HYPERAMYLASEMIA AFTER CARDIOPULMONARY BYPASS - PANCREATIC CELLULAR INJURY OR IMPAIRED RENAL EXCRETION OF AMYLASE

Background. Postoperative hyperamylasemia and even acute pancreatitis are associated with coronary bypass grafting (CABG). The mechanism of hyperamylasemia and pancreatic acinar cell damage was studied in 20 pa tients undergoing CABG. Methods. Serial blood and urine samples at eig ht time points before, during, and 24 hours after the CABG were collec ted. Salivary and pancreatic isoamylases, the fractional clearance of isoamylases (i.e., relative to creatinine clearance), pancreatic phosp holipase A(2) (a specific serum marker of pancreatic acinar cell injur y), 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. Hyperamyla semia occurred from 6 to 24 hours after the CABG and was mainly caused by pancreatic isoamylase. Serum pancreatic phospholipase A(2) concent ration remained unchanged, which excludes acinar cell damage. Although renal glomerular filtration was normal during CABG as measured by ser um cystatin C and creatinine clearance, the fractional clearance of is oamylases decreased. Conclusions. The decreased rate of excretion into urine, rather than pancreatic cellular damage, is the major source of hyperamylasemia after CABG.