PLASMA-CONCENTRATIONS OF CHOLECYSTOKININ AND NEUROTENSIN IN PATIENTS WITH CYSTIC-FIBROSIS

Citation
Kh. Herzig et al., PLASMA-CONCENTRATIONS OF CHOLECYSTOKININ AND NEUROTENSIN IN PATIENTS WITH CYSTIC-FIBROSIS, Scandinavian journal of gastroenterology, 32(4), 1997, pp. 315-319
Citations number
45
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00365521
Volume
32
Issue
4
Year of publication
1997
Pages
315 - 319
Database
ISI
SICI code
0036-5521(1997)32:4<315:POCANI>2.0.ZU;2-D
Abstract
Background: Regulation of pancreatic exocrine secretion is controlled by vagovagal reflexes and hormones. A negative feedback control mechan ism exists between the intraduodenal protease concentration and pancre atic enzyme secretion. In man cholecystokinin (CCK) is the major regul ator of postprandial pancreatic enzyme secretion. There is a 50% reduc tion of meal-stimulated secretion by the specific CCK receptor antagon ist loxiglumide,whereas atropine completely blocks postprandial secret ion. Neurotensin is released postprandially by nerval reflexes and fat . It has been claimed that both hormones are increased in patients wit h pancreatic insufficiency. Methods: We investigated CCK and neurotens in levels in patients with cystic fibrosis and pancreatic insufficienc y. In 35 patients (2-24 years old) with cystic fibrosis with steatorrh ea and in 15 patients (1.5-24 years old) with cystic fibrosis without pancreatic insufficiency pre- and post-prandial CCK and neurotensin pl asma levels were measured 3 days after pancreatic enzyme therapy had b een withdrawn. Nine patients (3-14 years old) who had no complaint of abdominal disease served as controls. Results: Basal and postprandial CCK plasma levels did not differ statistically in the three groups, wh ereas basal and postprandial neurotensin levels were significantly inc reased in the cystic fibrosis groups. The severity of the disease had no effect on the neurotensin levels. Conclusions: Cystic fibrosis pati ents with severe pancreatic insufficiency did not have increased CCK p lasma levels, suggesting that a CCK-mediated feedback mechanism of pan creatic enzyme secretion does not operate in our patients. In contrast , basal and postprandial neurotensin plasma levels were significantly increased in patients with cystic fibrosis but were independent of the severity of the pancreatic insufficiency.