Empagliflozin-Induced Delayed Onset Euglycemic Diabetic Ketoacidosis

Abstract

Abubakr Muhamad Maher Issa Sowilem

A large anion gap metabolic acidosis, a comparatively low blood glucose level (less than 11.1 mmol/L), and evidence of ketosis are the hallmarks of euglycemic diabetic ketoacidosis (EDKA) [1]. EDKA can be brought on by a variety of factors, including excessive alcohol use, a reduction in caloric intake, infections, dehydration, severe sickness, and bariatric surgery. If the case is identified early and treated properly, the prognosis is typically quite good [2]. By blocking glucose reabsorption in the kidney's proximal tubule, sodium glucose cotransporter-2 (SGLT2) inhibitors reduce blood glucose levels while boosting glucose excretion in the urine One of the SGLT2 inhibitors, empagliflozin, has a half-life concentration of 5.6–13.1 hours, a peak plasma concentration of 1.33–3.0 hours after treatment, and a stable trough concentration after sixth day of administration [3,4]. Other research has demonstrated that the pharmacological effects of SGLT2 inhibitors can last longer than 10 days, as seen by the development of glucosuria following a 10- day medication cessation [5].

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