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Urinary excretion of bile acids in bile duct-ligated rats.

BACKGROUND: In patients with complete bile duct obstruction, the only pathway of bile acid elimination is through the urine. However, the urinary excretion of various bile acid conjugates in the presence of bile duct obstruction has not been clarified. Given this factor, the urinary excretion of various bile acids was compared in rats that were bile duct-ligated for 3 days. METHODS: After urinary bladder cannulation, radiolabeled bile acids were intravenously injected, and urine samples were collected every 2 h for 6 h, and radioactivity was counted. RESULTS: Urinary excretion (cumulative percent dose during 6 h) of taurocholate and cholate was similar (19.3% and 16.8%). Urinary excretion of tauroursodeoxycholate, lithocholate, and taurolithocholate-sulfate was less effective (12.7%, 9.8% and 2.1%, respectively). Cholate was mostly conjugated with taurine, and lithocholate was mostly conjugated with taurine and further hydroxylated. CONCLUSIONS: These results indicate that unconjugated bile acids were taken up by the liver and excreted into the blood after further biotransformation even under conditions of complete bile duct obstruction. Although bile acid sulfates are the major bile acids in the urine of patients with obstructive jaundice, monohydroxylated bile acids are considered not to be so effectively excreted into the urine, even with conjugation with taurine and sulfate, in rats.

Animals↗

Intraductal papillary neoplasm of the bile duct extending superficially from the intrahepatic to extrahepatic bile duct.

Intraductal papillary neoplasm of the bile duct (IPNB) or liver is a recently noted rare disease, and its pathogenesis remains unclear. Here we present a case of IPNB with an interesting morphology, which was treated by resection of the right hemiliver and extrahepatic bile duct. A 79-year-old woman was found to have a high alkaline phosphatase level and slight dilatation of the right intrahepatic bile duct on imaging studies. The right intrahepatic bile duct became dilated over a 2-year period; however, no solid mass could be detected, and tumor markers were not elevated. Hepatic resection was scheduled because a mucin-producing bile duct carcinoma of the liver was suspected. A right hemihepatectomy was conducted, and the extrahepatic bile duct was also resected after malignant cells were found in the surgical stump of the right bile duct and in the bile itself. Macroscopically, diffuse dilatation of the intrahepatic bile duct was noted, but no solid component or mucin within the duct was found. Histopathological findings revealed carcinoma in situ, IPNB, in the majority of intrahepatic bile ducts, with no lymph node metastasis, and it extended continuously to the epithelium of the common bile duct. No tumor recurrence or biliary dilatation was observed at follow-up 2 years after surgery. It is important to consider malignancy in the presence of a dilated bile duct and in the absence of any cause of occlusion. Complete resection of IPNB results in a good prognosis and no recurrence.

Aged↗

Bile secretion in the fistulated pig: effect of the method used for bile reinfusion.

The aim of this work was to investigate the effects on bile secretion of flow rate and site of reinfusion of the collected bile to the animal. Thirty-two pigs weighing 50 +/- 3 kg at the beginning of the experiment were fitted with a reentrant fistula in the lower common bile duct and in the upper duodenum. Bile collected from the bile duct was reinfused in four different ways (four groups of 8 animals each): into the duodenum or the lower common bile duct at a constant flow rate using a peristaltic pump, or into the duodenum or the lower common bile duct at a rate mimicking the flow rate of the secretion using an automatic apparatus. Reinfusing the bile into the lower common bile duct at a rate mimicking the secretion rate provided a daily bile acid production about 21% higher than the level recorded with the other three methods. This was mainly due to a higher bile acid concentration since the bile flow was only slightly affected by the treatment.

Animals↗

Dynamics of bile flow through the human choledochal sphincter following exploration of the common bile duct.

The opening pressure and flow rates through the sphincter of Oddi using the patient's own bile to prime the system were measured daily in 17 patients after cholecystectomy and exploration of the common bile duct. The sequential changes in these parameters were correlated with preoperative serum bilirubin, bile bacteriology, biliary lipid composition, and bile viscosity. The opening pressure fell from an initial value of 17.2 +/- 1.9 to 9.1 +/- 0.9 cm bile (p less than 0.01) on the seventh postoperative day, indicating a self-limiting hold-up following stone extraction. The low opening pressure after the fifth to sixth day is well below the maximal hepatic secretory pressure and suggests that the bile flow into the duodenum may be continuous after cholecystectomy. The flow rate through the sphincter measured at a fixed pressure head of 30 cm of bile increased from 23.9 +/- 3.9 to 40.0 +/- 6.1 ml during the same period (p less than 0.01). Presumably, the latter represents the maximal flow rate of bile through the sphincter of Oddi under physiological conditions. These changes in flow could not be explained by alterations in the bile viscosity during the study period. The increase in flow rate was significant only in the nonjaundiced group and correlated positively with the phospholipid concentration in the bile. There were no significant differences in opening pressure, flow rates, and biliary lipid concentrations between patients with sterile bile and those with positive bile cultures.

