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Published on: September 18, 2014
Gallbladder motility and cholecystokinin secretion during continuous enteral nutrition
M Ledeboer1, A A Masclee, I Biemond
1Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands.
Objectives:
During total parenteral nutrition, gallbladder motility is impaired, resulting in sludge and stone formation. Little is known about gallbladder motility during prolonged enteral nutrition.
Methods:
We studied gallbladder motility during continuous enteral nutrition (CEN) in nine hospitalized patients with active inflammatory bowel disease. The patients received a polymeric diet (2000 kcal/24 h) by CEN through a nasogastric tube for a prolonged period. Gallbladder volumes were obtained daily by ultrasonography, starting from day 0 (before CEN) and on 7 consecutive days during CEN. At days 0, 1, 4, and 7, the gallbladder response to i.v. cholecystokinin (CCK-33; 0.5 Ivy Dog unit/kg/h) was studied. Plasma CCK levels were determined at regular intervals by radioimmunoassay.
Results:
No significant differences were observed on day 0 between patients and a group of nine healthy control subjects in fasting gallbladder volumes (19.4 +/- 2.3 and 19.6 +/- 2.4 cm3, respectively) and gallbladder contraction during CCK infusion (56 +/- 14% and 69 +/- 7%, respectively). During CEN, from day 1 to day 7, mean gallbladder volume remained significantly (p < 0.05) reduced compared with fasting gallbladder volume, and mean plasma CCK levels remained significantly (p < 0.05) increased compared with fasting levels. Although gallbladder volume was significantly reduced during CEN, the gallbladder contractile response to CCK was not affected; at days 1, 4, and 7, gallbladder contraction was 36-57%.
Conclusions:
During CEN, 1) gallbladder volume is significantly reduced and plasma CCK levels are significantly increased, 2) these effects are sustained over time (7 days), and 3) the gallbladder remains responsive to exogenous CCK. These results indicate that gallbladder contractility and gallbladder responsiveness to CCK are preserved during prolonged CEN in patients with inflammatory bowel disease.
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