A 29-year-old woman admitted for diabetic ketoacidosis (pH=7.272) had suffered fever and abdominal pain 5 days before admission and developed thirst 2 days before. Despite high plasma blood glucose (642 mg/d
l), her HbA
1c was 4.9%, within normal range. Serum and urinary C-peptide were low, under normal detection (0.1 ng/m
l) and 3.3 μg/day. Both serum amylase (242 IU/
l) and urinary amylase (754 IU/
l) were elevated. No signs of acute or chronic pancreatitis were detected. After starting insulin therapy, metabolic glucose impairment was immediately improved, but insulin therapy had to be continued (HbA
1c=6.8%, insulin dose ; 0.6 Unit/kg/day). After 2 years, no C-peptide response to arginine or glucagon was detected, but glucagon response to arginine was. Neither islet cell antibody (ICA) nor antiislet antigen 2 was detected. Anti-GAD antibody, which was checked every 6 months from the onset of overt diabetes, remains negative. These findings suggest that she had fulminant type 1 diabetes as proposed by Imagawa et al. Her HLA haplotypes were presumed to be A2-B54-
DRB1*
0405-DQB1*
0401 and A33-B44-
DRB1*
1302-DQB1*
0604. So far, anti nuclear antibody, low complement and autoantibodies against carbonic anhydrase II and lactoferrin have been detected, unlike in previous fulminant type 1 diabetes patients. It is thus important to observe whether autoimmune disease will develop in this case.
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