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PubMed1996

Tauroursodeoxycholic acid protects in vitro models of human colonic cancer cells from cytotoxic effects of hydrophobic bile acids.

Bile acids have been implicated as tumor promoters that enhance epithelial proliferation and the development of colonic tumors. This study investigated the effects of bile acids on the growth of in vitro models of human colonic epithelial cells. Cell lines with varying degrees of differentiation (Caco2, HT29, LS174T, and Lovo) were studied. Cell viability and number were measured by a tetrazolium (MTT) spectrophotometric assay. Enhanced cell growth was not observed with any bile acid over the range 10 nmol/L to 2.5 mmol/L. Cytotoxicity was consistently observed at concentrations of unconjugated bile acids greater than 0.1 mmol/L. The bile acid concentration at which 50% growth inhibition occurred was similar for all cell lines and increased in the following order: deoxycholic acid = chenodeoxycholic acid < taurodeoxycholic acid < ursodeoxycholic acid < taurochenodeoxycholic acid < cholic acid < tauroursodeoxycholic acid. Coincubation of tauroursodeoxycholic acid (TUDC) with taurodeoxycholic acid (TDC) or taurochenodeoxycholic acid (TDCD) reversed the short-term (30-minute) cytotoxicity and release of glycoprotein induced by TDC or TCDC regardless of differentiation status. In contrast, TUDC did not reverse the cytotoxicity of deoxycholic acid. Unconjugated ursodeoxycholic acid did not alter short-term cytotoxicity of any bile acid. These data indicate that bile acids do not stimulate cell growth in undifferentiated or differentiated colon cancer cell lines, in contrast to normal colonic epithelium in vivo. Bile acid cytotoxicity correlates with the relative hydrophobicity of the bile acid. Because tauroursodeoxycholic acid alters the cytotoxicity of hydrophobic bile acids in vitro, further understanding of bile acid interactions in the colon may have important implications in altering tumor promotion.

Bile Acids and Salts↗

PubMed1992

Hepatic uptake and processing of cholesterol and cholesteryl ester from chylomicron remnants: an in vivo study in the rat.

The metabolic fate of cholesterol in chylomicron remnants was studied after intravenous infusion into biliary drained rats. The remnants were radiolabelled with [3H]cholesterol in vivo, so that radioactivity was incorporated into both the unesterified (27% of label) and esterified (73% of label) cholesterol fractions, or with 14C-labelled unesterified cholesterol after exchange in vitro. Blood and bile samples were collected at intervals for 180 min, after which the animals were killed for analysis. The total amount of radioactivity found in the liver (46%) and bile (4.5%) after infusion of [3H] remnants was higher than that found when the label was 14C (33 and 2.7%, respectively). Radioactivity from 14C-labelled unesterified cholesterol was cleared more rapidly from the blood, but the distribution of the label between the lipoprotein fractions VLDL + LDL, HDL2 and HDL3 at the end of the experiment was similar to that found when total [3H]cholesterol was used. In experiments with both types of label, approximately 94% of the total radioactivity secreted into bile was associated with the bile acid, with only about 6% in biliary unesterified cholesterol, and these proportions did not change during 180 min. When the chylomicron remnants were labelled with total [3H]cholesterol the specific radioactivity of the bile acid, taurochenodeoxycholic acid, in the bile was approximately twice that observed when the label was unesterified [14C]cholesterol. The specific radioactivity of unesterified biliary cholesterol was very low in the latter case, but higher and more comparable to that of taurochenodeoxycholic acid in the former. Thus, the metabolic fate of chylomicron remnant cholesterol differs, depending on whether it is in the esterified or unesterified form, suggesting that hepatic cholesterol originating from the two fractions may mix to a different extent with the various intracellular pools. In addition, the experiments with 14C indicate that the behaviour of chylomicron remnant unesterified cholesterol resembles that exhibited by cholesterol in HDL more than that carried in VLDL or LDL.

Animals↗

PubMed1994

Papaverine inhibits bile acid excretion in isolated perfused rat liver.

