This study aimed at examining the mechanisms participating in excessive faecal
bile acid loss in
cystic fibrosis. The study was designed to define the relation between faecal fat and faecal
bile acid loss in patients with and without
cystic fibrosis related
liver disease; to assess terminal ileal
bile acid absorption by a seven day whole body retention of
selenium labelled homotaurocholic
acid (
SeHCAT); and to determine if small intestinal bacterial overgrowth contributes to faecal
bile acid loss. The study population comprised 40 patients (27 men; median age 18 years) with
cystic fibrosis (n = 8) and without (n = 32)
liver disease and eight control subjects. Faecal
bile acid excretion was significantly higher in
cystic fibrosis patients without
liver disease compared with control subjects (mean (SEM) 21.5 (2.4) and 7.3 (1.2) micromoles/kg/24 hours respectively; p < 0.01) and patients with
liver disease (7.9 (1.3) micromoles/kg/24 hours; p < 0.01). No correlation was found between faecal fat (g fat/24 hours) and faecal
bile acid (micromoles 24 hours) excretion. Eight (33%) of
cystic fibrosis patients had seven day
SeHCAT retention < 10% (normal retention > 20%).
SeHCAT retention in
cystic fibrosis patients with
liver disease was comparable with control subjects (30.0 (SEM) 8.3% v 36.8 (5.9)%; p = NS) while
SeHCAT retention in
cystic fibrosis patients who did not have
liver disease was significantly reduced (19.9 (3.8); p < 0.05). Although evidence of small bowel bacterial overgrowth was present in 40% of patients no relation was found between breath
hydrogen excretion, faecal fat, and faecal
bile acid loss. The results are consistent with the presence of an abnormality in terminal ideal function in patients with
cystic fibrosis who do not have
liver disease and that a defect in the ileal absorption of
bile acids may be a contributory factor to excessive faecal
bile acid loss. Faecal
bile acid loss in
cystic fibrosis is unrelated to the presence of intraluminal fat or intestinal bacterial overgrowth.