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Intestinal Bile Acid Malabsorption in Cystic Fibrosis Gut: First Published As 10.1136/Gut.34.8.1137 on 1 August 1993

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Intestinal Bile Acid Malabsorption in Cystic Fibrosis Gut: First Published As 10.1136/Gut.34.8.1137 on 1 August 1993 1137 Gutl993;34: 1137-1141 Intestinal bile acid malabsorption in cystic fibrosis Gut: first published as 10.1136/gut.34.8.1137 on 1 August 1993. Downloaded from S O'Brien, H Mulcahy, H Fenlon, A O'Broin, M Casey, A Burke, M X FitzGerald, J E Hegarty Abstract loss.9 '° In addition, intestinal bacterial over- This study aimed at examining the mecha- growth, resulting from prolonged intestinal nisms participating in excessive faecal bile acid transit and stasis," may result in deconjugation loss in cystic fibrosis. The study was designed and dehydroxylation of bile salts and contribute to define the relation between faecal fat and to impaired bile acid absorption and faecal bile faecal bile acid loss in patients with and acid loss. without cystic fibrosis related liver disease; to Excessive faecal bile acid losses have not been assess terminal ileal bile acid absorption by a found in all studies in adult patients with cystic seven day whole body retention of selenium fibrosis.32 This finding has been attributed to labelled homotaurocholic acid (SeHCAT); the increased prevalence of hepatic dysfunction, and to determine if small intestinal bacterial with associated impairment of bile acid synthesis overgrowth contributes to faecal bile acid loss. and contraction of the total bile acid pool, in The study population comprised 40 patients adults with cystic fibrosis.3 (27 men; median age 18 years) with cystic The objectives of this study in an adult fibrosis (n=8) and without (n=32) liver disease population of patients with cystic fibrosis were and eight control subjects. Faecal bile acid to: (1) define the relation between faecal fat and excretion was significantly higher in cystic faecal bile acid excretion in patients with and fibrosis patients without liver disease com- without liver disease; (2) to discover if a defect in pared with control subjects (mean (SEM) 21-5 the ileal bile acid active transport mechanism (2.4) and 7.3 (1.2) umol/kg/24 hours respect- contributes to faecal bile acid loss; and (3) to ively; p<001) and patients with liver disease assess the contribution of small bowel bacterial (7.9 (1.3) umol/kg/24 hours; p<001). No overgrowth to faecal fat and faecal bile acid correlation was found between faecal fat (g fat/ losses. 24 hours) and faecal bile acid (umol/24 hours) excretion. Eight (33%) of cystic fibrosis patients had seven day SeHCAT retention Methods http://gut.bmj.com/ <10% (normal retention >20%). SeHCAT retention in cystic fibrosis patients with liver PATIENTS disease was comparable with control subjects The study population comprised of 40 patients (30.0 (SEM) 8-3% v 36-8 (5.9)%; p=NS) while with cystic fibrosis admitted to the Adult Cystic SeHCAT retention in cystic fibrosis patients Fibrosis Centre for evaluation of their respira- who did not have liver disease was significantly tory or hepatic state, or both. Most patients were reduced (19-9 (3.8); p<005). Although receiving standard treatment with broncho- on September 27, 2021 by guest. Protected copyright. evidence of small bowel bacterial overgrowth dilators, antibiotic prophylaxis against pseudo- was present in 40% of patients no relation was monas or staphylococcal infections, or both, and found between breath hydrogen excretion, pancreatic enzyme supplements. The presence faecal fat, and faecal bile acid loss. The results of hepatic disease was determined by abnormal are consistent with the presence of an abnor- liver biochemistry tests (gammaglutamyl trans- mality in terminal ileal function in patients with ferase >50 IU/1, 5'nucleotidase >15 IU/1) of at cystic fibrosis who do not have liver disease least six months duration, histological evidence and that a defect in the ileal absorption of bile of fibrosis/cirrhosis on liver biopsy and the Gastroenterology and acids may be a contributory factor to excessive presence of portal hypertension, or both. Eight Liver Unit, faecal bile acid loss. Faecal bile acid loss in patients in whom there was no evidence of S O'Brien H Mulcahy cystic fibrosis is unrelated to the presence of gastrointestinal, pancreatic, or hepatobiliary H Fenlon intraluminal fat or intestinal bacterial over- disease served as a control population. A Burke growth. Dietary advice to achieve a total energy intake J E Hegarty (Gut 1993; 34: 1137-1141) of 120-150% of the recommended daily allow- Adult Cystic Fibrosis ance for age,'3 with approximately 40% of the Centre, total energy intake derived from fat, was given to M X FitzGerald Excessive faecal bile acid loss is well recognised each patient. All patients received fat and water Education and Research in patients with cystic fibrosis'" and has been soluble vitamin supplements and none were Centre, attributed to an inhibitory effect of intraluminal taking taurine