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Case of Euglycemic Ketoacidosis Induced by SGLT2 Inhibitors (Sodium-Glucose Cotransporter 2) in a Diabetic Patient

Liliya Ilieva, Mira Siderova, Savi Shishkov, Kiril Hristozov

Abstract

Introduction: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of hypoglycemic antidiabetic medications indicated for the treatment of type 2 diabetes by inhibiting the SGLT2 protein in the proximal renal tubule to prevent reabsorption of glucose and facilitate its removal by the kidneys.

Materials and Methods: We report case of a 38-year-old woman with unrecognized type 1 diabetes, who developed severe ketoacidosis caused by a sodium-glucose cotransporter 2 inhibitor - Forxiga (dapagliflozin).

Results: The patient was misdiagnosed with diabetes type 2 a month and a half before the hospital admission with initial complaints of polydipsia, polyuria, genital pruritus and insignificant weight reduction (1 kg). Family history revealed a mother and an aunt with type 2 diabetes. In this period, she received gliclazide (30 mg/day), metformin (3 x 850 mg/day) and dapagliflozin (10 mg/day). Four days before hospitalization, the woman complained of nausea, tachydyspnea with gradual deterioration of her general condition. At the hospital admission, the laboratory results showed severe metabolic acidosis (pH: 6.91), positive urinary ketones (+++) and blood glucose level: 11.7 mmol/L. The patient was admitted at the Clinic of Anesthesiology and Intensive Care with severe acidosis and impaired consciousness. The treatment included intravenous insulin, infusions and correction of the electrolytes and acid-base disorders followed by subcutaneous insulin treatment in a basal bolus regimen. An examination of a panel of antibodies revealed positive GAD 65 (+) with low C-peptide.

Conclusion: Diabetic ketoacidosis (DKA) is an acute complication of type 1 diabetes. Glucosuria, insulinopenia and hyperglucagonemia induced by SGLT2 inhibitors are the mechanisms behind normoglycemic ketoacidosis.


Keywords

diabetes, ketoacidosis, SGLT2 inhibitors, insulin, glucose


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