We investigated the effects of papaverine on bile acid excretion into bile in the presence of infusions of taurocholic acid, tauroursodeoxycholic acid, taurochenodeoxycholic acid and taurodehydrocholic acid in a single-pass, isolated perfused rat liver model. Although continuous infusion of papaverine (1.6 mumol/min) did not reduce bile acid excretion in the presence of low-dose (1.0 mumol/min) infusions of taurocholic acid or tauroursodeoxycholic acid, papaverine significantly inhibited biliary excretion of bile acids in the presence of low-dose taurochenodeoxycholic acid (-50%) and high-dose (3.0 mumol/min) taurocholic acid (-54%), tauroursodeoxycholic acid (-37%) and taurodehydrocholic acid (-31%). During continuous infusion of taurocholic acid (3 mumol/min), a 15-min infusion of papaverine (3.2 mumol/min) reduced bile acid excretion significantly; however, total uptake of bile acid was slightly decreased by the papaverine infusion. Bile acid excretion increased over the baseline value after the papaverine infusion was stopped and then returned to baseline. These results suggest that papaverine does not affect the uptake phase of bile acids at the sinusoidal membrane but may affect the intracellular transport phase or the excretory phase at the bile canalicular membrane. When taurocholic acid was infused at a constant rate of 3 mumol/min for 20 min without papaverine and then stopped, bile acid excretion decreased gradually and was nearly zero by 52 min. Cumulative bile acid excretion in the 52 min after the end of the infusion reached 3.3 +/- 0.2 mumol/gm liver and represented the storage capacity of the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Biochemical and physiological evidence that bile acids produced and released by lake char (Salvelinus namaycush) function as chemical signals.

It has been hypothesized that faeces of juvenile lake char (Salvelinus namaycush) may contain chemical cues that mediate behaviour of conspecifics. However, our knowledge of bile acids naturally produced and released by fish is limited. Using HPLC, we fractionated bile acids produced and released by lake char and examined their stimulatory effectiveness using electro-olfactogram recordings. Taurocholic acid, taurochenodeoxycholic acid, taurooxocholanic acid, taurooxodeoxycholic acid 3alpha-sulphate, trace amounts of taurolithocholic acid and an unidentified sulphated bile steroid were found in bile and faeces. Bile acids were either taurine amidated or sulphated, or both. Lake char released an average of 4 nmol min(-1) bile acids per kilogram of body weight into their tank water. Urinary bile acids accounted for only a small portion of total bile acids released into water. Water and faeces contained higher proportion of taurochenodeoxycholic acid and sulphated bile acids (relative to taurocholic acid) than bile. The electro-olfactogram recordings demonstrated that bile acids released by lake char were detectable by their olfactory system at nanomolar concentrations, which is well below the levels of bile acids released into water. The exquisite olfactory sensitivity of lake char to water-borne bile acids released by their conspecifics is consistent with a role for these compounds as important chemical signals.

Animal Communication↗

PubMed2004

What doesn't kill you makes you stronger: how hepatocytes survive prolonged cholestasis.

The goals of the current study are to examine the extent and mechanisms of apoptosis in cholestatic liver injury and to explore the role of the transcription factor nuclear factor-kappa B (NF-kappaB) in protection against bile acid-induced apoptosis. Cholestatic liver injury was induced by bile duct ligation in Wistar rats. Furthermore, primary cultures of rat hepatocytes were exposed to glycochenodeoxycholic acid (GCDCA), tauroursodeoxycholic acid, taurochenodeoxycholic acid, and to cytokines. Apoptosis was determined by TUNEL staining, active caspase-3 staining, and by activation of caspase-8, caspase-9, and caspase-3. Limited hepatocyte apoptosis and increased expression of NF-kappaB-regulated anti-apoptotic genes A1 and cIAP2 were detected in cholestatic rat liver specimens. Bcl-2 expression was restricted to bile duct epithelium. In contrast to taurochenodeoxycholic acid and tauroursodeoxycholic acid, GCDCA induced apoptosis in a Fas-associated protein with death domain-independent pathway in hepatocytes. Although bile acids do not activate NF-kappaB, NF-kappaB activation by cytokines (induced during cholestasis) protected against GCDCA-induced apoptosis in vitroby upregulating A1 and cIAP2. GCDCA induces apoptosis in a mitochondria-controlled pathway in which caspase-8 is activated in a Fas-associated protein with death domain-independent manner. However, bile acid-induced apoptosis in cholestasis is limited. This could be explained by cytokine-induced activation of NF-kappaB-regulated antiapoptosis genes like A1 and cIAP2.

Comment↗

PubMedDate not supplied

Effect of a taurine-supplemented diet on conjugated bile acids in biliary surgical patients.