Adolescent↗

Inhibition and induction of bile acid synthesis by ketoconazole. Effects on bile formation in the rat.

The effects of ketoconazole, an antimycotic agent, and metyrapone, an inhibitor of mixed function oxidases, on bile acid synthesis were compared in the rat both in vitro and in vivo. In rat liver microsomes, ketoconazole was much more potent than metyrapone in inhibiting the activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in the synthesis of bile acids. The I50 values were 0.42 microM and 0.91 mM for ketoconazole and metyrapone, respectively. Intraduodenal administration of ketoconazole caused a rapid, dose-dependent reduction of bile acid synthesis in eight-day bile diverted rats. A single dose of 50 mg/kg reduced bile acid synthesis to 5% of control value; the same dose of metyrapone caused a reduction to only 85%. Inhibition of bile acid synthesis by ketoconazole was followed by a marked overshoot. At 28 hr after injection of 50 mg/kg of the drug, formation of bile acids was stimulated maximally by 45% compared to control value and remained elevated for more than 20 hr thereafter. Synthesis of all primary bile acids was affected to the same extent. Cholesterol 7 alpha-hydroxylase activity in livers of ketoconazole treated (30 mg/kg) rats with an intact enterohepatic circulation was increased by 70% at 16 hr after i.p. injection of the drug. During the very large decrease of biliary bile acid output with ketoconazole, bile flow rate was relatively increased, due to stimulation of the bile acid-independent fraction of bile flow. The latter effect can probably be explained as caused by biliary secretion of osmotically active metabolites of ketoconazole.

Animals↗

Influence of tacrolimus on bile acid and lipid composition in continuously drained bile using a rat model. Comparative study with cyclosporine.

Cholestatic effects have been reported for cyclosporine (CsA), but information is still limited for tacrolimus (TCR). The purpose of this study was to investigate the influence of TCR on biliary bile acid and lipid composition as compared with CsA, using a continuously bile-drained rat model. Adult male Wistar rats received TCR (0.4 mg/kg, 1 mg/kg, and 4 mg/kg) or CsA (2.5 mg/kg, 10 mg/kg, and 25 mg/kg) by intramuscular injection (i.m.) daily for 10 days. On day 7, the common bile duct of all rats was cannulated, then bile was continuously collected for the following 3 days. Bile flow, bile acid secretion rate (BASR), and biliary lipids secretion were measured for each of the groups. TCR increased bile acid-dependent flow (BADF) but with no statistical significance. However, this agent did not influence total bile flow and biliary lipids secretion, while bile acid-independent flow (BAIF) was significantly reduced and bile acid synthesis (mainly cholic acid, CA, synthesis) was increased. In contrast, CsA was cholestatic, showing a tendency to reduce both BADF and BAIF. BASR was dose-dependently suppressed, especially in chenodeoxycholic acid (CDCA). Furthermore, biliary lipids secretions were also significantly decreased under a higher dose of CsA. TCR increased BADF with no influence on total bile flow, having a stimulating effect on CA production, although CsA dose-dependently diminishes CDCA production and consequently reduced bile secretion. Our results suggest that TCR is a less effective agent on cholestasis as compared to CsA.

Animals↗

Short-term feeding of a diet enriched in phospholipids increases bile formation and the bile acid transport maximum in rats.

