A 64 years old female patient had admitted to our hospital because of uncosciousness. One week before the admission, she had a fever and abdominal pain. The blood examination by her home doctor revealed slight increase of plasma amylase. Following these symptoms, she had unconsciousness and diabetic ketoacidosis, and the patient was transferred to our hospital. The plasma glucose level was 871 mg/dl and HbA1c was 7.0%. Blood gas analysis showed a pH of 7.067. The plasma and urine levels of C-peptide immunoreactivity (CPR) was 0.1 ng/ml and under 1.8 ug/day, respectively. The second day of admission, the electrocardiogram revealed ST elevation concomitant with increase creatine kinase and troponin I. The coronary angiography showed no coronary stenosis and left ventriculography revealed hypokinesis in apex lesion. To observe the pancreatic endocrine secretion, glucagon stimulation test was done. Blood sampling of CPR at 6 min after glucagon bolus intravenous administration was 0.1 ng/ml, indicating that insulin secretion was abolished. Both of anti GAD antibody and anti-IA-2 autoantibody were negative. Based on the results, this patient suffered a fulminant type 1 diabetes mellitus with takotubo cardiomyopathy. Takotubo cardiomyopathy is known as stress induced cardiomyopathy. Fulminant type 1 diabetes is a non-autoimmune disorder characterized by sudden onset. We report that fulminant type 1 diabetes mellitus is considered as one of cause for Takotubo cardiomyopathy.
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