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A source for healthcare professionals to access the latest data and information on the diagnosis, treatment and management of patients with gut related disorders

BAD

Physiology of bile acid diarrhoea

Professor Julian R.F. Walters

Consultant Gastroenterologist and Professor of Gastroenterology, Imperial College London, London, UK

Bile acid diarrhoea (BAD) is a common but under-recognised cause of chronic functional diarrhoea, accounting for up to a third of patients who otherwise would be labelled as diarrhoea-predominant irritable bowel syndrome (IBS-D).1,2

Bile acids normally undergo an enterohepatic circulation. This starts with the hepatic synthesis of bile acids from cholesterol, and then conjugation with glycine or taurine.3

The conjugated bile acids are then secreted via the bile ducts into the intestine, where they solubilise lipids into micelles to aid in their absorption. Bile acids undergo reabsorption, with active absorption of conjugated bile acids in the ileum. Uptake of bile acids by the hepatocytes then occurs, and they are subsequently resecreted.3 If bile acids enter the colon, diarrhoea can result.2

In BAD, an excess of bile acids is found in the colon, either because they are not absorbed in the small intestine, or due to overproduction.1 Bacterial metabolism changes bile acids, producing stimulation of colon secretions with watery diarrhoea, and increased motility.1

Methods that have been used for diagnosing BAD include measuring faecal bile acids, the tauroselcholic (75selenium) acid (SeHCAT) test, and various serum measurements of bile acid production and regulation.4,5

Biography

Professor Julian R.F. Walters is a Consultant Gastroenterologist and Professor at Imperial College London, London, UK. Professor Walters has contributed to more than 140 studies related to molecular and cellular function of the small intestine, in particular how the development and differentiation of the mucosal epithelial cells affects nutrient transport. This includes the effects of inflammatory diseases of the intestine causing malabsorption, such as coeliac disease and Crohn's disease, and the changes in gene expression during active disease and the repair process.

References

1. Wedlake L et al. Aliment Pharmacol Ther 2009;30:707–717.
2. Slattery SA et al. Aliment Pharmacol Ther 2015;42:3–11.
3. Chiang JYL. Compr Physiol 2013;3:1191–1212.
4. Valentin N et al. Gut 2016;65:1951–1959.
5. Pattni SS et al. Aliment Pharmacol Ther 2013;38:967–976.

Job number: JB57410GBl Date of Preparation: June 2019

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