Shared Pathogenic Features Between Serotonin Receptor Antagonist-Associated Diabetic Ketosis and Ketosis-Prone Type 2 Diabetes: A Case Report

Ketosis-prone type 2 diabetes (KPD) is characterized by male predominance, onset at a young age, obesity, and sudden onset of diabetic ketosis/ketoacidosis without precipitating factors, negative anti-islet autoantibodies, and β-cell function preservation after recovery from diabetic ketosis/ketoacidosis following temporal insulin therapy. However, its pathogenesis remains unknown. We encountered a 49-year-old obese man presenting with diabetic ketosis, i.e., ketonuria, plasma glucose 252 mg/dL, HbA1c 12.8%, without anti-islet autoantibodies, induced by dose escalation of quetiapine, a serotonin receptor antagonist. After discontinuing quetiapine and starting subcutaneous intensive insulin therapy, diabetic ketosis rapidly resolved. Following glycemic state stabilization, insulin therapy was discontinued on the 11^th day of the initiation of therapy. Instead, metformin and linagliptin were initiated, and his glycemic status remained well controlled thereafter. His clinical course closely resembled that of KPD, together with our literature review, suggesting the involvement of decreased serotonin production/action in the pathogenesis of KPD.