Endocrine Abstracts

KPD remains poorly understood. It is characterised by unprovoked hyperglycaemia with ketoacidosis at diagnosis, in the context of brief history of hyperosmolar symptoms and weight loss in individuals with no prior history of diabetes. The initiation of insulin therapy in these patients is accompanied by insulin-free periods, during which oral hypoglycaemic medications and diet achieve normoglycaemia. KPD has been reported predominantly in Africans, African Americans, Hispanics and, less commonly, Asians.

Case presentation: 29-year-old Zimbabwean lady (BMI of 49 kg/m²) presented to the A&E with a one-month history of osmotic symptoms and weight loss. She reported persistent vomiting of a week duration, and systemic reviews were unremarkable. Her Father and grandfather had type 2 diabetes, and her grandmother has type 1 diabetes. She has a history of polycystic ovarian syndrome and takes no regular medication. The Patient was dehydrated at presentation, and systemic examinations were unremarkable. She had a blood glucose of 23 mmol/l, PH of 7.249, bicarbonate of 10 mmol/l and ketone of >7 mmol/l. Other investigations showed sodium of 132 mmol/l, potassium of 4.0 mm/l, Urea of 2.5 mmol/l and Creatinine of 59 mmol/l. HBA1c was 116 mmol/mol, and there was no evidence of chest or urine infection. She was commenced on insulin infusion and then discharged home on basal-bolus (Lantus 20 units, Novorapid 8 units TDS) following the resolution of her DKA. She was followed up at the outpatient clinic within a month, during which she reported resolution of osmotic symptoms and weight gain, and SMBG revealed optimal glycaemic control with some episodes of symptomatic hypoglycaemia. GAD65 and Islet cell antibodies were negative, C-peptide was 2241 pmol per litre and urine ACR was 7.22 mg/g. Novorapid was stopped, Lantus was reduced to 10 units, and She was commenced on metformin and Ramipril. Her insulin was discontinued during further follow-up within three months, and HBA1c was 42 mmol/mol. The Patient remained well on oral hypoglycaemic agent with optimal glycaemic control. The classification of this heterogeneous condition still poses great challenge, though the recent Aβ classification gave some clarity to four different phenotypes (A⁺ β⁻, A⁻ β⁻, A⁺ β⁺, and A⁻ β⁺ ) with recognisable limitations. Moreover, the aetiopathogenesis of DKA remains largely debated; proposed mechanisms include prolonged glucotoxicity, increased oxidative stress, high glucagon levels and viral-induced insulin resistance with secretory defect. It is hoped that guidelines for the long-term management of this condition will be established by relevant authorities as the incidence of KPD in the UK is likely to increase.