Accelerated in vitro degradation of CCK-58 in blood and plasma of patients with acute pancreatitis.

Proteases released into the circulation during acute pancreatitis may hydrolyse circulating peptide hormones leading to altered regulatory functions. Cholecystokinin is a major regulator of postprandial gut function; stimulating pancreatic enzyme secretion, gallbladder contraction and diminishing food intake. Cholecystokinin-58 is the largest and most abundant form of this hormone in acid extracts of human intestine, and major amounts are released into the circulation after feeding. In order to test whether cholecystokinin-58 is degraded more rapidly due to the increased circulating of enzymes, this peptide was added to blood and plasma of patients with acute pancreatitis and incubated for various time intervals. The in vitro half life of cholecystokinin-58 was 10 +/- 1 minutes (mean +/- SE) in plasma and 11 +/- 1 min in blood from patients with acute pancreatitis, about four fold lower than the half life in plasma of healthy volunteers; 45 +/- 5 min. Degradation of cholecystokinin-58 produced immunoreactive forms of cholecystokinin that eluted in the positions of cholecystokinin-8 and cholecystokinin-33/39. We conclude that acute pancreatitis increases the degradation of CCK molecules.