Euglycemic Diabetic Ketoacidosis Following Ertugliflozin Initiation Precipitated by Norovirus Gastroenteritis
- 1Associate Professor, South Dakota State University College of Pharmacy and Allied Health Professions, Brookings, South Dakota
- 2Clinical Pharmacist, Transitions of Care, Avera McKennan Hospital & University Health Center, Sioux Falls, South Dakota
- 3Clinical Pharmacist, Northwestern Memorial Hospital, Chicago, Illinois
Abstract
Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are associated with an increased risk of euglycemic diabetic ketoacidosis (euDKA), a potentially life-threatening complication that can be difficult to recognize due to near-normal blood glucose levels. While infection is a known precipitant of DKA, viral gastroenteritis as a specific trigger for SGLT2 inhibitor-associated euDKA has not been well-characterized.
Case Report: A 36-year-old female with type 2 diabetes mellitus presented with severe metabolic acidosis (pH 6.85), anion gap of 23 mEq/L, and blood glucose of 165 mg/dL 1 week after initiating ertugliflozin 15 mg daily in the setting of recent norovirus exposure. The patient was treated per institutional DKA protocol with intravenous fluids, insulin infusion, and dextrose. Ertugliflozin was discontinued and the patient made a full recovery within 48 h.
Discussion: This case illustrates the synergistic mechanism by which norovirus gastroenteritis can precipitate euDKA in patients recently initiated on SGLT2 inhibitors. Viral gastroenteritis causes rapid volume depletion through vomiting and diarrhea, reduced oral carbohydrate intake, and counter-regulatory hormone activation - all of which compound the ketogenic effects of SGLT2 inhibition. Clinicians should counsel patients initiating SGLT2 inhibitors about sick day management and the importance of temporarily discontinuing these agents during acute gastrointestinal illness.
Related
- Euglycemic SGLT2 Inhibitor-Associated Ketoacidosis in a Nondiabetic Patient: A Case Report.
- Sodium-glucose cotransporter-2 inhibitor-associated euglycemic diabetic ketoacidosis in an adolescent with type 2 diabetes.
- Favorable CGM metrics do not exclude SGLT2 inhibitor-associated euglycemic diabetic ketoacidosis: an educational case report with narrative review of literature
- Case Report: Euglycemic diabetic ketoacidosis as the initial presentation of adult-onset autoimmune diabetes in a treatment-naïve man
- An unusual presentation of pituitary apoplexy precipitated by dengue haemorrhagic fever in a dialysis patient
BibTeX
@article{farley2026euglycemic,
title = {{Euglycemic Diabetic Ketoacidosis Following Ertugliflozin Initiation Precipitated by Norovirus Gastroenteritis}},
author = {T. Michael Farley and Sara Nezirevic},
journal = {AACE Endocrinology and Diabetes},
year = {2026},
month = may,
doi = {10.1016/j.aed.2026.05.004},
url = {https://doi.org/10.1016/j.aed.2026.05.004},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Euglycemic Diabetic Ketoacidosis Following Ertugliflozin Initiation Precipitated by Norovirus Gastroenteritis
AU - T. Michael Farley
AU - Sara Nezirevic
PY - 2026
DA - 2026/05/15
JO - AACE Endocrinology and Diabetes
DO - 10.1016/j.aed.2026.05.004
UR - https://doi.org/10.1016/j.aed.2026.05.004
AB - Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are associated with an increased risk of euglycemic diabetic ketoacidosis (euDKA), a potentially life-threatening complication that can be difficult to recognize due to near-normal blood glucose levels. While infection is a known precipitant of DKA, viral gastroenteritis as a specific trigger for SGLT2 inhibitor-associated euDKA has not been well-characterized. Case Report: A 36-year-old female with type 2 diabetes mellitus presented with severe metabolic acidosis (pH 6.85), anion gap of 23 mEq/L, and blood glucose of 165 mg/dL 1 week after initiating ertugliflozin 15 mg daily in the setting of recent norovirus exposure. The patient was treated per institutional DKA protocol with intravenous fluids, insulin infusion, and dextrose. Ertugliflozin was discontinued and the patient made a full recovery within 48 h. Discussion: This case illustrates the synergistic mechanism by which norovirus gastroenteritis can precipitate euDKA in patients recently initiated on SGLT2 inhibitors. Viral gastroenteritis causes rapid volume depletion through vomiting and diarrhea, reduced oral carbohydrate intake, and counter-regulatory hormone activation - all of which compound the ketogenic effects of SGLT2 inhibition. Clinicians should counsel patients initiating SGLT2 inhibitors about sick day management and the importance of temporarily discontinuing these agents during acute gastrointestinal illness.
SN - 3050-9157
ER -