Endotoxin and its binding proteins in chronic liver disease: the effect of transjugular intrahepatic portosystemic shunting
: Background: Gut‐derived endotoxin is insufficiently cleared by the diseased liver, and thus, is elevated in plasma of patients with chronic liver disease (CLD). Endotoxin action might be modified by binding to soluble CD14 (sCD14) and lipopolysaccharide‐binding protein (LBP), both of which have no...
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Published in | Liver (Copenhagen) Vol. 22; no. 5; pp. 380 - 387 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Munksgaard International Publishers
01.10.2002
Munksgaard |
Subjects | |
Online Access | Get full text |
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Summary: | : Background: Gut‐derived endotoxin is insufficiently cleared by the diseased liver, and thus, is elevated in plasma of patients with chronic liver disease (CLD). Endotoxin action might be modified by binding to soluble CD14 (sCD14) and lipopolysaccharide‐binding protein (LBP), both of which have not yet been sufficiently studied in CLD.
Methods: Endotoxin, sCD14 and LBP have been determined in peripheral blood of 72 patients and 39 control subjects, and in portal and hepatic venous blood of 12 patients during transjugular intrahepatic portosystemic shunt (TIPS) implantation.
Results: Peripheral endotoxin (average 3‐fold increased compared to controls), LBP, and sCD14 plasma levels were elevated in chronic liver disease irrespective of Child stage m, preserve/absence of cirrhosis or aetiology. LBP, and sCD14. Furthermore, endotoxin levels in the portal vein (38.1 ± 6.1 pg/ml) were only slightly elevated compared to the hepatic vein (29.2 ± 4.4 pg/ml), and peripheral endotoxin levels did not increase after TIPS.
Conclusions: Decreased hepatocellular function rather than hepatic blood shunting might be responsible for endotoxemia. The elevation in LBP and sCD14 levels may be a consequence of endotoxemia. |
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Bibliography: | istex:ECD70F89F7789CDA1026A6672B0B6EF2DFC27246 ArticleID:LIV1666 ark:/67375/WNG-XLT867QH-5 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0106-9543 1600-0676 |
DOI: | 10.1034/j.1600-0676.2002.01666.x |