Abstract
Disclosure: F.O. Asemota: None. S.H. Siddiqui: None. A.D. Manavalan: None.
Introduction: Euglycemic diabetic ketoacidosis (EDKA) is characterized by high-anion gap metabolic acidosis, ketosis, and near-normal glucose levels. Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) have cardiovascular and renal benefits in diabetes but may also induce prolonged EDKA. We present a case of prolonged EDKA associated with ertugliflozin use. Case: A 32-year-old male with type 2 diabetes diagnosed 6 years prior, complicated by gastroparesis presented with vomiting, pain, and poor oral intake. His home regimen included insulin lispro with meals and ertugliflozin 15 mg daily. Laboratory evaluation revealed: A1c 10.6%, glucose 245 mg/dL, pH 7.29, bicarbonate 14 mEq/L, and beta-hydroxybutyrate (BHB) >4 mmol/L. Urinalysis showed glucosuria ≥1000 mg/dL and ketones ≥160 mg/dL. The patient was initiated on intravenous insulin and dextrose for the management of ketoacidosis. Despite continued insulin infusion, glucose levels maintained in the 140-180mg/dl range and NPO status, serum bicarbonate remained low with persistently elevated BHB, and continued glucosuria > 1000 mg/dl. Insulin infusion rates were increased with supporting dextrose which ultimately led to the resolution of ketoacidosis on the ninth day of hospitalization. He was bridged to a basal and bolus insulin regimen. Glutamic acid decarboxylase antibody, IA2 antibody, Zinc transporter 8 antibody and islet cell antibody testing was negative. Ertugliflozin was discontinued on discharge. He was advised to follow up with his endocrinologist to evaluate for restoration of insulin secretion. Discussion: The rate of EDKA with SGLT-2i is estimated to range from 0.32-2.0 per 1000 patient years. SGLT-2i are associated with glucosuria, often leading to decreased insulin dosing, promoting increased hepatic gluconeogenesis. In addition, glucagon activity is upregulated through unclear mechanisms. Due to a negative fluid balance, cortisol and epinephrine levels are increased, further increasing insulin resistance and promoting ketosis, independent of insulin and glucagon levels. Risk factors for developing EDKA with SGLT-2 inhibitors include Type 1 diabetes, pancreatitis, bariatric surgery, gastroparesis, insulin reductions, ketogenic diet, starvation, dehydration, drug or alcohol use and stress. Ketonemia and glucosuria have been shown to persist for more than 10 days in SGLT-2i induced EDKA. Factors that predispose to prolonged ketoacidosis are not clear. However, it is proposed the higher rates of fixed dose insulin infusion supported by dextrose may be needed, as in our case, rather than lower and variable insulin dosing that is the standard of care for DKA in order for rapid and successful management.
Presentation: Monday, July 14, 2025