Poster Presentation The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2017

The enigmatic triad of diabetic ketoacidosis, severe hyper-triglyceridaemia and acute pancreatitis: A case report and review of the literature. (#262)

Danish Mahmud 1 2 , Rakesh Iyer 2
  1. Australian National University Medical School , Canberra, ACT
  2. Calvary Health, Bruce, ACT, Australia

Introduction:

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)

Clinical report:

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.

Discussion:

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)

  1. Singla AA, Ting F, Singla A. Acute pancreatitis secondary to diabetic ketoacidosis induced hypertriglyceridemia in a young adult with undiagnosed type 2 diabetes. JOP. 2015;16(2):201-4.
  2. Vergès B. Lipid disorders in type 1 diabetes. Diabetes Metab. 2009;35(5):353-60.
  3. Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterol. 2003;36(1):54-62.
  4. Balasubramanyam A, Nalini R, Hampe CS, Maldonado M. Syndromes of ketosis-prone diabetes mellitus. Endocr Rev. 2008;29(3):292-302.