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Wellington, New Zealand

Carroll R.W.,Diabetes and Research Center
Asia-Pacific Journal of Clinical Oncology

Multiple endocrine neoplasia type 1 (MEN1) is inherited in an autosomal dominant fashion and predisposes to the development of hyperplastic or neoplastic changes in the parathyroid and pituitary glands and the endocrine pancreas, along with numerous other characteristic tumors and features. The management of each entity differs to some degree from their sporadic counterparts, while the lack of a genotype-phenotype correlation requires lifelong clinical, biochemical and radiological screening for the development of new tumors. While the syndrome itself is relatively rare (a prevalence of 1-10/100000), it is likely that health-care practitioners from numerous specialities will occasionally encounter a patient with MEN1 and therefore a basic knowledge of the syndrome is important. In addition, many of the associated tumors are seen commonly in sporadic form, and a judicious policy is therefore required in deciding how thoroughly patients who develop these tumors should be screened for MEN1. The current literature on MEN1 is reviewed and key learning points are suggested for the clinician. © 2012 Wiley Publishing Asia Pty Ltd. Source

Krebs J.D.,University of Otago | Krebs J.D.,Diabetes and Research Center | Elley C.R.,University of Auckland | Parry-Strong A.,University of Otago | And 6 more authors.

Aims/hypothesis To compare the effectiveness of low-fat high-protein and low-fat high-carbohydrate dietary advice on weight loss, using group-based interventions, among overweight people with type 2 diabetes. Study design Multicentre parallel (1:1) design, blinded randomised controlled trial. Methods Individuals with type 2 diabetes aged 30-75 years and a BMI >27 kg/m 2 were randomised, by an independent statistician using sequentially numbered sealed envelopes, to be prescribed either a low-fat high-protein (30% of energy as protein, 40% as carbohydrate, 30% as fat) or a low-fat highcarbohydrate (15% of energy as protein, 55%as carbohydrate, 30% as fat) diet. Participants attended 18 group sessions over 12 months. Primary outcomes were change in weight and waist circumference assessed at baseline, 6 and 12 months. Secondary outcomes were body fatness, glycaemic control, lipid profile, blood pressure and renal function. A further assessment was undertaken 12 months after the intervention. Research assessors remained blinded to group allocation throughout. Intention-to-treat analysis was performed. Results A total of 419 participants were enrolled (mean±SD age 58±9.5 years,BMI 36.6±6.5 kg/m 2 and HbA 1c 8.1±1.2% (65 mmol/mol)). The study was completed by 70%(294/419). No differences between groups were found in change in weight or waist circumference during the intervention phase or the 12-month follow-up. Both groups had lost weight (2-3 kg, p<0.001) and reduced their waist circumference (2-3 cm, p<0.001) by 12 months and largely maintained this weight loss for the following 12 months. By 6 months, the difference in self-reported dietary protein between groups was small (1.1%total energy; p<0.001). No significant differences between groups were found in secondary outcomes: body fatness, HbA 1c, lipids, blood pressure and renal function. There were no important adverse effects. Conclusions/interpretation In a 'real-world' setting, prescription of an energy-reduced low-fat diet, with either increased protein or carbohydrate, results in similar modest losses in weight and waist circumference over 2 years. Trial registration: Australia New Zealand Clinical Trials Register ACTRN12606000490572 Funding: The Health Research Council of New Zealand (06/337). © 2012 Springer-Verlag. Source

Carroll R.W.,Diabetes and Research Center | Carroll R.W.,University of Otago | Murphy R.,University of Auckland

Monogenic forms of beta cell diabetes account for approximately 1%-2% of all cases of diabetes, yet remain underdiagnosed. Overlapping clinical features with common forms of diabetes, make diagnosis challenging. A genetic diagnosis of monogenic diabetes in many cases alters therapy, affects prognosis, enables genetic counseling, and has implications for cascade screening of extended family members. We describe those types of monogenic beta cell diabetes which are recognisable by distinct clinical features and have implications for altered management; the cost effectiveness of making a genetic diagnosis in this setting; the use of complementary diagnostic tests to increase the yield among the vast majority of patients who will have commoner types of diabetes which are summarised in a clinical algorithm; and the vital role of cascade genetic testing to enhance case finding. © 2013 by the authors; licensee MDPI, Basel, Switzerland. Source

