Plasma cholecystokinin concentrations in patients with pancreatic insufficiency measured by sequence-specific radioimmunoassays

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Abstract
It has been claimed that plasma cholecystokinin (CCK) concentrations are raised in patients with pancreatic insufficiency. We have measured plasma CCK concentrations in 32 patients with pancreatic insufficiency (22 alcoholic pancreatitis and 10 cystic fibrosis) and in 30 normal subjects by radioimmunoassays using antibodies with different specificties. Antibody 1703 binds to COOH-terminal forms of CCK containing at least 14 amino acid residues and does not cross-react with gastrins. Antibody T204 binds to all CCK-peptides containing the sulfated tyrosyl region and shows low cross-reactivity with sulfated gastrins but no binding to nonsulfated gastrins. Antibody 5135 binds to all COOH-terminal CCK-peptides and shows full cross-reactivity with gastrins. In patients with pancreatic insufficiency, plasma CCK concentrations (1.2±0.1 pmol/liter, antibody 1703; 2.0±0.2 pmol/liter, antibody T204; 12.5±1.4 pmol/liter, antibody 5135) were not significantly different from those in normal subjects (1.1±0.1 pmol/liter, antibody 1703; 2.2±0.3 pmol/liter, antibody T204; 10.5±0.9 pmol/liter, antibody 5135). Furthermore, plasma CCK concentrations in patients with pancreatic insufficiency due to alcoholic pancreatitis (1.2±0.1 pmol/liter, antibody 1703; 1.9±0.2 pmol/liter, antibody T204; 14.0 ±1.9 pmol/liter, antibody 5135) were not significantly different from those in patients with cystic fibrosis (1.2±0.2 pmol/liter, antibody 1703; 2.4±0.4 pmol/liter, antibody T204, 9.1 ±1.0 pmol/liter, antibody 5135). Cross-reactivity with gastrin accounted for almost all CCK-like-immunoreactivity measured with antibody 5135. Oral ingestion of 250 ml 20% Intralipid induced similar increases in plasma CCK in six patients with pancreatic insufficiency (4.3±1.5 pmol/liter, antibody 1703; 2.9±0.6 pmol/liter, antibody T204) as in seven normal subjects (5.0±0.9 pmol/liter, antibody 1703; 4.3±0.9 pmol/liter, antibody T204). It is concluded that CCK concentrations in fasting plasma are very low, that oral fat induces significant increases in plasma CCK, and that in patients with pancreatic insufficiency plasma CCK levels are not increased.