The occurrence of Diabetic Ketoacidosis (DKA), severe hypertriglyceridaemia (HTG) and acute pancreatitis (AP) is an uncommon triad of severe metabolic derangement, which has previously been reported in only handful of case reports.(1)
A 49 years old woman with type 2 Diabetes mellitus (diet controlled) presented to the Emergency department with severe abdominal pain for 3 days, on a background of 4 weeks of polyuria, polydipsia and lethargy. On examination, she was severely dehydrated and had central abdominal tenderness and guarding. Initial investigations revealed DKA (BGL: 40mmol/L, Ketones: 6mmol/L, arterial pH: 7.21), severe hypertriglyceridaemia (triglycerides: 64.2mmol/L) and acute pancreatitis (Lipase: 511 IU/L and CT scan evidence of AP). She was kept nil by mouth and treated in ICU with intravenous insulin infusion which resolved the metabolic derangements over 5 days. She was subsequently discharged from Hospital on basal bolus insulin regimen and a fibrate. On clinic review in 6 weeks, she was well, her glycaemic control was improved (HbA1c improved from 15.2% on hospital admission to 7.9%) and triglycerides were down to 2.92mmol/L. Her Anti GAD, IA-2 and Insulin antibodies were negative.
Our patient developed the triad of DKA, HTG and AP, with insulin deficiency the likely primary trigger for the metabolic derangements. It’s well known that Insulin deficiency leads to the development of DKA but Insulin plays an important role in lipid metabolism as well. Insulin is needed for optimal function of lipoprotein lipase, a key enzyme in lipid metabolism, and insulinopaenic states lead to its deactivation resulting in rise in triglycerides and chylomicrons.(2) Hypertriglyceridaemia and increased chylomicrons in turn, can cause acute pancreatitis.(3) Based on the pathogenic mechanism, insulin replacement therapy leads to reversal of these metabolic derangements. The case also highlights the emerging and increasingly recognised entity of ketosis-prone diabetes mellitus.(4)