Recent studies have shown that
cholecystokinin (CCK) is involved in the induction and development of
acute pancreatitis in experimental animals. In the present study we determined basal plasma CCK concentrations by a specific and sensitive radioimmunoassay using antiserum OAL656 in 17 patients with
acute pancreatitis due to
gallstone in the common bile duct (n = 7), alcoholic (n = 4), post endoscopic retrograde pancreatography (n = 1), and unknown causes (n = 4), and 37 patients with
cholelithiasis (n = 18) and
choledocholithiasis (n = 19). Plasma CCK concentrations in patients with
gallstone pancreatitis on hospital day 1 (mean +/- SEM, 6.78 +/- 1.39 pM) were significantly higher than those in patients with other causes (1.33 +/- 0.16 pM) or in 20 healthy control subjects (1.55 +/- 0.11 pM). There was no relationship between plasma CCK and serum pancreatic
enzyme levels, the severity of
acute pancreatitis, or serum
bilirubin concentrations. Plasma CCK levels in patients with acute symptomatic
cholelithiasis (n = 7; 4.35 +/- 0.90 pM) and
choledocholithiasis (n = 8; 4.52 +/- 1.17 pM) were significantly higher than those in patients without symptoms (
cholelithiasis, n = 11, 1.40 +/- 0.17 pM;
choledocholithiasis, n = 11, 1.88 +/- 0.49 pM) but tended to be lower than those in patients with
gallstone pancreatitis. These present observations suggest that the increase in plasma CCK levels in
gallstone pancreatitis appears not to be the cause but to be the result of
gallstone pancreatitis probably due to a transient disturbance of bile flow into the duodenum by stones or
edema of the bile duct. Our present results provide some evidence for the usefulness of
CCK receptor antagonists for the treatment of biliary colics and
acute pancreatitis.