Plasma concentrations of cholecystokinin in patients with duodenal ulcer disease

Cholecystokinin (CCK) is structurally similar to gastrin and is known to competitively inhibit the action of gastrin on the parietal cell, but little information has been accumulated about circulating levels of CCK in patients with duodenal ulcer (DU). In a group of 18 healthy volunteers (controls) and 22 DU patients (13 with active DU, nine with inactive DU), we stimulated endogenous release of CCK with oral administration of Lipomul corn oil. Plasma concentrations of CCK were measured by radioimmunoassay; ultrasonographic measurements of gallbladder volume were used as a biologic correlate for CCK in control patients and in patients with active DU. No significant difference was found in fasting plasma concentrations of CCK between controls (107 +/- 8 pg/ml) and DU patients (123 +/- 15 pg/ml), or in their total integrated release of CCK during the first hour after Lipomul ingestion (3.7 +/- 0.7 ng-min/ml in controls, 2.8 +/- 0.4 ng-min/ml in DU patients). Furthermore, no significant difference was found in integrated release of CCK between patients with active DU (2.9 +/- 0.6 ng-min/ml) and those with inactive DU (2.8 +/- 0.6 ng-min/ml). Gallbladder volume was highly correlated with plasma concentrations of CCK in controls (r = -0.91) and in active DU patients (r = -0.98). Patients with active DU had significantly smaller volumes of their resting gallbladders, they emptied less of their resting gallbladder contents in response to fat, and they showed diminished sensitivity to endogenously released CCK compared to controls. In six patients with active DU who underwent truncal vagotomy and drainage, integrated release of CCK increased significantly, from 1.9 +/- 0.6 ng-min/ml before vagotomy to 9.3 +/- 3.0 ng-min/ml after vagotomy. We found no evidence to suggest that abnormalities in release of CCK contributes to the development of duodenal ulcers. We speculate, however, that the increased release of endogenous CCK after truncal vagotomy may possibly play an etiologic role in the syndrome of postvagotomy diarrhea.