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Fecal bile acid excretion (FBAE) is a physiological process reflecting the net elimination of bile acids from the enterohepatic circulation into the stool. Under normal conditions, approximately 95% of bile acids are reabsorbed in the terminal ileum via the apical sodium-dependent bile acid transporter (ASBT), but certain therapeutic interventions aim to increase this excretion to treat metabolic and cholestatic disorders. Promoting FBAE forces the liver to convert systemic cholesterol into new bile acids, effectively lowering plasma LDL cholesterol levels, and helps reduce the systemic accumulation of toxic bile acids in patients with cholestasis. Conversely, pathologically high FBAE is a diagnostic hallmark of bile acid malabsorption (BAM), which leads to colonic irritation and chronic watery diarrhea. Pharmacological modulation of this process is primarily achieved using bile acid sequestrants like colestyramine or highly specific IBAT inhibitors like odevixibat and maralixibat.
Increased fecal bile acid excretion is achieved through either physical sequestration of bile acids in the intestinal lumen by resins or the pharmacological inhibition of the apical sodium-dependent bile acid transporter (ASBT/SLC10A2) in the terminal ileum.
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