Abstract
BackgroundFulminant type 1 diabetes mellitus (FT1D) is a newly established subtype of type 1 diabetes. Its etiology has not been fully elucidated. Several cases with FT1D have exhibited pancreatitis or myocarditis.Case presentationWe report a 31-year-old Japanese woman who showed upper abdominal pain and was admitted to a local hospital. She was initially diagnosed with acute pancreatitis based on serum amylase elevation and swelling of the pancreas on computed tomography. Four days after admission, she developed diabetic ketoacidosis and was transferred to our hospital. Her symptoms and laboratory findings met the FT1D criteria. On the 3rd hospital day, electrocardiography (ECG) showed ST-segment elevation, and serum cardiac enzymes were markedly elevated. Because she exhibited late gadolinium enhancement in the apical wall on contrast-enhanced cardiac magnetic resonance imaging, she was diagnosed as acute myocarditis. Abnormal ECG findings and elevations of biomarkers associated with myocarditis showed improvement on the next day.ConclusionsThis is the first case of FT1D accompanied by both pancreatitis and myocarditis and suggests that the pathophysiology of FT1D is related to the common etiology of acute pancreatitis and myocarditis.
Highlights
Fulminant type 1 diabetes mellitus (FT1D) is a newly established subtype of type 1 diabetes
This is the first case of FT1D accompanied by both pancreatitis and myocarditis and suggests that the pathophysiology of FT1D is related to the common etiology of acute pancreatitis and myocarditis
These specific clinical findings are shown at the onset of FT1D: 1) Hyperglycemia with diabetic ketoacidosis, 2) Plasma glucose level is greater than 16.0 mmol/L (288 mg/dL), whereas glycated hemoglobin level is less than 8.7%, 3) Urinary C-peptide excretion is less than 10 μg/day, while serum C-peptide level is less than 0.3 ng/mL (0.10 nmol/ L) at overnight fast, or 0.5 ng/mL (0.17 nmol/L) following intravenous glucagon load [1, 2]
Summary
This is the first case of FT1D accompanied by both pancreatitis and myocarditis and suggests that the pathophysiology of FT1D is related to the common etiology of acute pancreatitis and myocarditis.
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