ESA-SRB-AOTA 2019

Diabetic ketoacidosis, hypertriglyceridaemia and acute pancreatitis: a case series of the enigmatic triad (#585)

Kay Hau Choy 1 , Tegan van Gemert 2 , Zoran Apostoloski 2 , Jane Zhang 2
  1. Department of Endocrinology and Metabolism, Concord Repatriation General Hospital, Concord, NSW, Australia
  2. Department of Endocrinology, Wollongong Hospital, ISLHD, Wollongong, NSW, Australia

Background: The triad of diabetic ketoacidosis (DKA), hypertriglyceridaemia and acute pancreatitis is a rare phenomenon. Herein, we present a case series of two patients with this unique clinical scenario.

Results: Two male patients, aged 34 and 19 years, with no known history of diabetes mellitus or dyslipidaemia presented with acute epigastric pain. Radiological assessment revealed acute pancreatitis, with biochemistry showing concurrent diabetic ketoacidosis (DKA) and hypertriglyceridaemia in all cases. Our first patient—who had a triglyceride level of 91mmol/L (reference interval, <2.5mmol/L), HbA1c of 14.1%, pancreatic necrosis and multi-organ failure—received plasmapheresis. The other patient had a triglyceride level of 27mmol/L with HbA1c of 12.7% and achieved rapid resolution of metabolic derangements with intravenous insulin infusion. Both patients were managed in intensive care unit. All patients were discharged on combination lipid-lowering therapy and required ongoing subcutaneous insulin. Their triglycerides and glycaemic control were monitored regularly at clinical follow-up and no patients have had recurrence of pancreatitis or DKA.

Discussion: Acute pancreatitis and hypertriglyceridaemia can both be a cause of or a consequence of DKA.1 DKA is a state of profound insulin deficiency associated with dysregulated glucose and lipid metabolism. The resulting hypertriglyceridaemia may induce pancreatitis with direct toxicity to the acinar cells and pancreatic capillaries.2,3 Hypertriglyceridaemic-pancreatitis can precipitate beta-cell dysfunction, leading to transient insulin deficiency and potentially triggering DKA. Infusions of insulin, heparin and plasmapheresis have been used in addition to aggressive fluid repletion to lower triglycerides in different subsets of patients. Fibrates are the first-line long-term pharmacotherapy in patients with hypertriglyceridemia who are at risk of pancreatitis.1-3

Conclusion: A diagnosis of DKA in hypertriglyceridaemic-pancreatitis and vice versa is challenging due to the complex causal-effect relationship of the three concurrent conditions. Awareness of this uncommon triad is vital for early recognition and appropriate intervention.

  1. Simons-Linares CR, Jang S, Sanaka M, Bhatt A, Lopez R, Vargo J, at al. The triad of diabetes ketoacidosis, hypertriglyceridemia and acute pancreatitis. How does it affect mortality and morbidity?: A 10-year analysis of the National Inpatient Sample. Medicine 2019;98(7).
  2. Seth A, Rajpal S, Saigal T, Bienvenu J, Sheth A, Alexander JS, et al. Diabetic ketoacidosis-induced hypertriglyceridemic acute pancreatitis treated with plasmapheresis—recipe for biochemical disaster management. Clin Med Insights Gastroenterol. 2014;7: CGast-S18557.
  3. Singla AA, Ting F, Singla A. Acute pancreatitis secondary to diabetic ketoacidosis induced hypertriglyceridemia in a young adult with undiagnosed type 2 diabetes. JOP. J Pancreas. 2015;16: 201-4.