胆固醇胆结石早期复发的致病因素

胆石形成与胆汁中胆固醇的过饱和、胆固醇结晶快速成核及/或胆囊排空不全有关。本研究调查这些因素在胆囊结石复发中的意义。 材料与方法:20例胆囊结石患者在体外震波碎石和胆汁酸溶石治疗成功后,10例于12±2月内胆囊结石再次复发(复发组),另10例配对对照随访22±3月没有复发(未复发组)。 两组分别口服同位素标记的胆酸(CA)、鹅脱氧胆酸(CDCA)和脱氧胆酸(DCA)各50mg,用气液色谱分析仪——单离子分光光度计法测     

胆汁酸、微生物和代谢

<正>胆汁酸的结构1932年首先被描述,它被公认在脂肪吸收、胆固醇分泌和胆固醇结石形成的生理和病理生理过程中起着非常重要的作用。人初级胆汁酸-胆酸(CA)和鹅去氧胆酸(CDCA)由肝脏合成,分泌到肠道,经细菌生物转化形成次级胆汁酸包括脱氧胆酸(DCA)和胆石酸(LCA)。上世纪60年代以来,已公认胆汁酸代谢中微生物起重要作用。胆汁酸信号通路核受体法尼酯X受体(FXR)与Takeda G蛋白偶联受体5     

肝脏对胆汁形成和分泌的作用

胆汁由肝细胞制造,分泌进入胆道系统,进餐后胆囊收缩,将胆汁排入十二指肠,帮助脂肪和脂溶性物质吸收。一、胆汁成分胆汁是一种复杂的液体,固体成分不到5 %,与血浆等渗,主要由水、无机电解质和有机物如胆汁酸、磷脂、胆固醇和胆色素等组成(表1)。胆汁酸是胆汁中最主要的有机物质,分为初级胆汁酸和次级胆汁酸。初级胆汁酸与牛磺酸和甘氨酸形成结合胆汁酸,更具水溶性。肠道细菌将初级胆汁酸分解为脱氧胆酸和石胆酸称次级胆汁酸。脱氧胆酸在末端回肠重吸收,石胆酸大部分随粪排出,小部分重吸收。表1　胆汁的主要成分成分浓度mmol/L水占95 %电解…     

乙肝相关慢加急性肝衰竭患者粪便胆汁酸谱变化的研究

目的检测乙肝相关慢加急性肝衰竭患者粪便胆汁酸谱水平,了解其在疾病发展中的意义。方法选取20例乙肝相关慢加急性肝衰竭患者为观察组,随机选取14名体检健康者作为对照组。应用高效液相色谱(HPLC)法检测两组粪便胆汁酸(胆酸、石胆酸、脱氧胆酸、鹅脱氧胆酸、熊脱氧胆酸及总胆汁酸)的水平。结果观察组粪便胆酸水平高于对照组(P0.05),石胆酸、脱氧胆酸、鹅脱氧胆酸、熊脱氧胆酸及总胆汁酸水平与对照组相比差异无统计学意义(P0.05)。伴/不伴肝性脑病两组患者,伴/不伴腹水两组患者,Child-Pugh B级与C级两组患者胆汁酸水平差异无统计学意义(P0.05)。结论乙肝相关慢加急性肝衰竭患者粪便胆酸水平较正常人升高,但总胆汁酸和其他胆汁酸水平与正常人相比无显著差异。     

炎症性肠病患者血清胆汁酸谱的研究

背景:炎症性肠病(IBD)发病率不断升高,其病因和发病机制尚未完全明确。研究发现,胆汁酸代谢紊乱在实验性结肠炎的病理进程中起重要作用,但其与IBD发病的相关性尚未见报道。目的:探讨IBD患者血清胆汁酸谱的变化。方法:选取上海新华医院7名健康对照、15例溃疡性结肠炎(UC)和16例克罗恩病(CD),采用高效液相色谱-质谱法检测血清胆汁酸谱。结果:与对照组相比,UC和CD患者血清初级胆汁酸胆酸(CA)、鹅去氧胆酸(CDCA)、甘氨胆酸(GCA)、牛磺胆酸(TCA)、甘氨鹅去氧胆酸(GCDCA)含量无明显差异(P0.05);UC患者次级胆汁酸去氧胆酸(DCA)含量显著降低(P0.05),CD患者甘氨去氧胆酸(GDCA)和牛磺去氧胆酸(TDCA)含量显著降低(P0.05),UC和CD患者血清石胆酸(LCA)显著降低(P0.05)。结论:IBD患者血清胆汁酸谱发生显著改变,提示其可能参与IBD病理进程。     

