MON-624 Insulin Therapy in Steroid-Induced Ketoacidosis (SIKA) with Normoglycemia

Abstract Disclosure: G.I. Sydney: None. Background: Diabetic ketoacidosis (DKA) is traditionally associated with insulin deficiency; however, it can also occur in patients with well-controlled diabetes—or even in those without diabetes. Acute physiological stress triggers a surge in counter-regulatory hormones, including epinephrine, cortisol, and growth hormone, which collectively promote lipolysis and ketogenesis. Corticosteroids, particularly dexamethasone, exacerbate this metabolic disruption by potentiating the lipolytic effects of growth hormone and upregulating key enzymes such as hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL). This steroid-driven augmentation of ketogenesis can lead to profound metabolic acidosis, even in the absence of marked hyperglycemia. Case Presentation: An 85-year-old female with non-Hodgkin’s B-cell lymphoma developed immune effector cell-associated neurotoxicity syndrome (ICANS) following treatment with glofitamab. She was treated with high-dose dexamethasone (20 mg every 6 hours) for ICANS but subsequently developed acute nausea, vomiting, and tachypnea. Laboratory evaluation revealed severe metabolic derangement, including a bicarbonate level of 10 mmol/L (reference range: 20-30 mmol/L), an anion gap of 29 (reference range: 7-17), and markedly elevated beta-hydroxybutyrate at 8.85 mmol/L (reference range:<=0.27 mmol/L). Despite a glucose level of 161 mg/dL (reference range: 70-100 mg/dL), these findings were consistent with ketoacidosis. Given the profound ketosis and metabolic acidosis, an insulin infusion was initiated intended to suppress lipolysis and ketone production, while a concurrent dextrose infusion was administered to prevent hypoglycemia in the setting of relative normoglycemia. This approach successfully reversed the ketosis, and resolved the patients acidosis. Conclusion: This case underscores the complex pathophysiology of SIKA and the potential for corticosteroids to precipitate ketoacidosis independent of severe hyperglycemia. By amplifying the lipolytic effects of growth hormone and upregulating key enzymatic pathways, corticosteroids can provoke profound metabolic acidosis, necessitating a high index of suspicion for timely diagnosis. Recognizing SIKA as a distinct entity is crucial for appropriate management, with insulin serving as a potential key therapeutic agent, even in the absence of overt hyperglycemia. Presentation: Monday, July 14, 2025