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Changes in bilirubin pigments secreted in bile after liver transplantation
Author(s) -
Goresky Carl A.,
Gordon Ellen R.,
Sanabria JuanRamon,
Strasberg Steven M.,
Flye M. Wayne
Publication year - 1992
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840150517
Subject(s) - bilirubin , chemistry , bile pigments , glucuronidation , glucuronate , transplantation , glucuronide , biochemistry , glucuronosyltransferase , medicine , endocrinology , metabolism , biology , enzyme , microsome
The species of bile pigments secreted in T‐tube fistula bile after liver transplantation were ascertained by high‐performance liquid chromatography in 15 patients for 10 days after liver transplant. Nine glycosidic conjugates and unconjugated bilirubin were resolved by the analytical procedure. The principal pigments in bile and their proportions in normal patients were the following: bilirubin diglucuronide = 83.0% ± bilirubin monoglucuronide = 9.7% ± 1.4% (S.D.); bilirubin monoglucuronide monoglucoside = 4.0% 2.8% (S.D.); and bilirubin monoglucuronide monoxyloside = 1.5% ± 1.8% (S.D.). All of the other possible glucuronide, glucose and xylose monoconjugates and diconjugates and unconjugated bilirubin were also found, but each was normally less than 1% of the total. In 13 of the 15 transplant patients, a significant depression in proportions of bilirubin diglucuronide and elevation in proportions of bilirubin monoglucuronide were found after the transplant, with an accompanying but generally small increase in the proportions of the minor conjugates. In two patients with rejection of the transplant, the changes were of larger magnitude, with improvement occurring only with recovery from the rejection. In one of these patients, kidney failure was present, and in addition to the diglucuronide and monoglucuronide conjugates diglucoside and monoglucoside monoxyloside conjugates were found in plasma. The underlying metabolic abnormalities are not clear but likely reflect underlying abnormal intracellular cofactor levels for conjugation. Glycogen depletion with reduction of UDP‐glucuronate levels or reduced UDP‐glucuronate formation from UDP‐glucose, secondary to elevation of UDP‐xylose, could potentially account for the changes in pigment excretion. (H EPATOLOGY 1992;15:849–857).