O'Brien S, Mulcahy H, Fenlon H, O'Broin A, Casey M, Burke A, FitzGerald M X, Hegarty J E
Gastroenterology and Liver Unit, St Vincent's Hospital, Elm Park, Dublin, Ireland.
Gut. 1993 Aug;34(8):1137-41. doi: 10.1136/gut.34.8.1137.
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.
本研究旨在探讨参与囊性纤维化患者粪便胆汁酸过度丢失的机制。该研究旨在明确有无囊性纤维化相关肝病患者粪便脂肪与粪便胆汁酸丢失之间的关系；通过对硒标记的同型牛磺胆酸（SeHCAT）进行为期7天的全身潴留来评估回肠末端胆汁酸的吸收情况；并确定小肠细菌过度生长是否会导致粪便胆汁酸丢失。研究人群包括40例患者（27名男性；中位年龄18岁），其中患有囊性纤维化（n = 8）且无肝病（n = 32）以及8名对照受试者。无肝病的囊性纤维化患者的粪便胆汁酸排泄量显著高于对照受试者（分别为平均（标准误）21.5（2.4）和7.3（1.2）微摩尔/千克/24小时；p < 0.01）以及肝病患者（7.9（1.3）微摩尔/千克/24小时；p < 0.01）。未发现粪便脂肪（克脂肪/24小时）与粪便胆汁酸（微摩尔/24小时）排泄之间存在相关性。8例（33%）囊性纤维化患者的SeHCAT 7天潴留率<10%（正常潴留率>20%）。患有肝病的囊性纤维化患者的SeHCAT潴留率与对照受试者相当（30.0（标准误）8.3%对36.8（5.9）%；p =无显著性差异），而未患肝病的囊性纤维化患者的SeHCAT潴留率显著降低（19.9（3.8）；p < 0.05）。尽管40%的患者存在小肠细菌过度生长的证据，但未发现呼气氢排泄、粪便脂肪与粪便胆汁酸丢失之间存在关联。这些结果与无肝病的囊性纤维化患者回肠末端功能异常的存在相一致，并且胆汁酸回肠吸收缺陷可能是粪便胆汁酸过度丢失的一个促成因素。囊性纤维化患者的粪便胆汁酸丢失与肠腔内脂肪或肠道细菌过度生长的存在无关。
