Diabetic Ketoacidosis Associated With Painless Thyroiditis in a Patient Treated With an SGLT2 Inhibitor

While sodium-glucose cotransporter 2 (SGLT2) inhibitors provide substantial benefits for glycemic control and reduced cardiovascular and renal risks, they are also associated with an increased risk of diabetic ketoacidosis (DKA) because they stimulate lipolysis. Severe thyrotoxicosis, including thyroid crisis, is a recognized cause of DKA because it promotes lipolysis and increases ketone production. Here, we report the case of a 62-year-old man with type 2 diabetes and poor glycemic control who was taking an SGLT2 inhibitor and developed DKA associated with painless thyroiditis. The blood glucose and 3-hydroxybutyric acid levels normalized after initiation of insulin therapy and fluid infusions. The thyroid function normalized without additional treatment and remained stable during follow-up. The findings in this case indicate that thyrotoxicosis may amplify the risk of DKA in the presence of the ketogenic state triggered by SGLT2 inhibitor therapy, even when the thyrotoxicosis does not reach the severity of thyroid crisis, due to the interplay with the lipolytic metabolic changes induced by thyrotoxicosis. With the increasing use of SGLT2 inhibitors, careful monitoring is essential because these medications can lower the threshold for DKA, even when triggered by minor metabolic disturbances, particularly in patients with poorly controlled glycemia.