Endocrine Abstracts

A 35 year old otherwise healthy gentleman from Togo, was referred to our clinic with new onset diabetes and a glycated haemoglobin (Hba1c) of 119mmol/mol (13.1%). He initially presented to his general practitioner with polyuria and polydipsia, and 5 kg of weight loss. He denied any change in bowel habit and had no recent illnesses. Both parents had Type 2 Diabetes Mellitus (T2D). Initial blood tests revealed a blood glucose of 22.84 mmol/l, with positive ketones (1.2 mmol/l). Urinalysis showed glycosuria (1000 mg/dl) but was negative for nitrites and white cells. Renal, liver and thyroid function tests were all within normal limits. In addition, the patient had mild metabolic acidosis (Table 1). The markedly elevated blood glucose levels in association with ketoacidosis strongly suggested a diagnosis of Type 1 Diabetes Mellitus (T1D). The patient was admitted to the diabetes ward and treated with a fixed rate insulin infusion as per diabetic ketoacidosis (DKA) protocol. There was a fairly rapid improvement in both hyperglycaemia and ketonaemia within a few hours. Anti-glutamic acid (GAD), anti-insulinoma antigen 2 antibodies (IA2) and anti-insulin antibodies were all negative. The next day, the patient was discharged on a basal bolus regime of glargine and aspart after review by the inpatient diabetes team. The patient continues with regular clinic reviews. His glucose levels continued to improve with incremental insulin dose reductions and he remains on low dose metformin (500 mg daily), with normalisation of his Hba1c after 6 months.

Conclusions: A rapid response to insulin, negative testing for type 1 autoimmunity, in a young gentleman of African origin, suggested a diagnosis of ketosis prone/Flatbush diabetes was most likely. The aetiology of ketone-prone diabetes remains unknown. Further studies may help future therapies. A diagnosis of ketosis prone diabetes should always be borne in mind in patients of African ethnicity presenting with new onset diabetes and ketosis. Misdiagnosing patients with KPD as T1D can lead unnecessary treatment with long-term insulin therapy, with all its implications (e.g. hypoglycaemia, occupational impact).