Earlier studies suggested that the secretory rate maximum (SRm) of bile acid and the cholestasis which occurs after the SRm is reached may be determined by the hepatic or extrahepatic biliary phospholipid pool. We therefore investigated whether bile formation and the bile acid SRm could be influenced by feeding a diet enriched in phospholipids. Male rats were fed phospholipid (PLD) or triacylglycerol (TgD)-enriched diet for 3 days, and bile formation as well as biliary lipid output were measured on the 4th day. In other similarly fed groups, cholic acid was infused in stepwise increasing doses to determine the effect of PLD on the SRm of cholic acid. The plasma lipid levels were significantly lower in PLD and TgD diets compared to basal diet. But, while the levels of total cholesterol (CH), HDL-CH, and phospholipid (PH) were not significantly altered by PLD compared to TgD, the triacylglycerol levels were markedly increased by PLD. In the liver of PLD fed rats, triacylglycerol and CH ester contents decreased by 39 and 62%, respectively, while free CH and PH contents were not significantly changed. The PLD significantly augmented spontaneous bile flow, bile acid, PH and CH secretion rates compared to TgD diet (65, 124, 164 and 654%, respectively). The enhanced biliary secretory function was associated with an increase in pericanalicular vacuoles and diverticuli in centrilobular hepatocytes. Compared to TgD fed rats, PLD rats showed a 2-fold decrease in the ratio of cholic acid/chenodeoxycholic acid in bile and a significant decrease in the % contribution of taurine conjugated BA. The PH fatty acids in bile were similar in both groups except that in PLD group the % contribution of C18:2 was higher than in TgD group. No differences were found in plasma membrane CH/PH content or total fatty acid composition. During bile acid infusion, the SRm and the total cholic acid secreted were significantly higher in the PLD than in the TgD rats. Moreover, the cholestatic response observed after high bile acid dose was markedly reduced by PLD. The results show that short-term feeding of PLD induces changes in CH and bile acid metabolism which result in enhanced biliary output of CH and PH. The enhanced pool of biliary lipid may protect plasma membranes from the deleterious effects of high bile acid concentrations.

Animals↗

Adenovirus-mediated p53 gene transfer to the bile duct by direct administration into the bile in a rat cholangitis model.

BACKGROUND: Hepatolithiasis is a common disease in East Asia and its aggravating factor is bile duct stenosis because of refractory cholangitis. This study investigated the feasibility of gene therapy for bile duct stenosis by administration of p53 adenoviral vectors into the bile. MATERIALS AND METHODS: Adenoviral vectors (AxCALacZ or AxCAhp53) were injected transpapillarily into the bile in the bile duct in a rat model of cholangitis. The extent and duration of the gene expression was evaluated with X-gal staining and p53 immunostaining. The bile duct tissue was examined to evaluate the inhibitory effect on the proliferative changes at 3 and 7 days after administration, and Ki-67 labeling index was determined. RESULTS: beta-galactosidase was expressed in the bile duct epithelia, the bile duct wall and the surrounding connective tissue. The expression of beta-galactosidase was detected at 4 weeks after the administration. Mean thickness of the bile duct wall at 7 days was 343.2 +/- 14.0 microm for the AxCAhp53 group, 446.5 +/- 25.3 microm for the AxCALacZ group and 447.1 +/- 53.4 microm for the control group. The proliferation of the bile duct wall was significantly suppressed in the AxCAhp53 group (P < 0.05). Maximum thickness was 408.0 +/- 23.9 microm for the AxCAhp53 group (P < 0.05), 650.0 +/- 49.3 microm for the AxCALacZ group, and 590.0 +/- 64.3 microm for the control group. Mean Ki-67 labeling index for the three groups was 20.7% (P < 0.05), 34.4% and 37.4%, respectively. CONCLUSIONS: P53 gene transfer by administration of the adenoviral vector into the bile suppressed the proliferative changes in the bile duct in a rat cholangitis model.

Adenoviridae↗

Effect of various bile salts on calcium concentration and calcium carbonate saturation of rat bile.

To establish whether the calcium-binding capacities of the bile salts play an essential role in their stimulatory effects on biliary calcium secretion, we compared (1) the effects of tauro- and glycoconjugates of ursodeoxycholate (TUDC-GUDC) and cholate (TC-GC) on biliary calcium in bile fistula rats, and (2) the in vitro calcium-binding capacities of mixed micelles containing the same bile salts. The increase of biliary calcium depended on the infused bile salt in the following order: GUDC greater than GC = TUDC greater than GC). The same order was obtained in vitro, so that there was a linear relationship between the slopes of the [Ca] vs. [bile salts] regression lines in vivo and the binding percentages of the four bile salts. Biliary ionized calcium concentration was almost independent of bile salt concentration. However, hepatic bile was supersaturated with calcium carbonate in the presence of the four bile salts. Our results suggest that biliary calcium concentration increases in relation to the calcium-binding capacity of the various bile acids so that ionized biliary calcium remains in equilibrium with plasma. As a result, bile saturation with calcium is almost completely independent of bile salt secretion.

