ECE2023 Eposter Presentations Diabetes, Obesity, Metabolism and Nutrition (355 abstracts)
Taher Sfar University Hospital, The Endocrinology Department of the Taher Sfar University Hospital of Mahdia, Mahdia, Tunisia
Introduction: SGLT2 (sodium-glucose cotransporter 2) inhibitors are a molecule more and more used in type 2 diabetes. However, it can cause a metabolic decompensation in some cases. Euglycemic ketoacidosis may be atypical, misplacing and delaying the diagnosis. We investigated the precipitating factors of this metabolic complication in our case study and in the literature.
Presentation of the Case: We report the case of a normal BMI (19 kg/m2) ,66-year-old woman with incidentally discovered diabetes for 3 years, switched from dual oral antidiabetics to insulin analogues (basal-plus regimen (0.48 IU/kg/24 h)) a year before her hospitalization. Since the patient did not accept the multiple insulin injections, she was put on hypocaloric diet and changed to an insulin bedtime regimen with the addition of Dapagliflozin (10 mg/d). A few days later, she went to the emergency room with asthenia, epigastralgia, vomiting and dyspnea. At the workup, venous glucose was 10 mmol/l. On urine dipstick, glucosuria was two crosses and acetonuria was four crosses. On arterial blood gas, the patient presented a severe metabolic acidosis (PH=7.08, bicarbonates at 8) with hypocapnia (PCO2 at 27). The diagnosis of severe euglycemic ketoacidosis was retained and the patient was transferred to the intensive care unit where she received hydration, insulin therapy with an electric syringe pump with adapted potassium supplementation and discontinuation of oral antidiabetics. The ketoacidosis was resolved after three days. The insulin regimen was re intensified.
Discussion: Euglycemic ketoacidosis under iSGLT2 can be explained by several mechanisms, mainly the alteration of the insulin/ glucagon ratio. iSGLT2 increases glucagon production by directly stimulating pancreatic alpha cells but also in response to the decrease in blood glucose. Glucagon increases the activity of CPT-I (carnitine palmitoyl transferase-I) inducing the overproduction of ketone bodies1. Conditions such as relative insulin deficiency, low body mass index with reduced glycogen stores and a low carbohydrate diet are then predictive factors of ketoacidosis under iSGLT2[1]. Other precipitating factors may include pancreatic damage and alcoholism. In our case, the reduction of insulin doses, the hypocaloric diet and the low BMI could be the incriminating factors.
Conclusion: Euglycemic ketoacidosis under iSGLT2 is a rare and serious entity which can be overlooked in the face of normal blood glucose. A clinical attention should be carried to predictive factors.
Reference: 1. "Euglycemic ketoacidosis: a complication of SGLT2 inhibitors", Swiss Medical Journal. Diabetic Ketoacidosis and Sodium-Glucose Cotransporter-2 Inhibitors: A Focused Review of Pathophysiology, Risk Factors, and Triggers.