ObjectiveWe assessed the efficacy of routine glycated hemoglobin (HbA1c) testing to detect undiagnosed diabetes and prediabetes in an urban Australian public hospital emergency department (ED) located in an area of high diabetes prevalence.MethodsOver 6 weeks, all patients undergoing blood sampling in the ED had their random blood glucose measured. If ≥5.5 mmol/L (99 mg/dL), HbA1c was measured on the same sample. HbA1c levels ≥6.5% (48 mmol/mol) and 5.7–6.4% (39–46 mmol/mol) were diagnostic of diabetes and prediabetes, respectively. Hospital records were reviewed to identify patients with previously diagnosed diabetes.ResultsAmong 4580 presentations, 2652 had blood sampled of which 1267 samples had HbA1c measured. Of these, 487 (38.4%) had diabetes (either HbA1c≥6.5% or a prior diagnosis), and a further 347 (27.4%) had prediabetes. Among those with diabetes, 32.2% were previously undiagnosed.ConclusionsRoutine HbA1c testing in the ED identifies a large number of people with undiagnosed diabetes and prediabetes, and provides an opportunity to improve their care.

Access to proprietary closed‐loop insulin pump systems is limited. The use of Do‐It‐Yourself closed‐loop systems in Australia is growing. A 2017 Facebook group survey indicated that 20 individuals were actively looping with another 38 yet to commence despite the lack of regulatory body approval. Improved glycaemic control with less hypoglycaemia and better sleep were the main benefits. Local health professionals need to be aware of this technology.

It has been suggested that the primary site of damage in motor neuron disease (MND) is the cortical motor neuron, with secondary degeneration of spinal motor neurons. To test this hypothesis, we sought to determine if loss of corticomotoneurons in MND precedes spinal motor neuron loss. The density of corticomotoneurons was measured in 18 MND and 9 control cases using 10-microns horizontal sections of motor cortex in the hand/arm region. The density of spinal motor neurons was measured in 10-microns transverse sections of the lower cervical spinal cord. Corticomotoneuron and spinal motor neuron densities were decreased in MND cases compared to controls, but in MND cases there was poor correlation (r2 = 0.06) between corticomotoneuron and spinal motor neuron densities. The results indicate that corticomotoneuron and spinal motor neurons are lost at different rates in different MND patients, and that corticomoteneuron loss is unlikely to be a primary event in MND.