PubMedDate not supplied
In order to clarify whether there is a negative feedback mechanism for CCK secretion, we investigated plasma CCK bioactivity in patients suffering from chronic pancreatitis (CP) according to the characteristics of their pancreatic disease. Basal, meal-stimulated, and integrated release of plasma cholecystokinin (CCK) bioactivity was measured in 24 patients with CP and in 12 healthy controls. The values obtained were compared between the healthy control group and the CP group, and between subgroups of CP patients established on the basis of the presence/absence of several parameters: abnormal gastric emptying, abdominal pain, steatorrhea, pancreatic calcification, insulin-requiring diabetes mellitus, and impairment of pancreatic exocrine functions as indicated by secretin test. A bioassay method using pancreatic acini was used to measure plasma CCK bioactivity. In the control group, plasma CCK bioactivity increased from a basal value of 1.6 +/- 0.7 pmol/L to a maximal increase of 6.6 +/- 4.1 pmol/L, and the integrated CCK release following a test meal was 37.7 +/- 19.3 pmol/L.150 min. In the CP group, plasma CCK bioactivity increased from 1.6 +/- 0.9 pmol/L to a maximal increase of 8.2 +/- 8.7 pmol/L, and the integrated release of CCK was 43.0 +/- 37.7 pmol/L.150 min. None of the differences between them were significant. No significant differences in basal value, maximal increase, or integrated plasma CCK release were noted according to any of the parameters of the CP patients and the control group. Nor was there any correlation between impairment of pancreatic exocrine function and plasma CCK bioactivity. These results provide no evidence of a negative feedback mechanism between pancreatic exocrine dysfunction and CCK secretion.