抄録
A 52-year-old female was admitted because of unconsciousness. She suffered from peritonitis at the age of 30 years. She had been treated for hypertention since 38 years of age. Her blood glucose at admission was 33 mg/100 ml and she responded to the intravenous administration of glucose. The fasting levels of blood glucose ranged 52 to 80 mg/100 ml. Oral glucose loading revealed a diabetic glucose tolerance and hypoglycemic coma was not provoked by tolbutamide injection, although blood glucose fell 63 to 42 mg/100 ml at the time of 120 minutes. Total immunoreactive insulin (IRI) of untreated plasma was found more than 4, 000 μU/ml. Under the diagnosis of insulinoma, she was undergone laparotomy. On operation, adenoma of the pancreas was not revealed and the partial resection of the head of the pancreas was done.
Insulin content of the pancreas was 3.8 U/kg and the histological examination showed an increase in numbers of the Langerhans' islets.
Her plasma was proved to bind '311-insulin by the method of gel filtration with Sephadex G 50, paper chromatography or dextran-coated charcoal. The binding protein was identified to be gamma globulin upon paper electrophoresis and was absorbed by anti-human gamma globulin rabbit sera. Endogenous insulin as well as 131 I-insulin bound to patient's plasma was dissociated by acidification of plasma. Protein fraction, obtained by acidification and gel filtration of patient's plasma, reacted with pork, beef or human insulin. With insulin from bonito, however, her plasma did not show any immunological reaction. The maximal binding capacity of her plasma to human insulin was determined approximately as 5, 600 μU/ml. A positive skin anaphylaxis reaction was observed in a guinea pig immunized with patient's plasma but any precipitation reaction was not demonstrated by Ouchterlony method. It is concluded that the insulin binding protein is antibody to insulin and hat insulin antibody must be produced against endogenous insulin, since she had never received any insulin administration.
Clinical features, hypoglycemia, decreased glucose tolerance, increased level of IRI and hyperplasia of the pancreatic islets, were interpreted by the presence of insulin antibody in plasma. The patient findings were consistent with a case of insulin autoimmune syndrome coined by Hirata.
