BACKGROUND: Recent studies have shown that cholecystokinin (CCK) agonist, cerulein can induce acute pancreatitis in animals. The role of CCK in the induction of acute pancreatitis in humans is unclear. We investigated plasma CCK levels in alcoholic and biliary pancreatitis on admission and during the episode of acute pancreatitis. METHODS: Plasma CCK concentrations were determined by a specific and sensitive radioimmunoassay using CCK antiserum (Euro-Diagnostica, Malmö, Sweden) in 35 patients with acute alcoholic pancreatitis, in 27 patients with acute biliary pancreatitis, in 34 patients with nonpancreatic acute abdominal pain, and in 43 healthy subjects. The mean time from the first symptoms to the plasma sample was 31 (+/- 3.7) h in alcoholic pancreatitis patients and 25 (+/- 5.1) h in biliary pancreatitis patients. We also determined CCK levels in 20 patients during the episode of acute pancreatitis. Normal fasting level of CCK is < or = 1.12 pmol/L according to manufacturer. RESULTS: Basal plasma CCK concentrations were significantly lower both in alcoholic pancreatitis (mean +/- SEM, 0.04 +/- 0.03 pmol/L, p < 0.0001) and biliary pancreatitis patients (0.17 +/- 0.13 pmol/L, p < 0.0001) than in nonpancreatic acute abdominal pain patients (1.23 +/- 0.32 pmol/L) or healthy subjects (1.18 +/- 0.20 pmol/L). Plasma CCK levels also remained low until the patient was well-recovering and had started oral diet. CONCLUSION: Basal plasma CCK concentrations are significantly decreased in acute alcoholic and biliary pancreatitis after the first day from the beginning of the symptoms until the patient was well-recovering.
BACKGROUND: Recent studies have shown that cholecystokinin (CCK) agonist, cerulein can induce acute pancreatitis in animals. The role of CCK in the induction of acute pancreatitis in humans is unclear. We investigated plasma CCK levels in alcoholic and biliary pancreatitis on admission and during the episode of acute pancreatitis. METHODS: Plasma CCK concentrations were determined by a specific and sensitive radioimmunoassay using CCK antiserum (Euro-Diagnostica, Malmö, Sweden) in 35 patients with acute alcoholic pancreatitis, in 27 patients with acute biliary pancreatitis, in 34 patients with nonpancreatic acute abdominal pain, and in 43 healthy subjects. The mean time from the first symptoms to the plasma sample was 31 (+/- 3.7) h in alcoholic pancreatitispatients and 25 (+/- 5.1) h in biliary pancreatitispatients. We also determined CCK levels in 20 patients during the episode of acute pancreatitis. Normal fasting level of CCK is < or = 1.12 pmol/L according to manufacturer. RESULTS: Basal plasma CCK concentrations were significantly lower both in alcoholic pancreatitis (mean +/- SEM, 0.04 +/- 0.03 pmol/L, p < 0.0001) and biliary pancreatitispatients (0.17 +/- 0.13 pmol/L, p < 0.0001) than in nonpancreatic acute abdominal painpatients (1.23 +/- 0.32 pmol/L) or healthy subjects (1.18 +/- 0.20 pmol/L). Plasma CCK levels also remained low until the patient was well-recovering and had started oral diet. CONCLUSION: Basal plasma CCK concentrations are significantly decreased in acute alcoholic and biliary pancreatitis after the first day from the beginning of the symptoms until the patient was well-recovering.