胆汁酸与大肠癌相关性的荟萃分析

目的 为了阐明粪便中总胆汁酸和单一胆汁酸的浓度是否与大肠癌的发生有关,我们对目前所有相关文献进行了荟萃分析.方法 检索以下电子数据库:Pubmed、Embase、the Cochrane Controlled Trials Register、the Science Citation Index和中文科技期刊数据库.根据纳入标准,纳入有关评价粪便胆汁酸和大肠癌/腺瘤关系的观察性试验.文献必需报道了患者和对照组的粪便中总胆汁酸、鹅脱氧胆酸、脱氧胆酸或石胆酸的浓度.我们计算加权均数差(weighted mean difference,WMD)和95%可信区间(95%confidence interval,CI).通过漏斗图肉眼观察是否存在发表偏倚,并做Begg和Egger检验进一步验证.结果 我们检索到了20个病例对照研究或队列研究(共1226例).无论是固定效应模型,还是随机效应模型,对所有研究进行汇总后均未发现粪便中总胆汁酸和大肠癌/腺瘤存在联系(WMD0.61,95% CI 0.35～1.57)mg/g冻干粪).相比对照组,大肠癌/腺瘤巾鹅脱氧胆酸、脱氧胆酸和石胆酸的浓度显著增加,分别为WMD 0.16、0.40、0.32,95% CI 0.00～0.32,0.18～0.61,0.12～0.53 mg/g冻干粪.然而初级胆汁酸和次级胆汁酸浓度却并无差异.结论 粪便中总胆汁酸与大肠癌/腺瘤无关联,但鹅脱氧胆酸和石胆酸可能涉及大肠癌的发生,脱氧胆酸则可能同大肠癌和大肠腺瘤都存在联系.     

节食状态下大鼠体内胆汁酸的变化及其机制的研究

目的探讨长期节食状态下大鼠体内胆汁酸的变化及其机制。方法 20只健康雄性Wistar大鼠分为对照组和节食组, 每组10只。对照组大鼠正常量饮食, 节食组大鼠给予正常饮食量的50%饲养, 12周后麻醉, 采集各组大鼠血清、胆汁、肝脏和回肠组织样本, 分离腹部脂肪称重, 并计算腹部脂肪/体重比。计算胆汁流速。采用试剂盒和高效液相色谱串联质谱法测定各样本中总胆汁酸(TBA)及β-鼠胆酸(β-MCA)、牛磺β-鼠胆酸(Tβ-MCA)、胆酸(CA)、牛磺胆酸(TCA)、甘氨胆酸(GCA)、鹅去氧胆酸(CDCA)、甘氨鹅去氧胆酸(GCDCA)、去氧胆酸(DCA)、牛磺去氧胆酸(TDCA)、甘氨去氧胆酸(GDCA)、石胆酸(LCA)、甘氨石胆酸(GLCA)、牛磺猪去氧胆酸(THDCA)、牛磺熊去氧胆酸(TUDCA)、甘氨熊去氧胆酸(GUDCA)的浓度, 采用实时荧光定量聚合酶链反应测定肝脏和回肠组织法尼醇X受体(Fxr)"肠-肝轴"通路上胆汁酸相关核受体、代谢酶和转运体小异二聚体伴侣(Shp)、成纤维细胞生长因子15(Fgf15)、胆固醇7α-羟化酶(Cyp7a1)、甾醇12α-羟化酶(Cyp8b1...     

小肠动力障碍对胆固醇结石形成影响的研究进展

小肠动力障碍及小肠移行性复合运动(migrating motor complex,MMC)减弱对胆固醇结石形成的影响作用日益受到重视。小肠动力障碍及MMC减弱间接地使胆汁中脱氧胆酸(deoxycholic acid,DCA)浓度增高:DCA本身可以使肠转运减慢,肠道吸收胆固醇增加,胆汁中DCA比例过高直接抑制胆囊运动;DCA增强胆汁中胆固醇分泌;DCA增加富含胆固醇的“泡”(vesicles)不稳定性,增强胆汁胆固醇结晶形成。胆汁中DCA浓度增高,胆汁酸减少,胆囊运动减弱,从而促进胆固醇结石的形成。     