The effect of a taurine-supplemented diet on the level of conjugated bile acids in postoperative patients was investigated during two consecutive 5-day period. Eighteen hepatobiliary patients with choledochostomies and a specific T-tube insertion were collected and divided randomly into two groups. In group 1, an ordinary postoperative soft diet was prescribed for the first 5 postoperative days and then followed with a taurine-supplemented soft diet (40 mumol/kg per day) for 5 consecutive days. In group 2, the taurine-supplemented diet was prescribed in reverse. At the end of the two periods, on days 5 and 10, bile was collected via a T-tube with an inflatable balloon and low-pressure motor suction. Analysis of conjugated bile acids was done by high-performance liquid chromatography. The results showed that a taurine-supplemented diet increased the concentration of taurocholic acid, glycocholic acid, taurochenodeoxycholic acid, glycochenodeoxycholic acid, and total bile acid from 0.5, 1.9, 0.3, 1.4, and 4.7 mg/mL (on day 5) to 1.1, 3.5, 1.0, 2.6, and 8.9 mg/mL, respectively, on day 10 in group 1. Similar findings were noted in group 2. These results indicate that a taurine-supplemented diet may enhance the conjugation and secretion of bile acid in hepatobiliary patients.

Adult↗

PubMed1980

In vitro inhibition of platelet aggregation by bile salts.

In a series of in vitro experiments, the influence of bile salts on platelet aggregation by ADP or by collagen and on serotonin-14C release by collagen, was studied. Sodium salts of the following bile acids showed a clear inhibitory effect: glycochenodeoxycholic acid, taurochenodeoxycholic acid, glycocholic acid, taurocholic acid and cholic acid. Lowering the pH of the platelet-rich plasma resulted in decrease platelet aggregation by ADP and by collagen. Bile salts further enhanced the inhibitory effect of pH change. In contrast the sodium salt of chenodeoxycholic acid was the sole aggregation inducing bile salt we studied. Relating the above studies to the clinical situation of upper gastroduodenal mucosal haemorrhage, we suggest that biliary reflux as well as the acidic environment may contribute to a poor haemostatic response by impaired platelet aggregation in the upper gastrointestinal tract of otherwise normal human subjects.

Adenosine Diphosphate↗

PubMed2000

Bile salt independent flow during bile salt-induced choleresis and cholestasis in the rat: role of biliary thiol secretion.

AIMS/BACKGROUND: Previous studies have shown that the generation of the so-called "bile salt-independent flow" (BSIF) may be partly dependent on the hepatic availability and rate of canalicular secretion of osmotically active substances such as glutathione (GSH) and derived thiols. This study examined the role of common bile salts (BS) on the BSIF formation under both choleretic and cholestatic conditions, and on the relationship of the BSIF to the biliary thiol secretion. METHODS: Experiments were carried out in adult male Sprague-Dawley rats both in situ in the isolated perfused rat liver and in vivo. The effect of choleretic and cholestatic doses of BS on the biliary BS secretion rate (BSSR), BS-dependent flow (BSDF), and BSIF was evaluated. RESULTS: In the perfused rat liver, the infusion of low and physiological doses of taurocholic acid stimulated the biliary BSSR, BSDF, and BSIF. This was associated with increased biliary thiol secretion and thiol-dependent bile flow. In vivo administration of taurocholic acid, taurochenodeoxycholic acid or taurolithocholic acid in step-wise increasing doses leading to cholestasis showed that the onset of cholestasis was not accompanied by a significant decline in the BSSR or BSDF but rather by a marked inhibition of the apparent BSIE During cholestasis, the three BS produced a significant reduction of biliary thiol secretion, with a marked decrease in thiol-dependent bile flow sufficient to account for a major proportion of BSIF inhibition. This decline in thiol secretion occurred before the drop in biliary BS secretion and was more pronounced than the reduction in BS output. No change in hepatic thiol content was observed. Administration of free or glyco-conjugated BS also resulted in a significant decrease of BSIF during the cholestatic period, suggesting a common role for BSIF inhibition in BS-induced cholestasis. CONCLUSION: The changes in bile flow during BS-induced choleresis and cholestasis are mediated by changes in the portion of the BSIF regulated by the thiol secretion.

Animals↗

PubMedDate not supplied

Hepatoprotection in ethinylestradiol-treated rats is provided by tauroursodeoxycholic acid, but not by ursodeoxycholic acid.

Ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) have been suggested as potential treatments for drug-induced cholestasis. It was therefore decided to study the effects of administration of UDCA or TUDCA on individual serum bile acid concentration, conventional liver tests and associated hepatic ultrastructural changes in ethinylestradiol-treated (EE) rats mg/kg per day). Control rats were treated s.c. with propylene glycol. EE-treated rats were randomly assigned to receive daily i.p. injections of placebo, TUDCA or UDCA. Four rats in each group were treated for 4 consecutive days, and a second four for 14 days. After 4 days of treatment, the serum levels of cholic acid and taurocholic acid were significantly increased in EE-treated rats. None of the conventional liver tests were significantly different among the four groups. After 14 days of treatment the serum levels of cholic acid, chenodeoxycholic acid, glycocholic acid, glycochenodeoxycholic acid, taurocholic acid, taurochenodeoxycholic acid, bilirubin, alkaline phosphatase and gamma glutamyltransferase were significantly raised in EE and EE plus UDCA treated rats. EE plus TUDCA treated rats, however, had no significant changes in these individual serum bile acids or conventional liver tests. The ultrastructure of livers from EE plus TUDCA treated rats was similar to those of controls. On the other hand, EE and EE plus UDCA rats both showed a significant reduction in sinusoidal microvilli. These results show that treatment of rats for 4 days with EE induces significant rises in the serum concentrations of two individual bile acids and that TUDCA protects against this.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

Quantification of bile acids directly from plasma by MALDI-TOF-MS.

Matrix-assisted laser desorption/ionization (MALDI) time-of-flight mass spectrometry (MS) has proved to be a useful method for the quantification of bile acids directly from plasma. Six cholic acid derivatives were selected for analysis: taurocholic acid, taurochenodeoxycholic acid, taurolithocholic acid, glycocholic acid, glycochenodeoxycholic acid, and glycolithocholic acid. Solid-phase extraction (SPE) columns were used to preconcentrate and purify the plasma samples. Calibration curves averaged from 3 days were obtained for the bile acids, and then tested for their ability to accurately determine concentrations from one measurement. In summary, a simple, rapid method has been developed for the quantification of bile salts from plasma by MALDI-MS with SPE cleanup.

Bile Acids and Salts↗

PubMed1984

Inhibition of Na+-coupled solute transport by calcium in brush border membrane vesicles.

Intracellular Ca++ is known to influence Na+ flux in luminal membranes. Abnormally elevated Ca++ levels in some cells is believed to be the primary pathophysiologic defect in cystic fibrosis (CF). This in turn is thought to alter Na+ transport which accounts for certain clinical manifestations of this disease. Two Na+-dependent intestinal transport mechanisms have been reported to be suppressed or missing in CF. To examine whether alterations in cell Ca++ may account for these findings, studies were performed to examine the influence of Ca++ on Na+-solute co-transport across intestinal luminal membranes. Purified brush border membrane vesicles prepared from rat small bowel were preincubated in either Ca++-free buffer or buffer containing 2.5 mM CaCl2. Ca++ loaded vesicles showed marked inhibition of Na+ co-transport of taurocholic acid, taurochenodeoxycholic acid, glucose and valine when compared to controls. The uptake of Na+ was also significantly reduced by intravesicular Ca++. These data demonstrate that intravesicular Ca++ inhibits Na+-coupled solute transport as well as Na+ influx across intestinal brush border membranes. These data suggest that intracellular Ca++ may suppress Na+-dependent solute absorption in the intestine. Results presented here further support the theory that elevated intracellular Ca++ may account for intestinal malabsorption and other altered transport phenomena reported in CF.

Animals↗

PubMed1996

Reduction of bile secretion by prostaglandins in the rat in vivo.

