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Early primary biliary cholangitis is characterised by brain abnormalities on cerebral magnetic resonance imaging

Research output: Contribution to journalArticle

  • V. P. B. Grover
  • L. Southern
  • J. K. Dyson
  • J. U. Kim
  • M. M. E. Crossey
  • M. Wylezinska-arridge
  • N. Patel
  • J. A. Fitzpatrick
  • A. Bak-bol
  • A. D. Waldman
  • G. J. Alexander
  • G. F. Mells
  • R. W Chapman
  • D. E. J. Jones
  • S. D. Taylor-robinson

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    Rights statement: © 2016 The Authors. Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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http://doi.wiley.com/10.1111/apt.13797
Original languageEnglish
Pages (from-to)936-945
JournalAlimentary Pharmacology and Therapeutics
Volume44
Issue number9
Early online date8 Sep 2016
DOIs
Publication statusPublished - Nov 2016

Abstract

Background

Brain change can occur in primary biliary cholangitis (PBC), potentially as a result of cholestatic and/or inflammatory processes. This change is linked to systemic symptoms of fatigue and cognitive impairment.
Aim

To identify whether brain change occurs early in PBC. If the change develops early and is progressive, it may explain the difficulty in treating these symptoms.
Methods

Early disease brain change was explored in 13 patients with newly diagnosed biopsy-proven precirrhotic PBC using magnetisation transfer, diffusion-weighted imaging and 1H magnetic resonance spectroscopy. Results were compared to 17 healthy volunteers.
Results

Cerebral magnetisation transfer ratios were reduced in early PBC, compared to healthy volunteers, in the thalamus, putamen and head of caudate with no greater reduction in patients with greater symptom severity. Mean apparent diffusion coefficients were increased in the thalamus only. No 1H magnetic resonance spectroscopy abnormalities were seen. Serum manganese levels were elevated in all PBC patients, but no relationship was seen with imaging or symptom parameters. There were no correlations between neuroimaging data, laboratory data, symptom severity scores or age.
Conclusions

This is the first study to be performed in this precirrhotic patient population, and we have highlighted that neuroimaging changes are present at a much earlier stage than previously demonstrated. The neuroimaging abnormalities suggest that the brain changes seen in PBC occur early in the pathological process, even before significant liver damage has occurred. If such changes are linked to symptom pathogenesis, this could have important implications for the timing of second-line-therapy use.

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