胆汁酸代谢改变对肝癌发生影响机制的研究

目的探讨胆汁酸(bile acids,BAs)各组分在乙型肝炎(乙肝)相关性肝细胞癌(hepatocellur carcinoma,HCC)患者血浆中的浓度及组成比例变化,进一步探索其与HCC的关系。方法用液相色谱-质谱联用手段分别检测24例HCC患者、15例乙肝肝硬化患者、6例慢性乙肝患者及12例健康对照者血浆中的各BAs组分的变化。用实时荧光定量PCR与免疫组织化学法检测15例肝癌组织与癌旁组织中IL-1β的表达水平。结果在24例HCC患者中,BAs组分胆酸、鹅脱氧胆酸、牛磺脱氧胆酸、石胆酸、甘氨鹅脱氧胆酸、甘氨脱氧胆酸相比乙肝肝硬化与健康对照组有明显升高,差异均有统计学意义(P均0.05),其中石胆酸浓度在不同临床分期患者中差异有统计学意义,C期明显高于B期和A期。癌组织中IL-1β的表达水平低于癌旁组织。结论血浆胆汁酸中石胆酸的浓度增高与肝癌进展相关,有可能成为HCC进展的评价指标。     

婴幼儿的胆汁酸代谢及其异常

胆汁酸是由带羟基的类固醇和脂肪侧链构成，是胆汁的主要成份。其来源有二，一是在肝脏内胆固醇合成的初级胆汁酸(包括胆酸和鹅脱氧胆酸)，二是初级胆汁酸在肠道经细菌水解和7-α-脱羟基转变而来的二级胆汁酸(包括脱氧胆酸、石胆酸和熊脱氧胆酸)。     

Bile acid metabolism in patients with Crohn's disease in terminal ileum

Bile acid metabolism was studied by means of the fractional turnover rate or orally ingested 14C-labeled taurocholic acid and by gas chromatographic determination of fecal excretion of the bile acids cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), and lithocholic acid (LCA). Thirty patients with Crohn's disease (CD) of the small bowel, of whom 19 had been operated on with limited ileal resections, were studied and compared with 11 healthy volunteers. The unoperated group of CD patients did not show significant increase in bile acid excretion in the stools in contrast to the CD patients with ileal resection. The fecal excretion consisted mostly of primary bile acids, and a significant correlation between length of resection and bile acid excretion was found (rs = 0.81, p less than 0.01). The fractional turnover rate of CA + DCA was significantly increased in both unoperated (0.21 l/day) and operated (0.44 l/day) patients compared with normal controls (0.06 l/day). The bile acid pool of CA + DCA, however, was normal in patients with ileal resections, indicating a compensatory increase in bile acid synthesis. In unoperated patients the bile acid pool of CA + DCA was slightly decreased (3.1 mmol) compared with operated patients (6.2 mmol) and normal controls (4.8 mmol). The pool size was not significantly correlated to mean transit time of dietary residue, feces excretion, loss of weight, or amount of fat in feces. The mean transit time of dietary residue was decreased in both operated and unoperated CD patients.     

Biliary bile acids in the gall-bladder and the common bile duct of patients with anomalous pancreaticobiliary ductal junction

The high incidence of biliary tract carcinoma in patients with anomalous pancreaticobiliary ductal junction (APBDJ) with or without choledochal cyst (CC) has been well documented. Twenty-two patients with APBDJ were divided into three groups: Group A, four patients not associated with CC and biliary tract carcinoma; Group B, 13 patients with CC but without biliary tract carcinoma; and Group C, five patients with biliary tract carcinoma (four with and one without CC). Profiles of bile acids in the gall-bladder and/or common bile duct were analysed in these patients and compared with those in the control patients with cholecystlithiasis to examine the hypothesis that the levels of deoxycholic acid (DCA) and lithocholic acid (LCA) are elevated in patients with APBDJ because these secondary bile acids are mutagenic. Bile acids were quantified by gas—liquid chromatography. Total bile acid concentration in the gall-bladder bile was significantly lower in any group with APBDJ than that of controls. In the gall-bladder, increased proportion of chenodeoxycholic acid (CDCA) in Groups A and B, decreased proportion of DCA in Group B and increased proportion of cholic acid (CA) in Group C were found in bile. In the bile duct, total bile acid concentration and proportion of DCA were significantly low in bile from Group C and decreased proportion of DCA and increased proportion of CDCA were found in bile from Group B. In both the gall-bladder and hepatic bile, proportion of LCA was not significantly different between any intergroups. Thus no increase of DCA and LCA was found in either the bile from the gall-bladder and the bile duct of APBDJ patients. It is concluded that bile acid plays little role, if any, in the pathogenesis of biliary tract carcinoma in patients with APBDJ.     

