Hyperamylasemia, specific pancreatic enzymes, and hypoxanthine during recovery from diabetic ketoacidosis.
The contribution of the exocrine pancreas to hyperamylasemia in diabetic ketoacidosis was investigated by measuring total amylase, salivary and pancreatic isoamylases, cathodic trypsin-like immunoreactivity, and pancreatic lipase in 12 consecutive patients recovering from diabetic ketoacidosis. Hyperamylasemia was present in six of the patients [50%; expected incidence: 21.1-78.9% (95% confidence limits)]--in five with simultaneously increased activities of all three specific pancreatic enzymes, and in one with only increased salivary isoamylase. The serum concentration of hypoxanthine--an indicator of the cellular energy state--was above normal in all patients at admission. We found no differences in concentrations of hypoxanthine in serum of patients with or without hyperamylasemia or in patients with or without increases in the specific pancreatic enzymes. In none of the patients was the clinical course or the time--concentration curves of the pancreatic enzymes consistent with acute pancreatitis. The pathogenic mechanism leading to hyperamylasemia in diabetic ketoacidosis remains uncertain.
Møller-Petersen
J
J
Andersen
P T
PT
Hjørne
N
N
Ditzel
J
J
D000293:Adolescent; D000328:Adult; D000681:Amylases / Q000097:blood*; D016883:Diabetic Ketoacidosis / Q000097:blood / Q000201:enzymology*; D005260:Female; D006801:Humans; D019271:Hypoxanthine; D007042:Hypoxanthines / Q000097:blood*; D007517:Isoamylase / Q000097:blood; D008049:Lipase / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000201:enzymology*; D012016:Reference Values
D007042:Hypoxanthines; D019271:Hypoxanthine; D008049:Lipase; D000681:Amylases; D007517:Isoamylase