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Bile biochemistry following liver reperfusion in the recipient and its association with cholangiopathy.

Accepted version
Peer-reviewed

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Article

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Authors

Gaurav, Rohit 
Atulugama, Niroshan 
Swift, Lisa 
Butler, Andrew J 
Upponi, Sara 

Abstract

Cholangiocytes secrete bicarbonate and absorb glucose, producing bile with alkaline pH and low glucose content. These functions of cholangiocytes have been suggested as a marker of bile duct viability during normothermic ex situ liver perfusion (NESLiP), and are now monitored routinely post reperfusion in our centre. In this study, we reviewed the composition of bile immediately after reperfusion in liver transplant recipients to determine normal post-transplant parameters and the predictive value of bile biochemistry for the later development of cholangiopathy. After reperfusion of the liver graft, a cannula was placed in the bile duct to collect bile over a median 44 minute time period. The bile produced was analysed using a point of care blood gas analyser (Roche Cobas b221). 100 liver transplants (35 donation after circulatory death [DCD] and 65 donation after brain death [DBD]) were studied. Median bile pH was 7.82 (Interquartile range [IQR] 7.67 -7.98), median bile glucose 2.1 (1.4 - 3.7) mmol/L, median blood and bile pH difference 0.5 (0.37 - 0.62) and the median blood and bile glucose difference 7.1 (5.6 - 9.1) mmol/L. 12 recipients developed cholangiopathy over a median follow up of 15 months (IQR 11 - 20). Bile sodium (142 vs 147 mmol/L; p=0.02) and blood-bile glucose concentration differences (5.2 vs 7.6; p=0.001) were significantly lower and associated with ischaemic cholangiopathy. In conclusion, bile biochemistry may provide useful insights into cholangiocyte function, and hence bile duct viability. Our results suggest bile glucose is the most sensitive predictor of cholangiopathy.

Description

Keywords

Bile biochemistry, Cholangiopathy, Gas analyser, Liver Transplantation

Journal Title

Liver Transplantation

Conference Name

Journal ISSN

1074-3022
1527-6473

Volume Title

Publisher

Wiley-Blackwell

Rights

All rights reserved
Sponsorship
Department of Health (via National Institute for Health Research (NIHR)) (NIHR BTRU-2014-10027)