Abdominal pain and tenderness are common features in diabetic ketoacidosis, and serum amylase activity is abnormally raised in more than 50% of such episodes. To elucidate the origin and nature of hyperamylasemia in diabetic ketoacidosis, measurements of amylase activity by the Caraway method and analysis of its isoenzyme by cellulose-acetate gel electrophoresis were made in 10 episodes of diabetic ketoacidosis. The transition of amylase activity before and during treatment with small intravenous insulin boluses was investigated. The following results were obtained.
1) The serum amylase activity in each episode was low before treatment. The isoenzyme study revealed that pancreatic-type amylase was particularly decreased.
2) In 3 of 10 episodes, the amylase activity was abnormally raised during treatment with insulin. Isoenzyme analysis demonstrated that salivary-type amylase and not pancreatic-type amylase was responsible for the rise in these 3 episodes. No correlation was observed between abdominal pain and amylase activity.
3) Raised salivary-type amylase returned to normal during the initial 3 days of treatment. The amylase/creatinine clearance ratio was not increased in the 3 hyperamylasemic episodes. There was no clinical manifestation of abnormal salivary glands.
4) These findings demonstrate that pancreatitis is not usually the origin of the increase inamylase activity in diabetic ketoacidosis.
It is suggested that salivary-type hyperamylasemia in diabetic ketoacidosis is most often caused by acute changes of carbohydrate metabolism.