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Hyperamylasemia in Diabetic Ketoacidosis: Sources and Significance

FRANK VINICOR, M.D.; LARRY M. LEHRNER, M.D., Ph.D.; ROBERT C. KARN, Ph.D.; and A. DONALD MERRITT, M.D.
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Grant support: in part by Indiana University Diabetes Research and Training Center (PHS-P60-AM-20542-01), Indiana University Human Genetics Center (PHS-50-GM-21054), Regenstrief Institute, and the National Institutes of Health (Research Grant PHS-R01-GM-19178). Dr. Vinicor was a Research Associate, Veterans Administration Hospital (MRIS #9035); Dr. Karn was supported by a Career Development Award (1-K04-AM-00284-01).

Portions of this paper have appeared in abstract form: Diabetes. 1978;27(suppl 2):319.

▸Requests for reprints should be addressed to Frank Vinicor, M.D.; Regenstrief Institute-Indiana University School of Medicine, 1100 West Michigan Street; Indianapolis, IN 46223.


Indianapolis, Indiana


© 1979 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1979;91(2):200-204. doi:10.7326/0003-4819-91-2-200
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The origins and clinical significance of hyperamylasemia during diabetic ketoacidosis are unclear. We have therefore correlated important clinical and laboratory indices of diabetic ketoacidosis with sequential determinations of serum and urine amylase concentrations, amylase/creatinine clearance ratios, and specific amylase isozyme types. Hyperamylasemia occurred in 79% of our patients with diabetic ketoacidosis, often after admission to the hospital. Among these patients, 48% had pancreatic-type, 36% salivary-type, and 16% mixed-type (pancreatic and salivary) hyperamylasemia. There were no correlations between the presence, degree, or isozyme type of hyperamylasemia and most laboratory or clinical characteristics, including gastrointestinal symptoms. Patients with pancreatic-type hyperamylasemia tended to have higher amylase/creatinine clearance ratios, but it was not possible to unequivocably diagnose acute pancreatitis during diabetic ketoacidosis with current routine clinical or laboratory procedures.

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