Animals↗

Detection of hepatitis C virus in the bile and bile duct epithelial cells of hepatitis C virus-infected patients.

The pathobiology of hepatitis C virus (HCV) in the biliary system has not been clarified yet, although bile duct damage is a histological finding characteristic of chronic hepatitis C. In this study, we examined whether HCV infects bile ducts and is released into the bile. Twelve patients positive for serum HCV antibody were examined in this study, and eight were seropositive for HCV RNA by polymerase chain reaction (PCR). For those who underwent abdominal surgery, the bile was aspirated from the gall bladders by fine needle puncture. Five underwent wedge liver biopsy. Series of saline-diluted bile were assayed for HCV RNA by PCR to determine the HCV RNA titers. To examine HCV expression in the biliary system, the liver specimens were immunostained using monoclonal antibodies to the HCV proteins. HCV RNA was detected in the bile of 5 patients with high serum HCV RNA load (> or = 2.5 Meq/mL). Comparison of viral loads between serum and bile revealed that the HCV RNA level in the bile was as high as that in serum. Furthermore, immunohistological study showed that bile duct epithelial cells were infected with HCV. In contrast, HCV was not found in either the bile or bile duct of patients seronegative for HCV RNA or with low serum HCV load (< or = 1.1 Meq/mL). These findings suggest that the biliary system is involved in the pathobiology of HCV and that the bile is as highly infectious as the serum.

Aged↗

Altered bile acid profiles in duodenal bile and urine in diabetic subjects.

The bile acid composition in duodenal bile was analysed in 22 diet-treated and 11 insulin-treated middle-aged patients with diabetes mellitus and in 20 normoglycaemic controls. In 10 subjects with diabetes mellitus the bile acid profile in urine was also investigated. In the non-insulin-dependent diabetic patients the percentage of cholic acid was reduced and that of deoxycholic acid increased. As a highly significant finding there was a three-fold increase of the percentage of 12-ketolithocholic acid in duodenal bile in non-insulin-dependent diabetics, whereas the bile acid composition in insulin-dependent diabetics was similar to that in a control group. The percentage of 12-ketolithocholic acid in duodenal bile was positively correlated to the percentage in urine. In nine of the subjects studied, 12-ketolithocholic acid was the major individual bile acid in urine. It constituted 36.3 +/- 4.4% of the bile acids analysed and the excretion was 6.1 +/- 2.3 mumol 24 h-1. Together with 3 alpha, 12 beta-dihydroxy-5 beta-cholanoic acid it was predominantly present in the glycine conjugate fraction, whereas in bile its conjugation was similar to that of the other bile acids. The results may reflect an increased formation of secondary bile acids from cholic acid combined with a metabolic disturbance in non-insulin-dependent diabetics affecting the oxidoreduction of bile acids at C-12.

Adult↗

Effect of increased bile flow and bile acid secretion on the hepatic elimination of sodium valproate in the cat.

The effect of increased bile flow and hepatic bile acid flux on the systemic clearance and hepatic elimination of intravenously administered sodium valproate was studied in the bile fistula cat. Taurochenodeoxycholic acid (TCDC), tauro-3 alpha, 7 beta-dihydroxy-12-keto-5 beta-cholanoic acid (T12K), SC-2644, and secretin were infused intravenously to vary bile flow and biliary bile acid secretion. Control animals were infused with 0.15 mol/l NaCl. Less than 1% of the drug administered to controls appeared as unchanged valproate in the bile over 6 h. Although SC-2644, T12K, and secretin significantly increased biliary excretion of valproate, it did not exceed 2% of the intravenous dose. Biliary clearance was directly related to the rate of bile flow, but not to the bile acid flux. By contrast, 18-19% of the dose appeared in bile as metabolite in controls, and none of the choleretic agents significantly increased this percentage. As a result, systemic clearance of valproate was unaltered. We conclude that the movement of unchanged valproate into bile is consistent with a process of simple diffusion. The fact that choleretic agents do not increase metabolite excretion into bile suggests that metabolite formation may be the rate-limiting step in the hepatic elimination of valproate, rather than transport and excretion of metabolites into bile.

Animals↗

The role of acinar zone 3 hepatocytes in bile formation: influence of bromobenzene treatment on bile formation in the rat.