Bile secretion has been reported to be regulated by circulating hormones and by autonomic liver nerves. In the in situ perfused rat liver, prostaglandins reduce bile flow and bile acid secretion. The aim of this study was to investigate the regulation of bile secretion by prostaglandins in the in vivo situation. The bile duct and portal vein of anaesthetised Wistar rats were cannulated by polyethylene tubes. Bile flow was determined gravimetrically. Bile acids were quantified by the 3-alpha-hydroxy-steroid-dehydrogenase method and by high-pressure-liquid-chromatography (HPLC) separation. Administration of 1 microM prostaglandin F2 alpha into the portal vein over 5 minutes reduced bile flow from 1.57 microliter/min.g liver to 0.95 microliter/min.g liver and bile acids secretion from 148 to 81 nmol/100g/min. The administration of different doses (0.1 microM, 1 microM, 10 microM) of prostaglandin F2 alpha reduced hepatic bile secretion in a dose-dependent manner. Similar effects were observed after infusion of prostaglandin D2. However, the ratio of the bile acids (alpha-tauromuricholic acid), beta-tauromuricholic acid, taurocholic acid, taurochenodeoxycholic acid, and taurodeoxycholic acid) was unchanged by prostaglandin F2 alpha. In conclusion, infusion of prostaglandin F2 alpha into the portal vein results in a reduction of bile flow and bile acid secretion in a dose-dependent manner. These results suggest that the effect is linked to canicular bile secretion.

Animals↗

PubMed1982

Uptake of cholic acid by freshly isolated rat hepatocytes: presence of a common carrier for bile acid transports.

The mechanism of the uptake of cholic acids and the interaction of various bile acids on the cholic acid uptake were investigated using isolated rat hepatocytes. The uptake consisted of unsaturable and saturable processes at 0 degrees C and 37 degrees C, respectively. The activation energy found for the saturable process was 26.1 Kcal/mol. In the saturable process the rate of cholic acid uptake followed Michaelis-Menten kinetics with Km: 67 microM and Vmax: 1.43 nmoles/ml protein/min. The uptake was significantly inhibited by 2,4-dinitrophenol, and replacement of extracellular Na+ by choline did not decrease the uptake. The uptake of cholic acid was competitively inhibited by deoxycholic acid, taurocholic acid, glycocholic acid, chenodeoxycholic acid, taurochenodeoxycholic acid and glycochenodeoxycholic acid. It is concluded from the above results that the cholic acid uptake in isolated hepatocytes is mainly mediated by an energy-dependent and sodium-independent carrier-mediated transport process.

2,4-Dinitrophenol↗

PubMed2004

Bile acids induce a cationic current, depolarizing pancreatic acinar cells and increasing the intracellular Na+ concentration.

Biliary disease is a major cause of acute pancreatitis. In this study we investigated the electrophysiological effects of bile acids on pancreatic acinar cells. In perforated patch clamp experiments we found that taurolithocholic acid 3-sulfate depolarized pancreatic acinar cells. At low bile acid concentrations this occurred without rise in the cytosolic calcium concentration. Measurements of the intracellular Na(+) concentration with the fluorescent probe Sodium Green revealed a substantial increase upon application of the bile acid. We found that bile acids induce Ca(2+)-dependent and Ca(2+)-independent components of the Na(+) concentration increase. The Ca(2+)-independent component was resolved in conditions when the cytosolic Ca(2+) level was buffered with a high concentration of the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). The Ca(2+)-dependent component of intracellular Na(+) increase was clearly seen during stimulation with the calcium-releasing agonist acetylcholine. During acetylcholine-induced Ca(2+) oscillations the recovery of cytosolic Na(+) was much slower than the recovery of Ca(2+), creating a possibility for the summation of Na(+) transients. The bile-induced Ca(2+)-independent current was found to be carried primarily by Na(+) and K(+), with only small Ca(2+) and Cl(-) contributions. Measurable activation of such a cationic current could be produced by a very low concentration of taurolithocholic acid 3-sulfate (10 microm). This bile acid induced a cationic current even when applied in sodium- and bicarbonate-free solution. Other bile acids, taurochenodeoxycholic acid, taurocholic acid, and bile itself also induced cationic currents. Bile-induced depolarization of acinar cells should have a profound effect on acinar fluid secretion and, consequently, on transport of secreted zymogens.

Animals↗

PubMed1976

Comparison of the binding of various bile acids and bile salts in vitro by several types of fiber.

The binding in vitro of the sodium salts of cholic acid, chenodeoxycholic acid, deoxycholic acid, taurocholic acid, taurochenodeoxycholic acid, taurodeoxycholic acid, glycocholic acid, glycochenodeoxycholic acid, and glycodeoxycholic acid by alfalfa, bran, cellulose, lignin, and cholestyramine was measured. Cholestyramine bound an average of 81.3% of all the bile acids and salts tested whereas cellulose bound only negligible amounts (1.4%). Of the other substances tested, lignin bound 29.2%, alfalfa, 15.9% and bran, 9.0%. No distinct pattern of binding was discerned. It is therefore apparent that the validity of statements concerning the effect of fiber on bile salf metabolism rests upon the specificity of the composition of the fiber involved and the bile acids or salts tested.

