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Mechanism of bile acid diarrhoea
Professor Julian R.F. Walters
Professor Walters explores the classification of different causes of bile acid diarrhoea (BAD). Professor Walters describes the normal entrohepatic circulation of bile salts and what occurs when the system does not function correctly.
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So you have seen from Dave Sanders a classification of BAD; this came from Fromm and Malavrolti in 1986.
The first type that was found was the secondary type, so that was called type 1, due to ileal disease – that does not make sense, secondary to be type 1.
Type 2 came next and that was the primary disorder – Idiopathic bile acid malabsorption, or as I prefer to call it primary BAD.
And then you’ve seen from David Sanders the miscellaneous types including post-cholecystectomy, SIBO, radiation enteropathy – which is a term I know Professor Andreas doesn’t like – and microscopic colitis.
So Alan Hoffman was important in establishing the syndrome of ileal disease and the broken enterohepatic circulation: back in 1967 he described the type 1 secondary patients.
Hess Thayson from Denmark, in the 1973 in the Danish medical bulletin, and then in Gut in 1976, described the idiopathic patients.
So let’s just go through the pathophysiology, well the normal physiology of the enterohepatic circulation of bile salts. So, they’re made in the liver from cholesterol by CYP7A1. They are conjugated with glycine or taurine. They get secreted via the biliary tree into the intestine where they do their main work of solubilising lipids into micelles for absorption.
They then get reabsorbed in the distal intestine, where there is active transport of the conjugated bile acids. Now that’s the normal enterohepatic circulation, they go around, they get retaken back up, and resecreted.
It’s the bile salts that enter the colon which are the problem, these are the ones that cause diarrhoea. They do this by being in the colon, the excess bile acids either there because they are unabsorbed or there is an increase in production. The bacteria transform them by deconjugating and dehydroxylating them, and the bile acids then stimulate colonic secretion by anions, producing a watery stool and they may produce motility changes also.
So here are the typical bile acid kinetics. We know the secretion in a day is about 12 grams per day, but the bile acid pool size is only about 2–3 grams, and so they have to cycle. They go around 4–6 times a day and in each cycle 95% will be absorbed. The faecal bile acid lost per day is under half a gram, so only a small proportion of the bile acid pool size, and this gives and average half-life of about 3 days.
So, we can diagnose bile acid malabsorption in several ways. Here’s a review done by Michael Camilleris’ group in 2013 and he talked about the various things that could be used; faecal bile acid, serum C4, SeHCAT, and we have used glycocholate breath tests in the past.
Job number: JB57410GBe(1) Date of Preparation: June 2020
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Professor Sanders argues that many patients presenting with irritable bowel syndrome (IBS) have underlying diseases. He explores a series of studies that suggest approximately 25% of patients presenting with IBS symptoms have BAD as the underlying cause.
Professor Sanders highlights that many patients presenting with irritable bowel syndrome (IBS) have underlying diseases.
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