In primary care, bile acid diarrhoea (BAD) is often misdiagnosed as irritable bowel syndrome (IBS with predominant diarrhoea, IBS-D) because of under-recognition and symptom overlap. As recognition increases, GPs will play an increasing role in diagnosing and treating BAD. This review explores BAD’s recognition, diagnosis, and treatment.
What is bile acid diarrhoea (BAD)?
BAD is characterised by chronic diarrhoea because of abnormal bile acid (BA) metabolism or handling. Excess BAs overwhelm the terminal small bowel’s absorptive capacity, stimulating colonic fluid secretion and motility. 1 BAD may follow cholecystectomy, or be secondary to conditions such as Crohn’s disease, but most cases are idiopathic. A lack of clinician awareness leads to common misdiagnosis and mismanagement, resulting in unnecessary distress. A quality of life study found that 80% of people with BAD always had diarrhoea, with over half experiencing bloating, pain, and the need to be close to a toilet. Treatment improved these symptoms for most people. 2
Four subtypes of BAD are currently recognised (Box 1).
Box 1. Summary of the subtypes of BAD.
| Subtype | Mechanism | Associated conditions | Notes |
|---|---|---|---|
| Type I(Secondary) | Impaired BA absorption in terminal ileum due to bile transporter loss; ↓ FGF-19 so ↑ BA synthesis | Crohn’s disease, ileal resection, radiotherapy | May cause steatorrhoea; excess BAs ↑ colonic secretion and motility |
| Type II(Idiopathic) | Likely ↓ FGF-19, BA transporter mutations, rapid transit, dysbiosis | IBS-D, functional diarrhoea | Most common type; reduced FGF-19; linked to microbiota and genetics |
| Type III(Secondary) | Indirect BA malabsorption or ↑ motility | Cholecystectomy, coeliac disease, chronic pancreatitis, cystic fibrosis | Often overlooked; contributes to chronic diarrhoea |
| Type IV(Excessive synthesis) | ↑ Hepatic BA synthesis with normal absorption; ↓ FGF-19 | hypertriglyceridaemia, metformin | Emerging subtype; mechanism unclear |
BA = bile acid. BAD = bile acid diarrhoea. FGF-19 = fibroblast growth factor 19. IBS = irritable bowel syndrome. IBS-D = IBS with predominant diarrhoea.
↑ = increased, ↓ = reduced
The mechanisms underpinning BAD include increased hepatic BA synthesis, impaired ileal absorption, or disrupted feedback inhibition by fibroblast growth factor 19 (FGF-19). 1
What is the prevalence of BAD?
Investigating the prevalence of BAD is challenging because of underdiagnosis. However, one review found that 68% of patients diagnosed with IBS-D had bile acid malabsorption to some extent. 2
A further review found that 30% of people with functional bowel disorders had moderate BA malabsorption. 3 In a cohort study of 1071 people with chronic diarrhoea, 42.7% were diagnosed with BAD. Among patients without risk factors, 35.7% tested positive for BAD. 4 It is estimated that BAD affects at least 25% of people with chronic diarrhoea. Approximately 5% of adults in Western countries report chronic diarrhoea. This implies a population prevalence of BAD of at least 1% of adults in Western countries. Therefore, GPs will frequently encounter people with BAD.
Why is BAD often misdiagnosed?
The symptoms of BAD overlap with IBS and inflammatory bowel disease (IBD), as well as other gastrointestinal conditions such as microscopic colitis, leading clinicians to default to a diagnosis of IBS-D when IBD has been excluded. This delays appropriate treatment and worsens outcomes.
How can BAD be differentiated?
The clinical history is essential in diagnosing BAD, as other conditions increase the risk of developing it. These include Crohn’s disease affecting the terminal ileum or after ileal resection, cholecystectomy, coeliac disease, chronic pancreatitis, various pancreaticobiliary diseases, radiation bowel disease, and cystic fibrosis. Diarrhoea caused by metformin may also contribute to BAD. The absence of blood in the stool and a negative faecal calprotectin are key to ruling out IBD.
How is BAD diagnosed?
Mainly diagnosed in secondary care, diagnosis of BAD relies on demonstrating disruption in BA homeostasis. The 75Selenium-homotaurocholic acid test (75SeHCAT) is the gold standard test. Other tests include serum C4 level (a component of the cholesterol biosynthesis pathway), serum FGF-19 levels, and faecal BA quantification. However, access to these tests is currently limited, though C4 is becoming more widespread in specialist centres, and faecal bile acid kits have recently become available, with the potential for rollout into primary care for diagnosis. However, at this time, clinical suspicion should prompt referral to gastroenterology, where SeHCAT can be considered.
What is the pathway for managing BAD?
The management of BAD includes accurate diagnosis, medical management, adjunctive treatments, and monitoring (Figure 1).
Figure 1. Flowchart of the management of BAD. BAD = bile acid diarrhoea. IBS = irritable bowel syndrome. SeHCAT = Selenium homotaurocholic acid test.
Bile acid sequestrants (BAS), such as colesevelam, are the mainstay of treatment for BAD. Alternative BAS can be trialled, for example, colestyramine or colestipol.
BAS suffer from multiple issues, including poor tolerability (especially colestyramine), gastrointestinal side effects, and variable response rates. 5 However, BAS are associated with a significant increase in quality of life in BAD. 6 BAS need to be taken apart from other medications, but do not need to be taken with meals.
Dietary modifications can also be made, including trialling a low-fat diet for 4 weeks (<20% of total daily calories from fat), increasing soluble fibre intake, limiting alcohol and caffeine, and eating smaller, more frequent meals.
Recent experience suggests that GLP-1 inhibitors, for example, liraglutide, may be effective if patients are refractory or intolerant to BAS. Studies show a high efficacy in reducing stool frequency, suggesting that they may be superior to BAS, with minimal side effects. 7
How can management be improved?
Increasing clinician awareness of BAD, and incorporating early screening tests into primary care in the future, could result in earlier diagnosis and treatment. The recently launched lower GI pathway may prove helpful in practice, though BAD is probably not given due prominence. 8 Diagnostic tests need to be made more widely available, and more research is needed on the safety and efficacy of newer therapies. Furthermore, patient education on managing dietary fat and fibre intake could help manage symptoms. The recently funded National Institute for Health and Care Research COBALT study should prove very insightful in due course.
Conclusion
BAD is a commonly underdiagnosed condition because of its overlap with IBS-D. Greater clinical awareness and prompt investigation or referral to gastroenterology can improve outcomes. Early diagnosis, medical management, and patient education are essential for improving outcomes and quality of life, which is greatly impacted by BAD. 2 Further research into diagnostic tools and management strategies will continue to improve the quality of life for people suffering with BAD.
Competing interests
The authors have declared no competing interests.
References
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