The development of low-grade cerebral edema in cirrhosis is supported by the evolution of H-1-magnetic resonance abnormalities after liver transplantation

Citation
J. Cordoba et al., The development of low-grade cerebral edema in cirrhosis is supported by the evolution of H-1-magnetic resonance abnormalities after liver transplantation, J HEPATOL, 35(5), 2001, pp. 598-604
Citations number
41
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
JOURNAL OF HEPATOLOGY
ISSN journal
01688278 → ACNP
Volume
35
Issue
5
Year of publication
2001
Pages
598 - 604
Database
ISI
SICI code
0168-8278(200111)35:5<598:TDOLCE>2.0.ZU;2-X
Abstract
Background/Aims: Liver failure may cause brain edema through an increase in brain glutamine. However, usually standard neuroimaging techniques do not detect brain edema in cirrhosis. We assessed magnetization transfer ratio a nd H-1-magnetic resonance (MR) spectroscopy before and after liver transpla ntation to investigate changes in brain water content in cirrhosis. Methods: Non-alcoholic cirrhotics without overt hepatic encephalopathy (n = 24) underwent H-1-MR of the brain and neuropsychological tests. H-1-MR res ults were compared with those of healthy controls (n = 10). In a subgroup o f patients (n = 11), the study was repeated after liver transplantation. Results: Cirrhotic patients showed a decrease in magnetization transfer rat io (31.5 +/- 3.1 vs. 37.1 +/- 1.1, P < 0.01) and an increase in glutamine/g lutamate signal (2.22 +/- 0.47 vs. 1.46 +/- 0.26, P < 0.01). The increase i n glutamine/glutamate signal was correlated to the decrease in magnetizatio n transfer ratio and to neuropsychological function. Following liver transp lantation, there was a progressive normalization of magnetization transfer ratio, glutamine/glutamate signal and neuropsychological function. Accordin gly, correlations between these variables were lost after liver transplanta tion. Conclusions: Cirrhotic patients show reversible changes in magnetization tr ansfer ratio that are compatible with the development of low-grade cerebral edema. Minimal hepatic encephalopathy and low-grade cerebral edema appear to be the consequences of the metabolism of ammonia in the brain. (C) 2001 European Association for the Study of the Liver. Published by Elsevier Scie nce B.V. All rights reserved.