Changes in bile acid composition and effect on cytolytic activity of fecal water by ursodeoxycholic acid administration: a placebo-controlled cross-over intervention trial in healthy volunteers

BACKGROUND: Ursodeoxycholic acid (UDCA) has been shown to affect membrane-damaging effects of bile acids in vitro and fecal bile acid composition in rats. This study evaluates the effect of UDCA on fecal bile acid composition and on cytolytic activity of fecal water in man to clarify the potential chemopreventive role of UDCA for colorectal cancer. METHODS: In this placebo-controlled crossover intervention trial, the effect of 900 mg/day UDCA orally in 15 healthy volunteers was studied. At the end of each 4-week period, 72 h feces were collected. Total and individual bile acids in feces were determined by gas chromatography and soluble bile acids were analyzed by high-performance liquid chromatography. Cytolytic activity of fecal water was measured using an erythrocyte lysis assay. RESULTS: In feces, the percentages of primary bile acids-cholic acid (CA) and chenodeoxycholic acid (CDCA)-and of secondary bile acid-deoxycholic acid (DCA) - decreased after supplementation with UDCA, whereas those of UDCA and LCA increased from 2.7 +/- 0.4% to 23.7 +/- 2.6%, P < 0.0001 and from 26.2 +/- 1.2% to 49.4 +/- 1.8%, P < 0.0001 respectively. The concentrations of these two bile acids in fecal water also increased after UDCA administration from 7.8 +/- 1.9 micromol/l to 47.0 +/- 6.7 micromol/l (UDCA), P < 0.0001 and from 2.5 +/- 0.6 micromol/l to 18.3 +/- 4.1 micromol/l (LCA), P < 0.002, respectively. Cytolytic activity of fecal water was not affected by UDCA. CONCLUSION: These results do not support a protective effect of UDCA supplementation against colorectal cancer in man.     

Changes in Bile Acid Composition and Effect on Cytolytic Activity of Fecal Water by Ursodeoxycholic Acid Administration: a Placebo-Controlled Cross-over Intervention Trial in Healthy Volunteers

Background: Ursodeoxycholic acid (UDCA) has been shown to affect membrane-damaging effects of bile acids in vitro and fecal bile acid composition in rats. This study evaluates the effect of UDCA on fecal bile acid composition and on cytolytic activity of fecal water in man to clarify the potential chemopreventive role of UDCA for colorectal cancer. Methods: In this placebo-controlled crossover intervention trial, the effect of 900 mg/day UDCA orally in 15 healthy volunteers was studied. At the end of each 4-week period, 72 h feces were collected. Total and individual bile acids in feces were determined by gas chromatography and soluble bile acids were analyzed by high-performance liquid chromatography. Cytolytic activity of fecal water was measured using an erythrocyte lysis assay. Results: In feces, the percentages of primary bile acids--cholic acid (CA) and chenodeoxycholic acid (CDCA)--and of secondary bile acid--deoxycholic acid (DCA)--decreased after supplementation with UDCA, whereas those of UDCA and LCA increased from 2.7 ± 0.4% to 23.7 ± 2.6%, P < 0.0001 and from 26.2 ± 1.2% to 49.4 ± 1.8%, P < 0.0001 respectively. The concentrations of these two bile acids in fecal water also increased after UDCA administration from 7.8 ± 1.9 μmol/l to 47.0 ± 6.7 μmol/l (UDCA), P < 0.0001 and from 2.5 ± 0.6 μmol/l to 18.3 ± 4.1 μmol/l (LCA), P < 0.002, respectively. Cytolytic activity of fecal water was not affected by UDCA. Conclusion: These results do not support a protective effect of UDCA supplementation against colorectal cancer in man.     

