Bile Acid diarrhea: prevalence, pathogenesis, and therapy.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing disease mechanisms, epidemiology, diagnostics, and therapy
PubMed 25918262 · doi:10.5009/gnl14397
What was done
Narrative review of clinical and mechanistic evidence on bile acid diarrhea, covering its prevalence, underlying pathogenesis (including FGF-19 regulation, TGR5 signaling, and colonic transit), diagnostic methods, and treatment options.
What was found
The abstract notes that bile acid diarrhea affects an estimated 1% of the population and 25% to 50% of patients with functional diarrhea or diarrhea-predominant irritable bowel syndrome. Pathophysiology involves fibroblast growth factor 19 deficiency, genetic variations in bile acid circulation or the TGR5 receptor, increased mucosal permeability, enhanced water and electrolyte secretion, accelerated transit, increased fecal primary bile acids, and microbiome alterations. Diagnostic options include the selenium homotaurocholic acid test, serum C4, serum FGF-19, fecal bile acids, and empiric bile acid sequestrant trials. Medical therapies include bile acid sequestrants (cholestyramine, colestipol, colesevelam) and FXR agonists like obeticholic acid. No comparative statistical results or numerical treatment outcomes were reported in the abstract.
Why it matters
This review emphasizes that bile acid diarrhea is common yet frequently misclassified as functional diarrhea or IBS-D, underscoring actionable diagnostic pathways and targeted pharmacotherapies.
Limits
This is a narrative review without primary data, systematic search criteria, quality appraisal, or meta-analytic pooling. The abstract provides no specific diagnostic accuracy statistics, treatment effect sizes, or participant counts.
Cited by
- context Bile acts to lubricate the colon to maintain normal bowel transit.