Literature DB >> 2753411

Reversible gall bladder dysfunction in severe pancreatic insufficiency.

A A Masclee1, J B Jansen, F H Corstens, C B Lamers.   

Abstract

The present study was undertaken to examine the intestinal phase of cholecystokinin (CCK) secretion and gall bladder contraction in patients with severe pancreatic insufficiency. Plasma CCK concentrations, measured by radioimmunoassay, and gall bladder contraction by cholescintigraphy were studied in response to intraduodenal fat with and without addition of pancreatic enzymes. Fasting plasma CCK concentrations were in the same range in six patients with pancreatic insufficiency with (2.6 (0.2) pmol/l) and without (2.6 (0.3) pmol/l) addition of pancreatic enzymes and in six healthy subjects (2.0 (0.4) pmol/l). The integrated plasma CCK secretion in response to intraduodenal fat was significantly (p less than 0.005) reduced in the patients without addition of enzymes (46 (13) pmol/1.90 min) compared with healthy subjects (199 (22) pmol/1.90 min), but increased significantly (p less than 0.01) by the addition of pancreatic enzymes (174 (25) pmol/1.90 min) to values not significantly different from healthy subjects. Similarly, gall bladder emptying in response to intraduodenal fat was significantly (p less than 0.01) reduced in patients with pancreatic insufficiency without addition of enzymes (at 90 min: 35 (11)%) compared with healthy subjects (at 90 min: 66 (7)%) but significantly (p less than 0.01) increased by addition of pancreatic enzymes (at 90 min: 70 (8)%) to values not significantly different from healthy subjects. These results indicate that patients with severe pancreatic insufficiency have impaired gall bladder emptying after intraduodenal fat, which can be normalised by the addition of pancreatic enzymes. This impaired gall bladder emptying appears to be the result of a reduced plasma CCK response. Thus, intra-intestinal pancreatic enzymes play an important role in the intestinal phase of CCK secretion and gall bladder emptying.

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Year:  1989        PMID: 2753411      PMCID: PMC1434150          DOI: 10.1136/gut.30.6.866

Source DB:  PubMed          Journal:  Gut        ISSN: 0017-5749            Impact factor:   23.059


  14 in total

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Journal:  Lancet       Date:  1973-10-13       Impact factor: 79.321

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Journal:  Dig Dis Sci       Date:  1988-03       Impact factor: 3.199

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Journal:  Gastroenterology       Date:  1981-03       Impact factor: 22.682

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Journal:  J Clin Invest       Date:  1976-08       Impact factor: 14.808

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Authors:  J B Jansen; C B Lamers
Journal:  Clin Chim Acta       Date:  1983-07-15       Impact factor: 3.786

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Authors:  C Beglinger; M Fried; I Whitehouse; J B Jansen; C B Lamers; K Gyr
Journal:  J Clin Invest       Date:  1985-05       Impact factor: 14.808

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Authors:  J B Jansen; W P Hopman; C B Lamers
Journal:  Dig Dis Sci       Date:  1984-12       Impact factor: 3.199

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6.  Preduodenal mechanisms compensate completely for absent pancreatic enzymes to stimulate gallbladder after meals.

Authors:  J H Meyer; M Hlinka; D Jehn; Y G Gu
Journal:  Dig Dis Sci       Date:  1995-04       Impact factor: 3.199

7.  Gallbladder dynamics in chronic pancreatitis. Relationship to exocrine pancreatic function, CCK, and PP release.

Authors:  B Glasbrenner; P Malfertheiner; O Pieramico; S Klatt; R Riepl; H Friess; H Ditschuneit
Journal:  Dig Dis Sci       Date:  1993-03       Impact factor: 3.199

8.  Relation between gastric emptying of albumin-dextrose meals and cholecystokinin release in man.

Authors:  J B Jansen; M Fried; W P Hopman; C B Lamers; J H Meyer
Journal:  Dig Dis Sci       Date:  1994-03       Impact factor: 3.199

9.  Pancreatic polypeptide secretion in patients with chronic pancreatitis and after pancreatic surgery.

Authors:  E H Eddes; M Verkijk; H A Gielkens; I Biemond; W Bemelman; C B Lamers; A A Masclee
Journal:  Int J Pancreatol       Date:  2001

10.  Delayed release pancrelipase for treatment of pancreatic exocrine insufficiency associated with chronic pancreatitis.

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