Haeusler S.,Victoria University of Wellington | Parry-Strong A.,Diabetes and Research Center | Krebs J.D.,University of Otago
New Zealand Medical Journal

Aim Metformin, the most common hypoglycaemic agent used in type 2 diabetes, is associated with reduced serum vitamin B12 concentrations. This cross sectional observational study determines the prevalence of low vitamin B12 status in people with type 2 diabetes on metformin therapy in both primary and secondary care in New Zealand. Method All eligible patients seen in a secondary-care clinic over a 15-month timeframe were screened for low serum vitamin B12 concentrations. Additionally, patients from four primary health care providers were identified using metformin prescription data and offered the chance to participate in the audit. Results Prevalence of serum Vitamin B12 level <220 pmol/L was 18.7%. Positive correlations were observed between B 12 concentration, age and dosage and duration of metformin treatment. Māori and Pacific Islanders had higher mean serum B12 concentrations than Europeans but no difference in prevalence of low serum B12 concentrations. Conclusion Low serum B12 concentration is a common occurrence in people with type 2 Diabetes treated with Metformin. Age is an important factor which explains some of this association. Systematic screening in those receiving metformin is advisable, particularly for patients older than 50 years. © NZMA. Source

Mctavish L.,Diabetes and Research Center | Krebs J.D.,Diabetes and Research Center | Krebs J.D.,University of Otago | Weatherall M.,University of Otago | Wiltshire E.,University of Otago
Diabetic Medicine

Aim: To determine whether a weight-based hypoglycaemia treatment using 0.3 g/kg (or 0.2 g/kg) glucose effectively treats adults with Type 1 diabetes mellitus compared with an internationally recommended 15-g treatment. Methods: Patients with frequent hypoglycaemia were recruited from hospital-based diabetes clinics. The treatment for each hypoglycaemic episode, defined as capillary glucose <4.0 mmol/l, was randomly assigned to one of three protocols: 0.2 g/kg, 0.3 g/kg, or 15 g, using DextroTM glucose tablets (Dextro Energy, Krefeld, Germany). Each participant received each treatment in random order for up to 15 hypoglycaemic episodes. Capillary glucose was re-tested 10 min after treatment, with a repeat dose if still < 4 mmol/l. Results: The study recruited 34 participants aged 22-71 years, whose mean (sd) BMI was 25.2 (3.1) kg/m2 and HbA1c 63 (10.4) mmol/mol [7.9 (0.9)%]. Two people withdrew because they did not like the taste of the Dextro tablets and one was excluded because they used their own glucose preparation. Unadjusted for clustering within participants, the mean (sd) capillary glucose after 10 min was 4.67 (1.25) mmol/l for 0.3 g/kg (141 episodes), 4.29 (0.94) mmol/l for 0.2 g/kg (132 episodes), and 4.37(0.99) mmol/l for 15 g (136 episodes). Capillary glucose, adjusted for clusters and baseline, was higher after 10 min for 0.3 g/kg glucose compared with 15 g glucose; a difference of 0.26 (95% CI 0.04-0.48) mmol/l (P = 0.02), but not for 0.2 g/kg; -0.07 (95% CI -0.29-0.16) mmol/l (P = 0.56). Capillary glucose for only three hypoglycaemic episodes rose above 8 mmol/l. Conclusions: A weight-based protocol of 0.3 g/kg glucose appears more effective for treating symptomatic hypoglycaemia in adults with Type 1 diabetes than either the most common current recommendation of 15 g glucose or a 0.2 g/kg glucose dose. © 2015 Diabetes UK. Source

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