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A3340 - Euglycemic Diabetic Ketoacidosis in a Patient on a SGLT-2 Inhibitor Presenting with Acute Pancreatitis
Author Block: K. Badwal, T. Tariq; Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI, United States.
Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are a novel class of medications used for glycemic control in type 2 diabetes mellitus. Their mechanism of action involves preventing resorption of glucose at the proximal kidney, thereby promoting glucosuria and weight loss. Unfortunately, there have been reported incidences of euglycemic diabetic ketoacidosis in individuals taking this medication. This report describes a 25-year-old male with a history of type 2 diabetes on dapagliflozin who developed diabetic ketoacidosis. This gentleman initially presented with his third episode of pancreatitis secondary to elevated triglycerides. The patient remained on dapagliflozin while inpatient and his blood sugars were consistently between 110 and 220. Unfortunately, five days into admission the patient’s bicarbonate trended down to 5 with an anion gap of 36. His beta-hydroxybutyrate level was noted to be 6.06. He was ultimately admitted into the intensive care unit where he required an insulin drip and one treatment of plasma exchange therapy for hypertriglyceridemia. The patient’s diabetic ketoacidosis resolved and he was transitioned to basal insulin successfully. The patient’s oral agents were discontinued completely and he was discharged on an insulin regimen. SGLT-2 inhibitors have been found to be associated with euglycemic DKA and ketosis, most likely as a result of their non-insulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. The aim of this case report is to alert the physician about the possibility of euglycemic DKA in a patient on an SGLT-2 inhibitor presenting with an acute illness such as pancreatitis as seen with our individual. When identified, the physician should immediately discontinue the medication while remaining vigilant about the possibility of diabetic ketoacidosis even in the euglycemic state.