Role of bile acids and metabolic activity of colonic bacteria in increased risk of colon cancer after cholecystectomy

Since the metabolic activity of the colonic flora plays a definite role in colon cancer and an increased incidence of this disease is reported after cholecystectomy, we studied the metabolic activity of the colonic flora in a group of postcholecystectomy patients and matched controls by measuring, as representative end products of the bacterial metabolism, their fecal bile acids (BA), fecal 3-methylindole (SK) and indole (IN), and respiratory methane and hydrogen. Patients had significantly higher SK and lower IN, and, among BA, higher lithocholic (LCA) and chenodeoxycholic acid concentrations and LCA/deoxycholic acid ratio in the stools than controls. Similar differences from controls were reported for colon cancer. Comparable bacterial metabolic activities are thus operative in the large bowel of postcholecystectomized and colon cancer patients. This supports the biological plausibility of the association of cholecystectomy and colon cancer.     

Postprandial Conjugated and Unconjugated Serum Bile Acid Levels after Proctocolectomy with Ileal Pouch-Anal Anastomosis

Salemans JMJI, Nagengast FM, Tangerman A, van Schaik A, de Haan AFJ, Jansen JBMJ. Postprandial conjugated and unconjugated serum bile acid levels after proctocolectomy with ileal pouch-anal anastomosis. Scand J Gastroenterol 1993;28:786-790.

In patients with ileal pouch-anal anastomosis (IPAA) bile acid reabsorption may be impaired, and stasis may lead to deconjugation and dehydroxylation of bile acids as a result of bacterial overgrowth. We therefore studied fasting and postprandial conjugated and unconjugated serum levels of cholic (CA), chenodeoxycholic (CDCA), and deoxycholic acid (DCA) in 11 patients who underwent proctocolectomy with IPAA and in 11 healthy controls. Fasting levels of conjugated DCA but not CA and CDCA were significantly lower in IPAA patients. Postprandially, conjugated bile acid levels were significantly lower in IPAA patients. Postprandial unconjugated CA levels were significantly higher and CDCA levels tended to be higher in IPAA patients, whereas unconjugated DCA levels were lower in IPAA patients. These data suggest that reabsorption of conjugated bile acids is impaired after IPAA; deconjugation of bile acids may result from bacterial overgrowth secondary to stasis in the pouch; and dehydroxylation of bile acids is decreased after proctocolectomy with IPAA.     

Biliary bile acids in primary biliary cirrhosis: effect of ursodeoxycholic acid.

Bile acid composition in fasting duodenal bile was assessed at entry and at 2 years in patients with primary biliary cirrhosis (PBC) enrolled in a randomized, double-blind, placebo-controlled trial of ursodeoxycholic acid (UDCA) (10-12 mg/kg/d) taken as a single bedtime dose. Specimens were analyzed by a high-pressure liquid chromatography method that had been validated against gas chromatography. Percent composition in bile (mean +/- SD) for 98 patients at entry for cholic (CA), chenodeoxycholic (CDCA), deoxycholic (DCA), lithocholic (LCA), and ursodeoxycholic (UDCA) acids, respectively, were 57.4 +/- 18.6, 31.5 +/- 15.5, 8.0 +/- 9.3, 0.3 +/- 1.0, and 0.6 +/- 0.9. Values for CA were increased, whereas those for CDCA, DCA, LCA, and UDCA were decreased when compared with values in normal persons. Bile acid composition of the major bile acids did not change after 2 years on placebo medication. By contrast, in patients receiving UDCA for 2 years, bile became enriched with UDCA on average to 40.1%, and significant decreases were noted for CA (to 32.2%) and CDCA (to 19.5%). No change in percent composition was observed for DCA and LCA. Percent composition at entry and changes in composition after 2 years on UDCA were similar in patients with varying severity of PBC. In patients whose bile was not enriched in UDCA (entry and placebo-treated specimens), CA, CDCA, DCA, and the small amount of UDCA found in some of these specimens were conjugated to a greater extent with glycine (52%-64%) than with taurine (36%-48%). Treatment with UDCA caused the proportion of all endogenous bile acids conjugated with glycine to increase to 69% to 78%, while the proportion conjugated with taurine (22%-31%) fell (P <.05). Administered UDCA was also conjugated predominantly with glycine (87%).     

