Ileal absorption of bile acids in patients with chronic cholestasis

1996 ◽  
Vol 41 (12) ◽  
pp. 2417-2422 ◽  
Author(s):  
Olivier Chazouillères ◽  
Philippe Marteau ◽  
Mostefa Haniche ◽  
Raymond Jian ◽  
Raoul Poupon

1990 ◽  
Vol 22 (2) ◽  
pp. 93-100 ◽  
Author(s):  
R. Aldini ◽  
G. Ussia ◽  
A. Roda ◽  
Grilli Cilioni ◽  
R. Rizzoli ◽  
...  


1998 ◽  
Vol 114 ◽  
pp. A1334
Author(s):  
P. Sauer ◽  
A. Stiehl ◽  
P. Kloeters-Plachky ◽  
BA Fitscher ◽  
HD Riedel ◽  
...  


1993 ◽  
Vol 5 (4) ◽  
pp. 247-250 ◽  
Author(s):  
Sharif Eusufzai ◽  
Sverker Ericsson ◽  
Torsten Cederlund ◽  
Kurt Einarsson ◽  
Bo Angelin
Keyword(s):  


1987 ◽  
Vol 926 (2) ◽  
pp. 154-159 ◽  
Author(s):  
Charles O. Mills ◽  
Sajida Iqbal ◽  
Elwyn Elias




2019 ◽  
Vol 19 (3) ◽  
pp. 215-228 ◽  
Author(s):  
Benjamin L. Woolbright ◽  
Hartmut Jaeschke

Cholestasis results in blockage of bile flow whether the point of obstruction occurs extrahepatically or intrahepatically. Bile acids are a primary constituent of bile, and thus one of the primary outcomes is acute retention of bile acids in hepatocytes. Bile acids are normally secreted into the biliary tracts and then released into the small bowel before recirculating back to the liver. Retention of bile acids has long been hypothesized to be a primary cause of the associated liver injury that occurs during acute or chronic cholestasis. Despite this, a surge of papers in the last decade have reported a primary role for inflammation in the pathophysiology of cholestatic liver injury. Furthermore, it has increasingly been recognized that both the constituency of individual bile acids that make up the greater pool, as well as their conjugation status, is intimately involved in their toxicity, and this varies between species. Finally, the role of bile acids in drug-induced cholestatic liver injury remains an area of increasing interest. The purpose of this review is to critically evaluate current proposed mechanisms of cholestatic liver injury, with a focus on the evolving role of bile acids in cell death and inflammation.



Gut ◽  
1991 ◽  
Vol 32 (9) ◽  
pp. 1044-1048 ◽  
Author(s):  
S Eusufzai ◽  
S Ericsson ◽  
T Cederlund ◽  
K Einarsson ◽  
B Angelin


Hepatology ◽  
1990 ◽  
Vol 12 (5) ◽  
pp. 1206-1208 ◽  
Author(s):  
Philippe Marteau ◽  
Olivier Chazouiléres ◽  
Anne Myara ◽  
Raymond Jian ◽  
Jean-Claude Rambaud ◽  
...  


1989 ◽  
Vol 9 ◽  
pp. S61
Author(s):  
P. Marteau ◽  
O. Chazouillères ◽  
A. Myara ◽  
R. Jian ◽  
J.C. Rambaud ◽  
...  


2006 ◽  
Vol 96 (2) ◽  
pp. 365-370 ◽  
Author(s):  
Stéphane M. Schneider ◽  
Françoise Joly ◽  
Marie-France Gehrardt ◽  
Abdul M. Badran ◽  
Anne Myara ◽  
...  

Taurine deficiency in patients on long-term parenteral nutrition may be involved in cholestasis. We aimed to assess plasma taurine and tauro-conjugated bile acids in adults with short-bowel syndrome and their response to intravenous taurine. Thirty-two adult patients, who had been on taurine-free parenteral nutrition for a mean of 59(SE14) months for short-bowel syndrome, were studied retrospectively. In a second study, a subgroup of ten patients with chronic cholestasis received taurine-enriched (6·0(SE0·6)mg/kg per d) parenteral nutrition for 55(SE13) months. Post-absorptive plasma taurine and bile acid concentrations were measured and liver function tests routinely sampled. At baseline, plasma taurine was lower in patients with a jejunal length of less than 35cm (group A,n16) than in those with a jejunal length of 35cm or more (group B,n16): 43(SE3)v. 58(SE4)μmol/l (P=0·01). The groups were no different in terms of chronic cholestasis (1/6v.1/6 patients), total bile acids (26(SE13)v.14(SE5)μmol/l) or the ratio of tauro-conjugated:glyco-conjugated bile acids (5(SE2)v.8(SE 4)%, usual range 30–60%). After supplementation, there was an increase in plasma taurine level (63(SE8)v. 43(SE4),P=0·007) but was no change in either total bile acids or the ratio of tauro-conjugated: glyco-conjugated bile acids. There was a significant decrease in aspartate aminotransferase level. Long-term parenteral nutrition for short-bowel syndrome is associated with an impaired tauro-conjugation of bile acids (enterohepatic pool), irrespective of plasma taurine level (systemic pool) and despite long-term taurine intravenous supplementation.



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