These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Plasma cholecystokinin and somatostatin levels in chronic pancreatitis patients.
    Author: al-Eryani S, Duris I, Payer J, Huorka M, Kratochvílová H, Ondrejka P.
    Journal: Hepatogastroenterology; 2000; 47(33):869-74. PubMed ID: 10919050.
    Abstract:
    BACKGROUND/AIMS: The existence of a negative-feedback mechanism between pancreatic enzyme secretion and intraduodenal proteases and the role of cholecystokinin in its mediation in humans is debatable. The presence of such a feedback mechanism in chronic pancreatitis patients with exocrine enzyme deficiency possibly leads to an increase in cholecystokinin plasma levels. Somatostatin 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 levels in 30 patients with chronic pancreatitis (11 with severe chronic pancreatitis and 19 with mild chronic pancreatitis) were measured 14 days after discontinuation of enzymatic substitution therapy and then were compared with 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 healthy individuals (P < 0.01). Basal, somatostatin, cholecystokinin and postprandial somatostatin levels were not significantly higher than those in healthy subjects. There was no correlation between basal and postprandial levels of cholecystokinin and somatostatin in our study. CONCLUSIONS: The cholecystokinin postprandial plasma levels were significantly higher in all patients with chronic pancreatitis when compared with healthy individuals, which suggests the role of cholecystokinin in the feedback control of pancreatic secretion.
    [Abstract] [Full Text] [Related] [New Search]