POS-092 SGLT2 INHIBITOR – INDUCED EUGLYCEMIC DIABETIC KETOACIDOSIS IN GUILLAIN-BARRE SYNDROME: A CASE REPORT

Abstract

Introduction: Euglycemic diabetic ketoacidosis (EuDKA) is a rare but increasingly reported serious adverse effect of SGLT2 inhibitors. There is not much published literature on the incidence of EuDKA and the factors associated with it. Though SGLT2 inhibitors were introduced as glucose lowering agents, recent trials have demonstrated their favourable cardiovascular outcome in heart failure and ability to retard progression of proteinuric kidney disease, including in non-diabetics. Hence use of this class of drugs is anticipated to increase exponentially, given the combined high global burden of diabetes, coronary artery disease and chronic kidney disease. As we embark to use the SGLT2 inhibitors in different clinical scenarios, it becomes imperative to report their adverse effects encountered in uncommon clinical conditions as well. Case history: A 42-year-old gentleman with history of type 2 diabetes mellitus for 15 years and coronary artery disease, presented with difficulty in climbing stairs and walking for 5 days with progressive difficulty in getting up from bed. He did not have past history of covid infection and had been immunised with 1 dose of covid vaccine. On examination, patient had normal hemodynamics. There was flaccid quadriparesis with areflexia and truncal muscle weakness. Nerve conduction study confirmed acute demyelinating polyradiculoneuropathy. His baseline laboratory investigations revealed normal renal parameters but metabolic acidosis was noted at the time of admission. Patient was started on iv immunoglobulin 2mg/kg and the motor weakness improved from grade 2/5 to 4/5. However, the high anion gap metabolic acidosis worsened over the next 4 days and patient developed acidotic breathing. His sugars were within normal limits and the patient was on metformin, glimeperide, vildagliptin, voglibose and dapagliflozin. As blood lactate levels were normal with urine acetone positivity, euglycemic diabetic ketoacidosis secondary to SGLT2 inhibitor was suspected and all the oral hypoglycemic agents were stopped. He was started on hydration and insulin infusion. After 48 hours of stopping dapagliflozin, acidosis resolved completely and the patient was reintroduced back on the other 4 class drugs. At follow-up, there was no recurrence of acidosis and patient was able to walk with support and physiotherapy. Discussion: SGLT2 inhibitors cause glycosuria and directly induce glucagon release from pancreas. Combined with insulin deficiency, this results in lipolysis, fatty acid oxidation and ketogenesis. They also cause increased renal reabsorption of ketone bodies. The precipitating factors for EuDKA identified so far include abrupt reduction in insulin dosage, reduced oral intake, infections, surgery, excess alcohol use, volume depletion, type 1 diabetes and heavy physical exercise. This is the first reported case of SGLT2 inhibitor-induced EuDKA in a patient with Guillain-Barre syndrome. As symptoms of dehydration may not be significant due to lack of hyperglycemia in EuDKA, there may be a delay in the diagnosis of this complication. Conclusion: The possibility of EuDKA to be kept in mind while evaluating metabolic acidosis in a diabetic patient on SGLT2 inhibitors. Temporarily withholding the SGLT2 inhibitors during an intercurrent illness will prevent the occurrence of the above serious adverse effect.