Meal-related changes in plasma CCK bioactivity in patients with chronic pancreatitis

In order to clarify whether there is a negative feedback mechanism for CCK secretion, we investigated plasma CCK bioactivity in patients suffering Dom chronic pancreatitis (CP) according to the characteristics of their pancre atic disease. Basal, meal-stimulated, and integrated release of plasma cholecystokinin (C CK) bioactivity was measured in 24 patients with CP and in 12 health) contr ols. The values obtained were compared between the healthy control group an d the CP group, and between subgroups of CP patients established on the bas is of the presence/ absence of several parameters : abnormal gastric emptyi ng, abdominal pain? steatorrhea, pancreatic calcification, insulin-requirin g diabetes mellitus. and impairment of pancreatic exocrine functions as ind icated bg secretin test. A bioassay method using pancreatic acini was used to measure plasma CCK bioactivity. In the control group, plasma CCK bioacti vity increased from a basal value of 1.6 +/- 0.7 rho mol/L to a maximal inc rease of 6.6 +/- 4.1 rho mol/L, and the integrated CCK release following a test meal was 37.7 +/- 19.3 rho mol/L . 150 min. In the CP group, plasma CC K bioactivity increased from 1.6 +/- 0.9 pmol/L to a maximal increase of 8. 2 +/- 8.7 rho mol/L, and the integrated release of CCK was 43.0 +/- 37.7 rh o mol/L . 150 min. None of the differences between them were significant. N o significant differences in basal value, maximal increase, or integrated p lasma CCK release were noted according to ang of the parameters of the CP p atients and the control group. Nor was there any correlation between impair ment of pancreatic exocrine function and plasma CCK bioactivity. These resu lts provide no evidence of a negative feedback mechanism between pancreatic exocrine dysfunction and CCK secretion.