A Clinical Case of Clozapine-Induced Fatal Diabetic Ketoacidosis

RESULTS AND CONCLUSION: Significant increase in body mass index from 28.7 to 33.5 was observed during hospitalization. The blood glucose level, measuredafter his death, was found to be 500 mg/dL. Altered metabolism due to clozapinecan lead to dyslipidemia-mediated-pancreatic-beta- cell damage, decreased insulin secretion as well as insulin resistance. In DKA, low levels of insulin lead to an increased release of free fatty acids from adipose tissue. Acetyl coenzyme A (CoA), derived from the breakdown of free fatty acids, is metabolized by the Kreb’s cycle. In hepatocytes, excess acetyl-CoAis converted into ketone bodies( acetoacetateand β- hydroxybutyrate) and released into circulation. Ketone bodieshave a low pK a value and their high serum concentrations lead to DKA. In this patient, DKA was most probably clozapineinduced and had fatal consequences. Thus, recognizing potential risk factors, providing patient education, and increasing monitoring of patients on clozapineand other atypical antipsychoticsare critical to prevent the lifethreatening effects of DKA.