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March 7, 2001

Rapid Loss of Insulin Secretion in a Patient With Fulminant Type 1 Diabetes Mellitus and Carbamazepine Hypersensitivity Syndrome

Author Affiliations

Stephen J.LurieMD, PhD, Senior EditorIndividualAuthorJody W.ZylkeMD, Contributing EditorIndividualAuthor

JAMA. 2001;285(9):1153-1154. doi:10.1001/jama.285.9.1153

To the Editor: Type 1 diabetes mellitus (DM) is caused by severe insulin deficiency that typically results from autoimmune destruction of pancreatic β-cells, although in some cases (classified as "idiopathic") there is no evidence of autoimmunity.1 Recently, a novel etiology of the disease has been described as nonautoimmune fulminant type 1 DM,2 which involves abrupt onset of insulin-deficient hyperglycemia, high serum pancreatic enzyme concentrations, and neither diabetes-related autoantibodies nor evidence of insulitis in pancreatic biopsy specimens. We report a case of rapid-onset type 1 DM with diabetic ketoacidosis (DKA), for which the clinical course was precisely documented. Interestingly, the onset of diabetes coincided with development of hemolytic anemia due to carbamazepine-induced cold agglutinin disease.

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