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Dominic Cavlan, Shanti Vijayaraghavan, Susan Gelding, and William Drake

development of ketotic hyperglycaemia in our patient. Abrupt GH-mediated derangement of glycaemic control was demonstrated as long ago as 1958, when Luft et al . (4) used cadaveric GH to treat three type 1 diabetic patients with hypopituitarism and

Open access

Ved Bhushan Arya, Jennifer Kalitsi, Ann Hickey, Sarah E Flanagan, and Ritika R Kapoor

divided doses) on day 15 of life. Outcome and follow-up Within 48 h of commencing diazoxide, marked hyperglycaemia (highest bedside BG concentration 21.6 mmol/L) developed, which persisted despite weaning high-concentration glucose intravenous

Open access

Dured Dardari, Alfred Penfornis, and Agnes Hartemann

with established microvascular disease (i.e. retinopathy and nephropathy). Moreover, the rapid normalisation of hyperglycaemia may, in some cases, cause acute neuropathy affecting small peripheral nerve fibres ( 2 ). Charcot neuroarthropathy (CN) is a

Open access

Akihiko Ando, Shoichiro Nagasaka, and Shun Ishibashi

for 1 week. At that time, hyperglycaemia above 16.7 mmol/L (300 mg/dL) was found and treated by intravenous insulin therapy for 1 month. Subsequently, her growth and development were normal without medication. At 13 years of age, she became aware of

Open access

N Siddique, R Durcan, S Smyth, T Kyaw Tun, S Sreenan, and J H McDermott

diagnosis of DM. Basal-bolus insulin was instituted and resulted in resolution of hyperglycaemia and osmotic symptoms. Insulin was subsequently discontinued, and he was discharged on metformin 1000 mg twice a day and gliclazide modified release of 30 mg a

Open access

Benjamin G Challis, Chung Thong Lim, Alison Cluroe, Ewen Cameron, and Stephen O’Rahilly

MWS commonly present with diarrhoea, dehydration and symptoms associated with severe electrolyte depletion, particularly those related to hypokalaemia. Symptomatic hyperglycaemia and new-onset diabetes are very rare manifestations of MWS. Herein we

Open access

Ploutarchos Tzoulis, Richard W Corbett, Swarupini Ponnampalam, Elly Baker, Daniel Heaton, Triada Doulgeraki, and Justin Stebbing

hospitalisation, she rapidly developed hyperglycaemia and ketosis with blood glucose of about 20 mmol/L and ketones of 2.0 mmol/L, requiring reinstatement of intravenous insulin infusion for a few hours. In the following 2 days, blood glucose readings ranged

Open access

Snezana Burmazovic, Christoph Henzen, Lukas Brander, and Luca Cioccari

the first 24 h after admission, her urine output was 3880 mL. Investigation Initial laboratory analysis revealed severe hypernatraemia (serum sodium concentration 161 mmol/L), moderate hypokalaemia (3.2 mmol/L), hyperglycaemia (BGL: 35.4 mmol

Open access

Shivani Patel, Venessa Chin, and Jerry R Greenfield

follow-up Blood glucose levels were well controlled on basal bolus insulin. Her hyperglycaemia-associated symptoms had significantly improved. She required 20 units of glargine insulin (Lantus) and 1 unit of insulin aspart (NovoRapid) for every 10 g of

Open access

Chad Bisambar, Andrew Collier, Fraser Duthie, and Carron Meney

Background Non-functional duodenal neuroendocrine tumours can present with hyperglycaemia and cause diabetes. This is in the absence of gluconeogenic hormones such as somatostatin and glucagon. Case presentation A previously well 40