Background: Fulminant 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 presentation: We 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. Conclusions: 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.

Background: Postprandial syndrome is characterized by hunger, weakness and anxiety neurosis occurring after meals. Although abnormal glucagon response has been suggested, inaccuracies of the conventional glucagon measurement method have prevented from precise analysis. Recently, a more reliable dual-antibody sandwich enzyme-linked immunosorbent assay for glucagon has been developed. Methods:We conducted a 75 g oral glucose tolerance test (OGTT) extending to 4 hours in 14 patients with idiopathic postprandial syndrome. In addition to blood glucose and insulin, we have measured glucagon concentrations using the novel method and analyzed retrospectively.Results: Median (lower quartile, upper quartile) of age and BMI were 40 years old (30, 49) and 24.9 (23.1, 26.2), respectively. The OGTT revealed that one patient had a diabetic pattern, and two were glucose intolerant. Fasting insulin was 7.6 U/mL (6.8, 8.8) and reached 73.7 (54.3, 82.6) at 30 min. Insulin remained elevated until 180 min. The fasting glucagon was 21.1 pg/mL (16.1, 33.8), falling at 60 min to a nadir of 6.9 (3.5, 10.3), onethird of the baseline, then remaining suppressed until 180 min. Furthermore, we have found that two types of glucagon dynamics: one is lower fasting glucagon with further suppression and the other is normal or higher fasting glucagon with subsequent big drop.Conclusions: These data suggest that glucagon suppression is stronger in patients with idiopathic postprandial syndrome than in normal subjects previously reported. The present data will contribute to further understanding and future research of this syndrome.