Serum-Bile-Acids in the Stagnant-Loop Syndrome

Lewis, Barbara; D, Panveliwalla; Tabaqchali, Soad; Wootton, I. D. P.

doi:10.1016/s0140-6736(69)91238-0

Cited by 71 publications

(29 citation statements)

References 10 publications

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“…In patients with small bowel overgrowth or ileal resection, increased concentrations ofserum unconjugated bile acids have been found (42,46) which may serve as substrates for hepatic and extrahepatic bile acid UDP-glucuronosyltransferase(s). This assumption is supported by the description of a patient with chronic malabsorption, who excreted glucuronides of otherwise unconjugated mainly 6a-hydroxylated bile acids in urine, which amounted to 20% of the total urinary bile acid excretion (47).…”

Section: Discussionmentioning

confidence: 99%

Hepatic and extrahepatic glucuronidation of bile acids in man. Characterization of bile acid uridine 5'-diphosphate-glucuronosyltransferase in hepatic, renal, and intestinal microsomes.

Matern¹,

Matern²,

Farthmann³

et al. 1984

J. Clin. Invest.

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Abstract. Microsomal UDP-glucuronosyltransferase activity toward the bile acids (chenodeoxycholic, deoxycholic, ursodeoxycholic, lithocholic, and glycolithocholic) has been detected in human specimens of liver, kidney, and intestinal mucosa. The characteristics of hepatic and extrahepatic UDP-glucuronosyltransferase activities toward these bile acids were compared with respect to kinetic parameters and other catalytic properties. Whereas no organspecific differences in the affinities of individual bile acids to hepatic and extrahepatic UDP-glucuronosyltransferases were observed, the individual bile acids showed reaction rates in liver that were about twice the rates estimated in kidney and about twice to three times the rates observed in duodenal mucosa. In intestinal mucosa the rate of chenodeoxycholic acid glucuronidation exhibited a progressive decrease from duodenum to colon, where it was 30%o of the duodenal level.

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Section: Discussionmentioning

confidence: 99%

Hepatic and extrahepatic glucuronidation of bile acids in man. Characterization of bile acid uridine 5'-diphosphate-glucuronosyltransferase in hepatic, renal, and intestinal microsomes.

Matern¹,

Matern²,

Farthmann³

et al. 1984

J. Clin. Invest.

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“…Increased concentrations of fasting serum unconjugated bile acids have been found in patients with small bowel bacterial overgrowth and ileal 26 resection. The explanation for this finding was the increased bacterial degradation of the conjugated bile acids coupled with the less efficient hepatic clearance of unconjugated bile acids from the peripheral circulation.…”

Section: Discussionmentioning

confidence: 99%

Diurnal changes in serum unconjugated bile acids in normal man.

Setchell¹,

Lawson²,

Blackstock³

et al. 1982

Gut

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SUMMARY Unconjugated bile acids were measured using gas chromatography-mass spectrometry in the serum of two subjects throughout a 24 hour period and in two other subjects over a six hour period after breakfast. Unconjugated bile acids were found in all samples of serum and included cholic, chenodeoxycholic, deoxycholic, 3f3,7a-dihydroxy-5,/-cholanic (isochenodeoxycholic), ursodeoxycholic, 3/3,7,B3dihydroxy-5,/3cholanic (iso-ursodeoxycholic), 3,& hydroxy-5-cholenoic, and lithocholic acids. The maximum concentration of each bile acid generally occurred between breakfast and dinner and total unconjugated bile acid concentrations attained levels of between 2-3 ,umol/l. Concentrations increased after breakfast and were often as high as 30-40% of the conjugated bile acid glycocholate, but returned to fasting levels in the absence of lunch. The intestinal absorption of unconjugated bile acids is therefore of greater quantitative importance than was previously thought.

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“…Although this could indicate hepatic dysfunction, increased serum bile acid concentrations have also been described in the blind loop syndrome and following ileal resection where there are excess quantities of free bile acids in the intestine (Lewis, Panveliwalla, Tabaqchali, and Wootton, 1969).…”

Section: Discussionmentioning

confidence: 99%

Liver structure and function in cholelithiasis: Effect of chenodeoxycholic acid

Bell¹,

Mok²,

Thwe³

et al. 1974

Gut

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SUMMARY Although, in suitable patients, oral chenodeoxycholic acid (CDCA) dissolves gallstones, the results of recent animal studies suggest that it might be hepatotoxic. Liver function was therefore studied in patients with gallstones before and during treatment with CDCA and liver biopsies were carried out both in patients with cholelithiasis given bile acid therapy and in those who had been given no medical treatment. In 25 patients treated with 0.5-1 5 g CDCA/day (7-20 mg kg body weight-' day-') there was no significant change in serum bilirubin, albumin, globulin, transaminase, isocitric dehydrogenase, alkaline phosphatase, and gamma glutamyl transpeptidase levels before and at monthly intervals during six months' treatment. The kinetics of bromsulphthalein (BSP) clearance and its apparent transport maximum were not significantly changed during CDCA therapy. The mean fasting serum bile acid concentrations of 18.0 ± SEM 1.2 ,umoles/litre before and 20.0 ± 3.5 j&moles/litre during treatment were both significantly greater than control values. Liver histology was not appreciably different in 11 patients treated with CDCA from that in eight patients with untreated cholelithiasis and in three patients who had received CDCA three to four months before biopsy. These results suggest that in doses of 0.5 to 1.5 g/day CDCA is not hepatotoxic in man.Oral chenodeoxycholic acid (CDCA) improves cholesterol solubility in bile (Thistle and Schoenfield, 1971) and in suitable patients it dissolves gallstones (Danzinger, Hofmann, Thistle, and Schoenfield, 1972;Bell, Whitney, and Dowling, 1972;Thistle and Hofmann, 1973), but, as with any new drug, the benefits of treatment with CDCA must be weighed against possible complications. One such potential complication is hepatic dysfunction and indeed Small (1971) predicted that this might happen either as a direct effect of CDCA itself on the liver, or indirectly through the formation of lithocholic acid, the bacterial metabolite of CDCA, which is known to be hepatotoxic.Although the initial reports of CDCA treatment 1Presented in part at

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Serum-Bile-Acids in the Stagnant-Loop Syndrome

Cited by 71 publications

References 10 publications

Hepatic and extrahepatic glucuronidation of bile acids in man. Characterization of bile acid uridine 5'-diphosphate-glucuronosyltransferase in hepatic, renal, and intestinal microsomes.

Hepatic and extrahepatic glucuronidation of bile acids in man. Characterization of bile acid uridine 5'-diphosphate-glucuronosyltransferase in hepatic, renal, and intestinal microsomes.

Diurnal changes in serum unconjugated bile acids in normal man.

Liver structure and function in cholelithiasis: Effect of chenodeoxycholic acid

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