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

## TL;DR

A case report links a drug that blocks serotonin receptors to a type of diabetes with sudden ketosis, suggesting a shared cause with a rare form of type 2 diabetes.

## Contribution

The report suggests serotonin dysfunction may play a role in the pathogenesis of ketosis-prone type 2 diabetes.

## Key findings

- A patient developed diabetic ketosis after increasing quetiapine, a serotonin receptor antagonist.
- Discontinuing quetiapine and starting insulin therapy resolved the ketosis quickly.
- The patient's recovery resembled ketosis-prone type 2 diabetes, suggesting a shared pathogenic mechanism.

## Abstract

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 11th 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.