Endocrine Abstracts

Background: Diabetes is the commonest cause of ketoacidosis, with alcoholic and starvation ketoacidosis encountered less frequently. We present a case of high anion gap metabolic acidosis whose features were not categorigal for usual causes.

Case presentation: A 42-year-old female patient was admitted with a 3 day history of nausea, vomiting and abdominal pain, that begun 1 day after binge alcohol intake, on the background of alcohol excess. AKI, transaminitis and high anion gap metabolic acidosis were noted: lactate 7.6 mmol/l, pH 7.08, venous glucose 18.1 mmol/l, on urinalysis glucose 1+, ketones 4+, blood ketones 6.7 mmol/l. Amylase was mildly elevated and liver imaging showed hepatosteatosis. Due to the triad of a metabolic acidosis with hyperglycaemia and ketonaemia, a new diagnosis of insulinopenic diabetes was considered with a differential of alcoholic ketoacidosis and chronic pancreatitis, and the patient was treated with the DKA protocol followed by initiation of basal bolus insulin. AntiGAD and IA2 antibodies were negative, C-peptide 1971 pmol/l with paired venous glucose 8.7 mmol/l and HbA1c 27 mmol/mol. The patient self-discharged and didn’t attend of outpatient reviews in the diabetes clinic. 10 months later she presented with a 3 day history of epigastric pain and vomiting, and reported having discontinued all insulin a week prior. On presentation a metabolic acidosis was noted with glucose 12 mmol/l and blood ketones 6.6 mmol/l. FRII was initiated during which she rapidly developed hypoglycaemia. Repeat HbA1c was 29 mmol/mol. A week after her discharge she reported repeated hypoglycaemia while on insulin glargine 6 units once daily.

Discussion: The differential diagnosis of alcoholic from diabetic ketoacidosis in the setting of hyperglycaemia is challenging in a patient without a history of diabetes who reports alcohol excess, and hyperglycaemia in alcoholic ketoacidosis is reported in 11% of cases. Underlying chronic pancreatitis is likely to exacerbate the hyperglycaemia.