Ileal absorption of bile acids in patients with chronic cholestasis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-12

AUTHORS

Olivier Chazouillères, Philippe Marteau, Mostefa Haniche, Raymond Jian, Raoul Poupon

ABSTRACT

The effect of cholestasis on ileal bile acid absorption is controversial in animal models (up- or down-regulation) and unknown in humans. We therefore studied values of the selena homotaurocholic acid (SeHCAT) test before and after long-term administration (>3 months, 13-15 mg/kg/day) of ursodeoxycholic acid (UDCA) in 27 patients with chronic cholestatic liver diseases (24 women, 3 men; mean age, 50 years; 24 primary biliary cirrhosis, 2 secondary biliary cirrhosis, 2 others). The control group consisted of 14 healthy volunteers. Seven-day SeHCAT percentage retention was identical in the 12 untreated cholestatic patients (serum bilirubin, 75+/-42 micromol/L, alkaline phosphatase, 4.2+/-1.0 N; mean+/-SEM) and in the control group (43.6+/-2.9 and 43.8+/-4.2%, respectively). In the 22 patients treated by UDCA for 38+/-8 months, SeHCAT percentage retention was 20.3+/-3.0%. In the seven patients with the SeHCAT test done before and after UDCA treatment (16+/-5 months), SeHCAT percentage retention decreased significantly under UDCA therapy (42.0+/-4.4 vs 19.4+/-4.1%; P < 0.02). We conclude that, in patients with chronic cholestasis (1) SeHCAT percentage retention is not altered-taken together with the known defect of biliary excretion, this lack of increase in SeHCAT percentage retention argues against up-regulation of bile acid ileal transport; and (2) UDCA treatment induces a decrease in the SeHCAT percentage retention-this effect may be related primarily to a decreased bile acid ileal absorption. More... »

PAGES

2417-2422

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf02100137

DOI

http://dx.doi.org/10.1007/bf02100137

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1000664450

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9011452


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