Phosphate is important for normal mineralisation of bone. Phosphate is important in its own right for neuromuscular function, and profound hypophosphataemia can be accompanied by encephalopathy, muscle weakness and cardiomyopathy. Hypophosphataemia can be due to intracellular uptake of phosphate from the extracellular fluid, reduced intestinal phosphate absorption, increased renal excretion, decreased renal tubular absorptive capacity and genetic defects in renal tubule phosphate transporters.

I was diagnosed with type 1 diabetes when I was 17, just days after finishing my A level exams. I had lost 5kg in weight and experienced extreme thirst and tiredness over the previous few weeks, but I put that down to exam stress and was looking forward to recovering over the summer. “Luckily,” my very elevated blood glucose levels were picked up on a routine blood test before I went into diabetic ketoacidosis. In one day, I went from a normal 17 year old, preparing to apply to medical school, to someone with a chronic illness, controlled by multiple injections and finger pricks a day.

Editor – We read with interest the paper by Jalal et al.1 Sherwood Forest Hospitals, has provided non-training clinical fellowships since 2002.2 An account of how it addresses the issues raised in the paper by Jalal et al has been reported.3 Many overseas doctors are trained through traditional undergraduate medical curricula which do not emphasise communication and leadership skills, in contrast to significant emphasis on communication and leadership skills in the UK. It is a significant cultural shift for them to make the transition to settings where skills of communication and teamwork are given high priority in the clinical setting and assessed through work place based assessments using an electronic portfolio. Our programme addressed this challenge through 8 weeks of a supervised supernumerary period in a supported environment, designed to expose the clinical fellows gradually to the work environment through an extended period of induction mentoring and coaching with a gradual transition to the new work environment to enable the fellows overcome language, communication, clinical and work-cultural challenges and adapt to the UK healthcare system. Overseas doctors, who are employed in non-training positions, do not by right receive the training and educational opportunities offered to trainees in the National Training Programme and are not monitored by the Guardian for Safe Working Hours. Our programme addressed this issue by providing a study leave allocation, protected time for personal and professional development as well as deployment of the gripes tool.4 Leadership, management and educational governance of the Clinical Development Fellowship Programme is through a committee comprising the executive medical director, director of postgraduate medical education and senior human resources staff. The success of the programme was reflected in the programme outcomes which showed that 49% of fellows gained a training grade post and another 19% appointed to trust grade posts with responsibility at registrar grade during or at the end of the programme. The programme has also shown a reduction in variable pay costs as well as overall costs of employing non-training grade junior doctors. Introduction of the programme has resulted in a fall in both the total spend and spend on agency employed locum doctors.

The prevalence of type 2 diabetes mellitus is expected to rise in the frail elderly population, which will have significant consequences for the health economy. Symptoms of hypoglycaemia can be subtle in the elderly. Hypoglycaemia accounts for more hospital admissions than hyperglycaemia. Treatment targets are set based on the risk of adverse events resulting from treatment and the benefits expected from tighter glycaemic control. The different medications available are discussed including the different types of insulin, in particular relation to usage in older adults. The choice of therapy is based on the targets, comorbidities and the characteristics of each antidiabetic agent. Deintensification of therapy should be considered in patients who experience adverse effects. Treatment guidelines should be formulated based on the above principles, as many current guidelines do not incorporate deintensification of therapy.

Objectives: Adrenal gland hypertrophy can be related to acute stress with abnormal adrenal function tests. It may not always need treatment. Material and methods: An acute presentation of adrenal gland hypertrophy following an abdominal emergency, with subsequent hypoadrenalism was investigated. Results: Adrenal medullary and cortical function fully recovered without treatment. Conclusions: We postulate that the adrenal glands became enlarged and hypertrophied during an acute stress event, possibly caused by acute adrenal medullary hypersecretion and subsequent cortical hyposecretion. A wait and watch policy should be followed if no other clinical symptoms and signs of adrenal disease are present. CT scan remains an important diagnostic tool.