supplementation. A O'Broin unhydrolysed triglycerides on the intestinal and Department of absorption of bile acids. Some studies, however, Nuclear Medicine, have shown no correlation between faecal fat FAECAL FAT AND BILE ACID ANALYSIS St Vincent's Hospital, excretion and faecal bile acid loss suggesting that Faecal fat and faecal bile acid analysis was Elm Park, Dublin, Ireland additional factors are responsible for bile acid performed on 17 patients with cystic fibrosis (five M Casey Thus in vitro with liver disease) and eight control subjects. Correspondence to: malabsorption in cystic fibrosis.3 Dr J E Hegarty, Liver Unit, studies have shown a defect in the terminal ileal Faecal samples were collected over three days St Vincent's Hospital, Elm bile acid active transport mechanisms in patients during which at least 50 grams of fat were Park, Dublin 4, Ireland. in vivo, day. The dietary intake over the 72 Accepted for publication with cystic fibrosis, which if present ingested per 15 December 1992 would also contribute to excessive faecal bile acid hour collection period was noted and fat intake 1138 O'Brien, Mulcahy, O'Broin, Casey, Burke, FitzGerald, Hegarty TABLE I Clinicalfeatures ofcysticfibrosis patients with and TABLE III Hydrogen breath tests in cysticfibrosis patients without liver disease with and without liver disease Gut: first published as 10.1136/gut.34.8.1137 on 1 August 1993. Downloaded from No liver Liver No liver Liver disease disease p disease disease p (n=32) (n=8) Value (n=28) (n=5) Value Median age in years (range) 20 (13-32) 15 (14-21) NS Fasting breath H2 (ppm) Men:women 22:10 5:3 NS > 12<75 5 3 NS Pancreatic supplements 30/32 6/8* NS >75 8 0 NS Meconium ileus equivalent 17/32 5/8 NS Fasting H2< 12 ppm Body weight (%IBW x 100% post sucrose 3 1 NS (SEM)) 84-2(2-8) 84 5(2 8) NS H2 breath test Positive 16/28 4/5 NS IBW=Ideal body weight; NS=not significant; *=one patient Negative 12/28 1/5 NS pancreas sufficient. H2=hydrogen; ppm=parts per million; NS not significant. calculated in grams/day. Three day stool collec- tion were stored at - 20°C and were subsequently microcurie (37 kBq) of SeHCAT was given orally analysed for fat and bile acid content. in capsule form to each subject. Whole body retention (% of dose) of selenium radioactivity was measured on two occasions using a shallow FAECAL FAT MEASUREMENT shield whole body counter (Camberra Accuscan) Faecal fat analysis was performed using the three hours and seven days after ingestion of the method of van de Kamer'4 and expressed as g fat/ radiolabelled isotope. g stool/24 hours. The coefficient offat absorption (CFA) was calculated from the daily dietary fat intake and the daily stool fat output and expres- HYDROGEN BREATH TEST ANALYSIS sed as a percentage ofthe daily fat intake. Increased breath hydrogen excretion after the ingestion of glucose and increased breath hydro- Daily fat intake (g)-daily stool output (g) gen excretion in the fasting state, is a useful CFA indicator of intestinal bacterial overgrowth. 8I9 Daily fat intake (g) Hydrogen breath tests were performed on 33 patients with cystic fibrosis including five FAECAL BILE ACID MEASUREMENT patients with cystic fibrosis related liver disease Bile acids were extracted from a 100 mg aliquot and eight control subjects. None of the patients of dried homogenate of faeces. Fifty microlitres had ingested lactulose in the preceding 36 hours. http://gut.bmj.com/ of [14C]-sodium cholate was added as an internal Breath hydrogen concentration was measured standard to allow assessment of recovery rates at using an exhaled hydrogen monitor (Keymed). the end of the extraction procedure. Bile acids After an overnight fast (minimum 10 hours) two were hydrolysed under alkaline conditions at 20 ml aliquots of end expiratory breath samples 220°C and were subsequently neutralised with were obtained using a modified Haldane-Priestly hydrochloric acid and extracted with diethyl- tube. Breath hydrogen was measured immedi- ether. Total faecal bile acids were measured ately and if less than 12 parts per million (ppm) on September 27, 2021 by guest. Protected copyright. using a 3a-hydroxysteroid dehydrogenase assay'5 50 g of sucrose was given orally. After ingestion and expressed as .tmol bile acid/g stool/24 hours. of sucrose, breath hydrogen was measured at 20 The results were also expressed as mg glyco- minute intervals for 160 minutes. If during this cholate equivalent bile acid/g stool/24 hours by period breath hydrogen increased by 100% or adding a glycocholate standard to the stool more the test was considered abnormal. If the specimen before analysis. fasting breath hydrogen was greater than 12 ppm fasting was continued for up to 14 hours and a breath hydrogen persistently greater than 12 SELENIUM HOMOTAUROCHOLIC ACID (seHCAT) ppm at the end of this period was considered RETENTION abnormal. The seven day retention of 75selenium labelled homotaurocholic acid (SeHCAT), a bile acid specifically absorbed by an ileal active transport EFFECT OF ANTIMICROBIAL TREATMENT mechanism,.
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