM, that they be immediately referred for investigation and management of risk factors, which might predispose to renal failure and stroke.

ImportanceFive‐year survival rates in patients undergoing vitrectomy for diabetic retinopathy (DR) vary from 68% to 95%. No study has been conducted in an Australian population.BackgroundWe aimed to determine the survival rates of patients undergoing diabetic vitrectomy in an Australian population.DesignRetrospective audit, tertiary centre hospitals and private practices.ParticipantsAll individuals in South Australia and the Northern Territory who underwent their first vitrectomy for diabetic complications between January 1, 2007 and December 31, 2011.MethodsAn audit of all eligible participants has been completed previously. Survival status as of July 6, 2018 and cause of death were obtained using SA/NT DataLink. Kaplan‐Meier survival curves and multivariate cox‐regressions were used to analyse survival rates and identify risk factors for mortality.Main outcome measuresFive‐, seven‐ and nine‐year survival rates.ResultsThe 5‐, 7‐ and 9‐year survival rates were 84.4%, 77.9% and 74.7%, respectively. The most common cause of death was cardiovascular disease. Associated with increased mortality independent of age were Indigenous ethnicity (HR = 2.04, 95% confidence interval [CI]: 1.17‐3.57, P = 0.012), chronic renal failure (HR = 1.76, 95% CI: 1.07‐2.89, P = 0.026) and renal failure requiring dialysis (HR = 2.32, 95% CI: 1.25‐4.32, P = 0.008).Conclusions and relevanceLong‐term survival rates after diabetic vitrectomy in Australia are similar to rates reported in other populations. Indigenous ethnicity and chronic renal failure were the most significant factors associated with long‐term mortality. This information can guide allocation of future resources to improve the prognosis of these high risk groups.

The 10-year all-cause mortality rate of Indigenous Australians over the age of 40 years and living in remote communities of Central Australia was 29.3%. This is more than double that of the Australian population as a whole. Mortality was significantly associated with visual acuity at recruitment. Further work designed to better understand this association is warranted and may help to reduce this disparity in the future.

PURPOSE. Few studies have explored the association of genetic variants in microRNA genes and binding sites with diabetic retinopathy (DR) in type 1 diabetes. We conducted a genome-wide scan for single nucleotide polymorphisms (SNPs) in these genes by using data from a genomewide association study (GWAS). METHODS. All known SNPs were imputed from our GWAS data (n ¼ 325) of DR cases and diabetic controls (no DR). Relevant SNPS were extracted using miRNASNP and PolymiRTS (version 2) databases. v 2 tests and logistic regression (adjusting for age, sex, duration of diabetes, HbA1c, and hypertension) were used to test the association between the imputed SNPs and DR phenotypes (any DR, nonproliferative DR [NPDR], proliferative DR [PDR], diabetic macular edema [DME], and sight-threatening DR defined as PDR, severe NPDR, or clinically significant macula edema [CSME]) compared with diabetic controls. Top-ranking SNPs were genotyped in a larger cohort (N ¼ 560) to confirm their association with DR. RESULTS. Three SNPs (rs10061133, rs1049835, rs9501255) were selected and genotyped in the final cohort. Rs10061133 in MIR449b was protective of sight-threatening DR (odds ratio [OR] ¼ 0.32, P ¼ 3.68 3 10 À4) and PDR (OR ¼ 0.30, P ¼ 8.12 3 10 À4), and the associations became more significant as the cohort increased in size. CONCLUSIONS. Rs10061133 in MIR449b is significantly associated with a decreased risk of PDR and sight-threatening DR in Caucasian patients with type 1 diabetes. This can guide future studies on genetic risk profiling and on developing microRNA-related therapies for sightthreatening DR.