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  Vol. 285 No. 9, March 7, 2001 TABLE OF CONTENTS
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Rapid Loss of Insulin Secretion in a Patient With Fulminant Type 1 Diabetes Mellitus and Carbamazepine Hypersensitivity Syndrome

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

To the Editor: Type 1 diabetes mellitus (DM) is caused by severe insulin deficiency that typically results from autoimmune destruction of pancreatic {beta}-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.

Report of a Case

A 77-year-old woman without history of alcohol use developed DKA after 2 weeks of inpatient treatment for allergic skin reactions. She had been treated with carbamazepine (200 mg/d) for 1 month for postherpetic neuralgia before developing . . . [Full Text of this Article]



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