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> Dr. Unger reports he is a consultant for and serves on the speakers bureau of Janssen Pharmaceuticals.
SOURCE : Peters AL, et al. Euglycemic diabetic ketoacidosis: A potential complication of treatment with sodium-glucose cotransporter 2inhibition. Diabetes Care 2015;38:1687-1693.
Diabetic ketoacidosis (DKA) occurs in approximately 5% of patients with type 1 diabetes and is defined by a triad of hyperglycemia (blood glucose > 250 mg/dL), anion-gap acidosis, and increased plasma ketones. Euglycemic DKA (euDKA) is considered rare, but may be underreported. Risk factors for euDKA include meal skipping, alcohol intake, and inhibition of gluconeogenesis. Patient 1 was a 40-year-old female with type 1 diabetes and a body mass index of 26.5 kg/m 2 . Prior to canagliflozin initiation, her A1c was 11.4%. As her glycemic control improved within 2 weeks, the patient reduced her basal insulin dose by 50%. Two weeks later, she developed a febrile illness resulting in reduced oral intake. She was therefore consuming fewer carbohydrates and using less insulin. In the emergency department (ED) her blood glucose was 220 mg/dL and serum ketones were positive. Her blood gas showed a pH of 6.9.
A second patient with type 1 diabetes was prescribed canagliflozin as adjunctive therapy to her insulin pump regimen. Her baseline A1c was 7%. The patient walked through an amusement park for 12 hours before becoming ill. After reducing her basal insulin dose, the patient awoke the next morning with a migraine headache. Over the course of 5 days, her headache persisted. A neurologist prescribed steroids. Although her blood glucose was 120 mg/dL, the patient’s urine ketone test was positive. She self-managed the euglycemia with oral-glucose-containing fluids, insulin, and antiemetics. As her ketones resolved, so did her migraine, nausea, and vomiting.
COMMENTARY
Personally, I have discontinued my off-label use of sodium-glucose cotransporter-2 (SGLT2) inhibitors in patients...