[Impairment of humoral regulation of exocrine pancreatic function in chronic pancreatitis].

AIM

To elicit the role of cholecistokinin (CCK), biogenic amines, bile acids (BA) in development of functional pancreatic insufficiency (PI) in chronic pancreatitis (CP).

MATERIAL AND METHODS

Blood concentrations of CCK, serotonin and acetylcholin, fecal concentration of elastase (E-1), BA spectrum in the blood and duodenal content were studied in 46 CP patients (20 patients with alcoholic pancreatitis--AP and 26 patients with biliary pancreatitis--BP) and 15 healthy controls.

RESULTS

In AP patients E-1 fell to 78.4 +/- 6.3 mcg/g (severe exocrine PI), while in BP patients E-1 was 170.0 +/- 28.9 mcg/g. CCK in AP and BP decreased to 0.33 +/- 0.03 and 0.45 +/- 0.03 ng/ml, respectively (control--1.60 +/- 0.02 ng/ml, respectively, p < 0.05). AP and BP patients had a rise in the absolute concentration and percentage of the total fraction of the taurodioxicholanic acids to 10.2 +/- 1.6 and 15.0 +/- 2.3%, respectively, (control 9.5 +/- 1.2%) in duodenal bile. The concentration of glycocholic acid fell to 24.1 +/- 1.6 and 23.7 +/- 3.7%, respectively, (control--36.4 +/- 2.4%, p < 0.05). AP patients had more significant decrease of taurocholic acid--to 4.5 +/- 0.7% (control--9.2 +/- 0.7%, p < 0.05). In the peripheral blood of AP patients there was an elevated basal level of serotonin and acetylcholine in the presence of low cholinesterase activity. After meal, acetylcholine concentration lowered in high secretion of serotonin.

CONCLUSION

Depending on severity of destructive changes in the pancreas, AP and BP patients had different degree of exocrine insufficiency which may be secondary to the absence of acetylcholine rise in the blood after meal. Alterations in the composition of the conjugates of cholic and taurodioxicholanic BA lead to alterations of CCK blood concentration and, therefore, to changes in exocrine pancreatic secretion. Imbalance between serotonin and acetylcholine levels after meal evidences for defects in conventional regulatory interrelations. Decreased threshold of nociceptors activation in simultaneous enhancement of afferent nociceptive flows may entail pain syndrome in CP.