Skip to main content
ENDO 2026 Main banner

Diabetes and Vascular Disease

SAT-618 - Recurrent Euglycemic Diabetic Ketoacidosis Associated with GLP-1 Receptor Agonist Therapy in Type 2 Diabetes Mellitus

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT

    Late-Breaking Poster Presenter(s)

  • QG

    Qetevan Gvazava, MD

    Resident Physician
    Luminis Health Anne Arundel Medical Center
    Annapolis, Maryland, United States

    • Co-Author(s)

  • PU

    Pulkita Uppal, MD

    Chief Resident Physician
    Luminis Health Anne Arundel Medical Center
    Annapolis, United States

    • Senior Author/Primary Investigator(s)

  • NM

    Nargiz Muganlinskaya, MD

    Program Director
    Luminis Health Anne Arundel Medical Center
    Annapolis, Maryland, United States

Background
Euglycemic diabetic ketoacidosis (eDKA), defined as DKA with blood glucose < 250 mg/dL, is an increasingly recognized complication predominantly associated with sodium-glucose cotransporter-2 (SGLT2) inhibitors. While glucagon-like peptide-1 receptor agonists (GLP-1 RAs) suppress glucagon secretion and theoretically reduce ketogenesis, emerging evidence suggests a potential paradoxical association with eDKA. We present a case of recurrent eDKA temporally associated with two different GLP-1 RAs, highlighting an important safety consideration for these widely prescribed medications.

Case Presentation
A 38-year-old female with type 2 diabetes mellitus presented with 1–2 days of nausea, vomiting, and shortness of breath. Home blood glucose readings ranged from 127–200 mg/dL. Her medications included metformin and dulaglutide.
On presentation, vital signs were stable. Physical examination was notable for dry mucous membranes. Laboratory evaluation revealed high anion gap metabolic acidosis with ketosis, consistent with diabetic ketoacidosis, despite relatively normal blood glucose levels. Venous blood gas confirmed metabolic acidosis.
The patient was diagnosed with euglycemic DKA and treated with intravenous fluids, insulin infusion, and dextrose with electrolyte replacement. She was admitted to the intensive care unit for close monitoring. No infectious or other precipitating causes were identified. Lactate and renal function were within normal limits.
Notably, the patient had a prior episode of eDKA one year earlier, attributed to semaglutide, which had been discontinued and replaced with dulaglutide.
The patient’s metabolic abnormalities resolved within 24 hours. Dulaglutide was discontinued, and she was discharged on metformin with outpatient endocrinology follow-up.

Conclusion
This case highlights an emerging safety signal of euglycemic DKA associated with GLP-1 receptor agonist therapy, with recurrence across different agents in the same class. Clinicians should maintain heightened awareness of this potentially life-threatening complication, particularly in patients presenting with nausea, vomiting, and dyspnea, even with normal or mildly elevated glucose levels. Patient education regarding medication management during periods of decreased oral intake and prompt medical evaluation for persistent gastrointestinal symptoms is essential. Further pharmacovigilance and mechanistic studies are needed to elucidate the relationship between GLP-1 RAs and eDKA and identify high-risk populations.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*