title: Hyperamylasemia after cardiopulmonary bypass: pancreatic cellular injury or impaired renal excretion of amylase?
abstract: BACKGROUND
  Postoperative hyperamylasemia and even acute pancreatitis are associated with coronary artery bypass grafting (CABG). The mechanism of hyperamylasemia and pancreatic acinar cell damage was studied in 20 patients undergoing CABG.
  
  
  METHODS
  Serial blood and urine samples at eight time points before, during, and 24 hours after the CABG were collected. Salivary and pancreatic isoamylases, the fractional clearance of isoamylases (i.e., relative to creatinine clearance), pancreatic phospholipase A2 (a specific serum marker of pancreatic acinar cell injury), and cystatin C (a sensitive marker of glomerular filtration rate) were measured.
  
  
  RESULTS
  Mild serum hyperamylasemia (300 to 1000 units/L) was found in 11 of 20 (55%) and severe (> 1000 units/L) in 6 of 20 (30%) patients with no signs of clinical acute pancreatitis. Hyperamylasemia occurred from 6 to 24 hours after the CABG and was mainly caused by pancreatic isoamylase. Serum pancreatic phospholipase A2 concentration remained unchanged, which excludes acinar cell damage. Although renal glomerular filtration was normal during CABG as measured by serum cystatin C and creatinine clearance, the fractional clearance of isoamylases decreased.
  
  
  CONCLUSIONS
  The decreased rate of excretion into urine, rather than pancreatic cellular damage, is the major source of hyperamylasemia after CABG.
authors.affiliation: Departments of Surgery, Anesthesiology, and Intensive Care, Kuopio University Hospital, Finland.
authors.forename: H
authors.initials: H
authors.lastname: Paajanen
authors.forename: P
authors.initials: P
authors.lastname: Nuutinen
authors.forename: A
authors.initials: A
authors.lastname: Harmoinen
authors.forename: M
authors.initials: M
authors.lastname: Pöyhönen
authors.forename: O
authors.initials: O
authors.lastname: Pitkänen
authors.forename: I
authors.initials: I
authors.lastname: Nordback
authors.forename: J
authors.initials: J
authors.lastname: Grönroos
authors.forename: T J
authors.initials: TJ
authors.lastname: Nevalainen
mesh_terms: D000681:Amylases / Q000097:blood* / Q000652:urine; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001026:Coronary Artery Bypass; D003404:Creatinine / Q000378:metabolism; D055316:Cystatin C; D015891:Cystatins / Q000097:blood; D015853:Cysteine Proteinase Inhibitors / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007517:Isoamylase / Q000097:blood*; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000201:enzymology / Q000473:pathology*; D010741:Phospholipases A / Q000097:blood; D054467:Phospholipases A2; D011183:Postoperative Complications / Q000175:diagnosis*; D011446:Prospective Studies; D012044:Regression Analysis
chemical_list: D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; D015891:Cystatins; D015853:Cysteine Proteinase Inhibitors; D003404:Creatinine; D010741:Phospholipases A; D054467:Phospholipases A2; D000681:Amylases; D007517:Isoamylase