Reduced cortical thickness in patients with acute-on-chronic liver failure due to non-alcoholic etiology

Yadav, S.K., Gupta, R.K., Saraswat, V.A., Rangan, M., Thomas, M.A., Rutella, S. ORCID: 0000-0003-1970-7375, Danese, S., Wang, E., Marincola, F.M. and Haris, M., 2015. Reduced cortical thickness in patients with acute-on-chronic liver failure due to non-alcoholic etiology. Journal of Translational Medicine, 13, p. 322. ISSN 1479-5876

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Abstract

Background:
Acute-on-chronic liver failure (ACLF) is a form of liver disease with high short-term mortality. ACLF offers considerable potential to affect the cortical areas by significant tissue injury due to loss of neurons and other supporting cells. We measured changes in cortical thickness and metabolites profile in ACLF patients following treatment, and compared it with those of age matched healthy volunteers.
Methods:
For the cortical thickness analysis we performed whole brain high resolution T1-weighted magnetic resonance imaging (MRI) on 15 ACLF and 10 healthy volunteers at 3T clinical MR scanner. Proton MR Spectroscopy (1H MRS) was also performed to measure level of altered metabolites. Out of 15 ACLF patients 10 survived and underwent
follow-up study after clinical recovery at 3 weeks. FreeSurfer program was used to quantify cortical thickness and LC- Model software was used to quantify absolute metabolites concentrations. Neuropsychological (NP) test was performed to assess the cognitive performance in follow-up ACLF patients compared to controls.
Results:
Significantly reduced cortical thicknesses in multiple brain sites, and significantly decreased N-acetyl
aspartate (NAA), myo-inositol (mI) and significantly increased glutamate/glutamine (glx) metabolites were observed in ACLF compared to those of controls at baseline study. Follow-up patients showed significant recovery in cortical thickness and Glx level, while NAA and mI were partially recovered compared to baseline study. When compared to controls, follow-up patients still showed reduced cortical thickness and altered metabolites level. Follow-up patients had abnormal neuropsychological (NP) scores compared to controls.
Conclusions:
Neuronal loss as suggested by the reduced NAA, decreased cellular density due to increased cerebral hyperammonemia as supported by the increased glx level, and increased proinflammatory cytokines and free radicals may account for the reduced cortical thickness in ACLF patients. Presence of reduced cortical thickness, altered
metabolites and abnormal NP test scores in post recovery subjects as compared to those of controls is associated
with incomplete clinical recovery. The current imaging protocol can be easily implemented in clinical settings to evaluate and monitor brain tissue changes in patients with ACLF during the course of treatment.

Item Type: Journal article
Publication Title: Journal of Translational Medicine
Creators: Yadav, S.K., Gupta, R.K., Saraswat, V.A., Rangan, M., Thomas, M.A., Rutella, S., Danese, S., Wang, E., Marincola, F.M. and Haris, M.
Publisher: BioMed Central
Date: 6 October 2015
Volume: 13
ISSN: 1479-5876
Identifiers:
NumberType
10.1186/s12967-015-0679-6DOI
679Publisher Item Identifier
Rights: © 2015 Yadav et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Divisions: Schools > School of Science and Technology
Depositing User: Jill Tomkinson
Date Added: 13 Sep 2016 13:46
Last Modified: 09 Jun 2017 14:05
URI: http://irep.ntu.ac.uk/id/eprint/28505

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