Objective: To illustrate an unusual mechanism causing hypoglycaemia. Material and methods: A 76-year-old man presented with episodes of agitation and confusion and was resuscitated with oral glucose gel when found to be hypoglycaemic. Results: A CT scan for an abdominal mass confirmed a solitary fibrous tumour (SFT). The sarcoma multidisciplinary team suggested conservative management. The patient's episodic hypoglycaemia was managed with diet modification including corn-based starch, scheduled snacks and dexamethasone. Glucose levels were within normal range at discharge from hospital. The patient was referred to the palliative care team for follow-up. Conclusion: SFTs causing non-islet cell tumour hypoglycaemia are difficult to treat., Copyright © EFIM 2015.

Objectives: To investigate the association between the fat mass and obesity related (FTO) gene rs9939609 and near melanocortin-4-receptor (MC4R) gene rs17782313 polymorphisms with obesity measures and metabolic parameters in urban and rural dwelling Sri Lankans. Methods: 535 subjects (60.9% female) from the general adult population (ages 18-70 years) representative of both urban (28.4%) and rural areas of residence were recruited by multi-stage random sampling. Body mass index (BMI), waist circumference (WC) and waist-to-hip ratio (WHR) was obtained by standard methods. DNA extracted from whole blood was genotyped using real-time PCR. Results: The FTO risk genotypes (AA + AT) were associated with higher BMI (p = 0.03) and WC (p = 0.05) measures as well as categorical obesity (BMI >= 27.5 kg m(-2) definition) (OR 1.69 95% CI 1.11-2.56, p = 0.01). The near MC4R risk genotypes (CC + CT) were associated with greater BMI (p = 0.03) as well as categorical obesity (BMI >= 25 kg m(-2) definition) (OR 1.57 95% CI 1.11-2.22, p = 0.01). In addition the MC4R risk genotype carriers (CC + CT) had significantly higher fasting blood sugar (FBS) levels compared to the 'TT' genotype carriers independent of BMI (p = 0.05). Urban living was associated with significantly greater BMI values for FTO risk genotypes compared to rural living (p = 0.02). Conclusions: FTO and near MC4R variants are associated with obesity measures in Sri Lankan populations whilst urban living accentuates the obesogenic effect of the FTO polymorphism. (C) 2016 Asia Oceania Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.

We investigate the effects of exenatide on excessive daytime sleepiness (EDS), driving performance and depression score in patients with type 2 diabetes with EDS. Eight obese patients with diabetes but without obstructive sleep apnoea (OSA) participated in a placebo-controlled single-blind study during which multiple wakefulness and sleep latency test, Epworth score, driving performance, depression score, fasting glucose and glycated haemoglobin (HbA1c) levels were assessed at baseline, end of placebo and treatment phase at baseline and after 22 weeks of treatment. Mean (±standard error of the mean) age, body mass index (kg m2) and HbA1c [mmol mol−1 (%)] of patients at baseline were 50 ± 4.9 years, 37.6 ± 1.1 and 65 ± 19 (8.06 ± 0.41), respectively. When compared to placebo, exenatide treatment was associated with a decrease in both subjective and objective sleepiness, based on the Epworth score reduction and the sleep latency increase assessed by multiple objective sleepiness and sustained attention (OSLER) tests, respectively. Mean sleep latency time (adjusted for change in HbA1c and weight) were 32.1 ± 1.7, 29.1 ± 1.7 and 37.7 ± 1.7, respectively ( P = 0.002). Modelling for covariates suggested that improvement in mean sleep latency time is predicted by changes in weight ( P = 0.003), but not by changes in HbA1c ( P = 0.054). Epworth sleepiness score was reduced significantly (values for placebo versus exenatide: 11.3 ± 1.2 versus 5.7 ± 1.3; P = 0.003). No significant change was noted in the depression score and driving performance. Exenatide is associated with a significant reduction in objective sleepiness in obese patients with type 2 diabetes without OSA, independent of HbA1c levels. These findings could form a basis for further studies to investigate the pathophysiological mechanisms of sleepiness in obese patients with type 2 diabetes.