The role of zone 3 hepatocytes in bile formation was determined when they were selectively destroyed by 3.8 mmol/kg b.w. of bromobenzene injected i.p. for 48 h, as compared to appropriate controls. Bromobenzene treatment resulted in 29 +/- 4.4% hepatic lobule necrosis localized in the zone 3 hepatocytes. Although bile flow and bile salt-independent flow were not affected, this treatment was associated with a significant reduction in bile salt, and phospholipid secretion. The bile salt pool and bile salt synthesis were also significantly decreased. These results suggest that necrosis of zone 3 hepatocytes induced by bromobenzene reduced bile acid synthesis which decreased bile salt pool and affected bile salt and phospholipid secretion rates. However, necrosis of zone 3 hepatocytes did not affect bile flow or the bile salt-independent flow, suggesting that hepatocytes of zones 1 and 2 maintained the normal bile salt-independent flow when zone 3 hepatocytes were damaged.

Animals↗

The effects of bile salt and raw bile on the intestinal absorption of micellar fatty acid in the rat in vitro.

1. The uptake, esterification and transport of [(14)C]oleic acid were studied using sacs of rat everted small intestine incubated in 25 ml. of a buffered mixture of sodium taurocholate, glyceryl mono-oleate and (14)C-labelled oleic acid in micellar form.2. Intestine obtained from bile fistula rats (bile duct cannulated 48 hr previously) showed elevated rates of (14)C uptake into the tissue total lipid compared with sham-operated controls.3. Nearly all of the excess (14)C uptake in the bile fistula group was in the form of free fatty acid. Both groups showed similar rates of [(14)C]oleic acid incorporation into tissue triglyceride and also similar, though small, amounts transported into the serosal fluid.4. In further experiments using intestine from bile fistula rats the addition of 1 ml. of fresh rat bile to the incubation mixture reduced the (14)C uptake to approximately control levels. The addition of 2-3 ml. of fresh bile similarly reduced the uptake and increased (14)C incorporation into the triglycerides of mucosal tissue and serosal fluid.5. These responses were not entirely the result of the bile salts contained in fresh bile since increasing the taurocholate concentration per se caused uptake, esterification and transport all to increase. In the presence of the higher taurocholate concentration the addition of fresh bile still caused a decrease in (14)C uptake.6. There was no significant effect of either fresh bile or taurocholate on the transport of the 3-O-methyl analogue of D-glucose under comparable conditions.7. It is concluded that raw bile contains one or more components other than bile salts which may be important in determining fatty acid absorption.

Animals↗

Gall stone disease without gall stones--bile acid and bile lipid metabolism after complete gall stone dissolution.

Although bile acid and bile lipid metabolism have been studied in established cholelithiasis, little is known about them in patients destined to develop gall stones, but in whom the stones have not yet appeared (prestone gall stone disease). After confirmed complete gall stone dissolution and withdrawal of treatment, gall stones recur frequently. Before the stones reappear, these patients have 'poststone gall stone disease'. In 13 such patients we confirmed complete gall stone dissolution with two normal cholecystograms and in 11 of the 13 by normal ultrasonography, measured bile acid and bile lipid composition in fasting duodenal bile, bile acid synthesis from marker corrected three day faecal bile acid excretion, bile acid pool size using an abbreviated isotope dilution technique, 'steady-state' bile lipid secretion using a duodenal amino acid perfusion system and then calculated the enterohepatic cycling frequency of the bile acid pool and the relationship between pool size and body weight. The results confirm that after withdrawal of treatment the biliary cholesterol saturation index reverts to levels (1.6 +/- SEM 0.4) comparable with those before dissolution therapy first began (1.6 +/- 0.2; NS). The mean bile acid pool size in the 13 patients of 4.4 +/- 0.5 mmol was comparable with that in untreated gall stone patients. Pool size was significantly smaller in the nine non-obese patients (3.5 +/- 0.3), than in the four obese (6.0 +/- 0.8; p less than 0.05). It also correlated significantly with body weight (r = 0.72) and with %IBW (r = 0.79). The coefficients of variation for biliary bile acid, phospholipid and cholesterol secretion were high, but the mean hourly secretion rates were of the same order as those seen in untreated gall stone patients studied with the amino acid duodenal perfusion stimulus. These results provide a baseline for assessing the response to postdissolution treatment and may indicate metabolic events leading to gall stone formation.

