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Normal or increased bile acid uptake in isolated mucosa from patients with bile acid malabsorption.

Journal article
Authors Antal Bajor
Anders Kilander
Anita Fae
Cecilia Galman
Olof Jonsson
Lena Öhman
Mats Rudling
Henrik Sjövall
Per-Ove Stotzer
Kjell-Arne Ung
Published in Eur J Gastroenterol Hepatol
Volume 18
Issue 4
Pages 397-403
ISSN 0954-691X
Publication year 2006
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Medicine, Department of Internal Medicine
Institute of Clinical Sciences
Pages 397-403
Language en
Subject categories Urology and andrology

Abstract

Introduction: Bile acid malabsorption as reflected by an abnormal 75Se-labelled homocholic acid-taurine (75SeHCAT) test is associated with diarrhoea, but the mechanisms and cause-and-effect relations are unclear. Objectives: Primarily, to determine whether there is a reduced active bile acid uptake in the terminal ileum in patients with bile acid malabsorption. Secondarily, to study the linkage between bile acid malabsorption and hepatic bile acid synthesis. Methods: Ileal biopsies were taken from patients with diarrhoea and from controls with normal bowel habits. Maximal active bile acid uptake was assessed in ileal biopsies using a previously validated technique based on uptake of 14C-labelled taurocholate. To monitor the hepatic synthesis, 7[alpha]-hydroxy-4-cholesten-3-one, a bile acid precursor, was assayed in blood. The 75SeHCAT-retention test was used to diagnose bile acid malabsorption. Results: The taurocholate uptake in specimens from diarrhoea patients was higher compared with the controls [median, 7.7 (n=53) vs 6.1 [mu]mol/g per min (n=17)] (P<0.01) but no difference was seen between those with bile acid malabsorption (n=18) versus diarrhoea with a normal 75SeHCAT test (n=23). The 75SeHCAT values and 7[alpha]-hydroxy-4-cholesten-3-one were inversely correlated. Conclusions: The data do not support bile acid malabsorption being due to a reduced active bile acid uptake capacity in the terminal ileum. (C) 2006 Lippincott Williams & Wilkins, Inc.

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