Bile Acids and Salts↗

PubMed1978

Bile acid structure and biliary lipid secretion. II. A comparison of three hydroxy and two keto bile acids.

The effect of five bile acids on biliary lipid secretion was studied in the pentobarbital-anesthetized cat. The dihydroxy acid, taurohyodeoxycholic acid, was indistinguishable from another dihydroxy acid, taurochenodeoxycholic acid, but secretion of both phospholipid and cholesterol was considerably reduced with two mono-keto dihydroxy acids, tauro-3alpha,12alpha-dihydroxy-7-keto-5beta-cholanoic acid and tauro-3alpha,7alpha-dihydroxy-12-keto-5beta-cholanoic acid. The effect of a trihydroxy bile acid, taurocholic acid was as previously described. The effect of the keto bile acids may be explained by the ability of these bile acids to solubilize lipid, but such an explanation is inadequate for the difference between di- and trihydroxy bile acids. An intracellular effect of bile acid is postulated.

Animals↗

PubMed1995

Relationship between bile acid transplacental gradients and transport across the fetal-facing plasma membrane of the human trophoblast.

Bile acids and bilirubin are synthesized by the fetal liver very early on during intrauterine life. The main fate of these compounds is to be transferred to the mother. This excretory role of the placenta is primarily determined by the ability of the trophoblast to transport them, which is believed to occur mainly by carrier-mediated processes. The aim of this study was to investigate the role of the cholephilic organic anion exchanger located in the fetal-facing plasma membrane of the human trophoblast in placental "biliary-like" function. No relationship between the magnitude of transplacental gradients for total bile acids and bilirubin was found. However, transport studies, which were carried out by using purified plasma membrane vesicles derived from the fetal-facing pole of the human trophoblast, revealed that [14C]taurocholate transport was affected by both another bile acid (taurochenodeoxycholic acid) and a non-bile acid cholephilic organic anion (bromosulfophthalein). On plotting the ability of different major bile acid species to inhibit radiolabeled taurocholate uptake by these vesicles versus their concentrations in fetal serum or the magnitude of their transplacental gradients, inverse relationships were found. Lower fetal serum concentrations and transplacental gradients were found for bile acid species with higher abilities to affect this transport and presumably to interact with the carrier. By contrast, the magnitude of the transplacental gradient for bile acid species was not correlated with their hydrophobic/hydrophilic balance, as would be expected if diffusion across the lipidic structures of the placental barrier would be the major pathway for the flux of bile acid across this organ.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

PubMed1990

Serum unconjugated primary and secondary bile acids in patients with cholangiocarcinoma and hepatocellular carcinoma.

Serum unconjugated primary bile acids (cholic acid, chenodeoxycholic acid), secondary bile acids (lithocholic acid, deoxycholic acid), conjugated primary bile acids (glycocholic acid, glycohenodeoxycholic acid, taurocholic acid, taurochenodeoxycholic acid) and total bile acids were measured in 25 and 75 male patients with cholangiocarcinoma and hepatocellular carcinoma respectively. Twenty-one healthy male volunteers served as controls. Other biochemical parameters, i.e. bilirubin, transaminases, albumin, globulin and cholesterol were also studied. Conjugated bile acids and total bile acids were elevated in both patient groups when compared with those of controls. The presence of unconjugated primary bile acids and secondary bile acids was noted in the patient groups, whereas, they were not detectable in controls. The appearance of these serum bile acids may be useful as a marker for early diagnosis of cholangiocarcinoma and hepatocellular carcinoma in people at-risk such as those who have chronic infection with Opisthorchis viverrini. Differentiation between the two types of tumor may be possible by using other parameters such as alpha-fetoprotein or other tumor markers newly discovered. An increase of the trihydroxy bile acids: dihydroxy bile acids and glycine conjugated bile acids: taurine conjugated bile acids ratios was shown in the patient groups. The latter may be due to the proportion of the increase of taurine conjugates being greater than the increase of glycine conjugates. The other biochemical parameters were significantly elevated in the patient groups except for albumin which was significantly decreased. The sensitivity of the tests for cholic acid, chenodeoxycholic acid, alkaline phosphatase and gamma glutamyl transferase was high.

Adenoma, Bile Duct↗