Plasma cholecystokinin and somatostatin levels in chronic pancreatitis patients

Citation
S. Al-eryani et al., Plasma cholecystokinin and somatostatin levels in chronic pancreatitis patients, HEP-GASTRO, 47(33), 2000, pp. 869-874
Citations number
39
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATO-GASTROENTEROLOGY
ISSN journal
01726390 → ACNP
Volume
47
Issue
33
Year of publication
2000
Pages
869 - 874
Database
ISI
SICI code
0172-6390(200005/06)47:33<869:PCASLI>2.0.ZU;2-A
Abstract
Background/ Aims: The existence of a negative-feedback mechanism between pa ncreatic enzyme secretion and intraduodenal proteases and the role of chole cystokinin in its mediation in humans is debatable. The presence of such a feedback mechanism in chronic pancreatitis patients with exocrine enzyme de ficiency possibly leads to an increase in cholecystokinin plasma levels. So matostatin has been used in many studies in the therapy of pain in chronic pancreatitis and plays a role in the regulation of cholecystokinin levels, however data on its plasma levels are still lacking. Methodology: Basal and the postprandial cholecystokinin and somatostatin le vels in 30 patients with chronic pancreatitis (11 with severe chronic pancr eatitis and 19 with mild chronic pancreatitis) were measured 14 days after discontinuation of enzymatic substitution therapy and then were compared wi th the levels taken from 25 healthy subjects. Results: The cholecystokinin postprandial plasma levels were significantly higher in patients with chronic pancreatitis when compared with those of he althy individuals (P<0.01). Basal, somatostatin, cholecystokinin and postpr andial somatostatin levels were not significantly higher than those in heal thy subjects. There was no correlation between basal and postprandial level s of cholecystokinin and somatostatin in our study. Conclusions: The cholecystokinin postprandial plasma levels were significan tly higher in all patients with chronic pancreatitis when compared with hea lthy individuals, which suggests the role of cholecystokinin in the feedbac k control of pancreatic secretion.