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Progress in idiopathic bile acid malabsorption
  1. Division of Gastroenterology, Department of Medicine
  2. University of California, San Diego, USA

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Bile acid malabsorption, whether caused by an inborn absence of the ileal transport system or by resection of the terminal ileum, causes diarrhoea because of the secretory effect of malabsorbed dihydroxy bile acids in the colon. There is now increasing evidence that bile acid malabsorption is also present and plays a causal role in many patients with intermittent or chronic diarrhoea who have no ileal pathology. Many of these patients have been labelled with the diagnosis of irritable bowel syndrome.1 In this issue, Fracchiaet al (see page 812) provide new information on this syndrome by defining biliary bile acid and lipid composition in 13 well characterised patients with idiopathic bile acid malabsorption.

Bile acids are secreted by the liver entirely in conjugated form. The conjugated bile acid anion is impermeable to cell membranes and too large to pass the paracellular junctions of the biliary and intestinal tract. The highly efficient conservation of bile acids, which is responsible for the accumulation of a recycling bile acid pool, results from both carrier mediated and passive absorption. Carrier mediated absorption is mediated mainly by an apical transporter located in the ileal enterocyte. This transporter, which has been cloned and characterised by Dawson and colleagues,2 is now termed the “apical bile salt transporter” (abst) because it is also present in the renal tubular epithelial cell and in the cholangiocyte. Passive absorption of unconjugated bile acids that are formed by bacterial enzymes present in the distal small intestine and colon also contributes to the efficient conservation of bile acids. The combination of active and passive absorption of bile acids in the small intestine means that …

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