Adult↗

Comparison of gall bladder bile and endoscopically obtained duodenal bile.

In 10 patients with gall stone disease (eight women, two men; mean (SD) age 47.4 (13) years), bile was obtained by endoscopic aspiration after stimulation of the gall bladder with ceruletid and also by fine needle puncture of the gall bladder under local anaesthetic. The total lipid concentration of the puncture bile samples was mean (SD) 11.9 (4.7) g/dl, significantly higher than the endoscopic bile samples (3.9 (3.3) g/dl, p less than 0.001). Total bile acids, phospholipids, and biliary cholesterol (expressed in mol%) and cholesterol saturation index showed no significant differences between the two types of samples. The glycocholic acid concentration in the endoscopically obtained bile (27.7 (6.6) mol% v 23.3 (5.4) mol%; p less than 0.01) was significantly higher than the puncture bile samples. Puncture bile exhibited a significantly shorter nucleation time (3.5 (3.3) days v 19.6 (11.9) days; p less than 0.001). For determination of the nucleation time, endoscopic bile aspiration after gall bladder stimulation with ceruletid led to adequately concentrated samples in 50% of the study subjects. Cholesterol monohydrate crystal formation in native bile was observed in six samples of puncture bile and in three samples of the endoscopically obtained bile. The presence of cholesterol crystals and the determination of nucleation time in the puncture bile were the best discriminants between cholesterol and pigment gall stones and correlated well with computed tomogram analysis.

Adult↗

Regulatory volume decrease stimulates bile flow, bile acid excretion, and exocytosis in isolated perfused rat liver.

To study the effect of volume regulation on bile secretory function, isolated perfused rat livers (IPRL) were exposed to hypotonic stress (45 mM NaCl) while bile flow and the biliary excretion of bile acids and horseradish peroxidase (HRP) were assessed. Hypotonic stress induced a biphasic increase in bile flow, which rose in the first minute from 1.1 +/- 0.2 to 1.7 +/- 0.1 microliter.min-1.g liver-1 (P less than 0.01), an effect attributed to rapid osmotic equilibration of water, then increased further between 3 and 5 min to 1.6 +/- 0.1 microliter.min-1.g liver-1 (P less than 0.01, followed by a subsequent return to baseline. HRP excretion in bile increased during the second peak of bile flow from 0.9 +/- 0.2 to 1.1 +/- 0.2 ng.min-1.g liver-1, P less than 0.01. Pretreatment with colchicine but not lumicolchicine completely abolished the latter increase in bile flow and HRP excretion as did BaCl2 (1 mM), an inhibitor of both K+ channels and regulatory volume decrease (RVD) in hepatocytes. When sodium taurocholate was infused (1 mumol/min), hypotonic stress induced an even larger increase in the second peak of bile flow (5.1 +/- 0.7 microliters/g liver, P less than 0.01) and higher rates of bile acid excretion than in control perfusions with bile acid (126.2 +/- 21.0 vs. 99.0 +/- 17.1 nmol.min-1.g liver-1, P less than 0.05). These data suggest that both bile flow and bile acid excretion are stimulated during RVD by mechanisms that involve both K+ channels and microtubule-dependent exocytosis at the canalicular (apical) membrane domain.

Animals↗

The role of bile carcinoembryonic antigen in diagnosing bile duct cancer.

It is known that the fluids bathing tumors might contain a higher level of the carcinoembryonic antigen (CEA) than those found in the blood. Therefore, we evaluated the role of bile CEA in diagnosing bile duct cancer. One hundred and thirty two patients were prospectively studied. The patients were divided into 3 groups: the bile duct cancer (n=32), pancreatic cancer (n=16), and benign biliary diseases (n=84) groups. Bile samples were obtained on the next day of the biliary drainage procedures. The mean bile CEA level in those with bile duct cancer (120.6 +/- 156.9 ng/mL) was significantly higher than those with pancreatic cancer and benign biliary diseases (32.0 +/- 28.5 ng/mL, 29.3 +/- 56.3 ng/mL). Using the level of 20 ng/mL, the sensitivity and specificity of bile CEA in the diagnosis of bile duct cancer from benign biliary diseases were 65.6% and 66.7%, respectively. Both the bile CEA and total bilirubin level were found to be an independent factor linked to bile duct cancer. This study result suggests that bile CEA level is a useful supplementary test for diagnosing bile duct cancer.

Adult↗