7 alpha-dehydroxylating bacteria enhance deoxycholic acid input and cholesterol saturation of bile in patients with gallstones

BACKGROUND & AIMS: Excessive deoxycholic acid (DCA) in the bile acid pool with cholesterol supersaturation of bile is prevalent in patients with cholesterol gallstones (CGs). This study examined whether this is caused by enhanced conversion of cholic acid (CA) to DCA by intestinal bacteria. METHODS: Ten patients with CGs with DCA excess (DCA/CA pool ratio, > 1.5) and 10 patients with low DCA (ratio, < 1.0) were compared for CA and DCA kinetics, ileal absorption of 75-Se-homotaurocholic acid (75-SeHCAT), and CA-7 alpha-dehydroxylation activity of the fecal microflora; the effects of ampicillin treatment on DCA excess were studied in 7 patients. RESULTS: Patients with DCA excess and low DCA differed (P < 0.01) in the pool size of CA (mean, 5.8 vs. 34) and DCA (28 vs. 11 mumol/kg) and DCA input (8.8 vs. 3.5 mumol.kg-1.day-1. Whereas 75-SeHCAT excretion was similar, CA-7 alpha-dehydroxylation activity and levels of fecal 7 alpha-dehydroxylation bacteria were 3- fold and 1000-fold higher (P < 0.01) in patients with DCA excess, respectively. Ampicillin treatment decreased (P < 0.02) CA-7 alpha- dehydroxylation activity and DCA pool size, expanded the CA pool to normal size, and lowered cholesterol saturation of bile. CONCLUSIONS: Increased CA-7 alpha-dehydroxylation activity of the intestinal microflora may be an important factor for CG formation or growth in these patients. (Gastroenterology 1996 Dec;111(6):1611-20)     

Effects of bile acids on proliferation and ultrastructural alteration of pancreatic cancer cell lines

AIM: Pancreatic cancer in the head is frequently accompanied by jaundice and high bile acid level in serum. This study focused on the direct effects of bile acids on proliferation and ultrastructural alteration of pancreatic cancer. METHODS: Pancreatic cancer cell lines PANC-1, MIA PaCa-2 and PGHAM-1 were explored in this study. The cell lines were cultured in media supplemented with certain bile acids, CA, DCA, LCA, TCDC, TDCA and GCA. Their influence on cell growth was measured with MTI- assay after 72 h of incubation. Cell cycles of PANC-1 cells in 40μM of bile acids media were analyzed by flow cytometry. Ultrastructural alteration of PANC-1 cells induced by DCA was observed using scanning and transmission electron microscope (SEM and TEM). RESULTS: At various concentrations of bile acids andincubation time, no enhanced effects of bile acids on cell proliferation were observed. Significant inhibitory effects were obtained in almost all media with bile acids. DCA and CA increased the percentage of G0+G1 phase cells, while GCA and TDCA elevated the S phase cell number. Alter 48h of incqbation in DCA medium, PANC-1 cells showed some structural damages such as loss of their microvilli and vacuolization of organelles in cytoplasm. CONCLUSION: Bile acids can reduce proliferation of pancreatic cancer cells due to their direct cytotoxicity. This result implies that elevation of bile acids in jaundiced serum may inhibit pancreatic cancer progression.     

Diet,fecal bile acids,and neutral sterols in carcinoma of the colon

Increased concentrations of fecal bile acids and neutral sterols or their degradation products have been linked to certain diets and are implicated in colonic carcinogenesis. We measured fecal bile acid and neutral sterol concentrations by thin-layer and gas-liquid chromatography in 15 patients with colonic adenocarcinoma, 23 controls, and 16 patients with nongastrointestinal cancer. We compared these results with dietary intake. Detailed dietary histories showed no differences among the groups in the ingestion of calories, protein, fiber, fat, or carbohydrate. A wide variation in fecal concentration of individual bile acids and neutral sterols was found within each group, but no significant differences in the total bile acid or total neutral sterol per gram dry weight feces were found. Decreased coprostanol, coprostanone, and lithocholic acid excretion was found in the colon cancer group compared with controls. The fecal excretion of all bile acids and neutral sterols was lower significantly in the nongastrointestinal cancer patients with liver metastases as compared with those without. We conclude that total bile acid and total neutral sterol excretion is similar in the three groups, all ingesting similar diets. We cannot confirm reported increased excretion of total bile acids nor excessive bacterial conversion to degradation products in colonic cancer patients. Hepatic metastases correlate with decreased fecal excretion of both bile acids and neutral sterols, which may be due to diminished hepatobiliary excretion.