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Catecholamines and inflammation in advanced liver disease: more closely intertwined than expected?
  1. Hans Dieter Nischalke1,
  2. Christina Nischalke1,
  3. Franziska Schmalz1,
  4. Christine Möller1,
  5. Benjamin Krämer1,
  6. Alexandra Funken1,
  7. Adrian Goldspink1,
  8. Jacob Nattermann1,2,
  9. Christian Strassburg1,2,
  10. Philipp Lutz1,2
  1. 1 Department of Internal Medicine I, University Hospital Bonn, Bonn, Germany
  2. 2 Partner Site Bonn/Cologne, German Center for Infection Research (DZIF), Bonn, Germany
  1. Correspondence to Dr Philipp Lutz, Department of Internal Medicine I, University Hospital Bonn, Bonn 53127, Germany; Philipp.Lutz{at}

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Recently, Weiss et al discovered that a catecholamine metabolite, 4-hydroxy-3-methoxyphenylglycol sulfate (MOPEG sulfate), is associated with death after 28 days in patients with acutely decompensated cirrhosis.1 The authors hypothesise that systemic inflammation, an important prognostic factor,2 may be connected to the intensity of the stress-induced alarm reaction in the central nervous system, triggering release of norepinephrine, which is later metabolised to MOPEG sulfate. However, immune cells may also produce catecholamines,3 offering another link between systemic inflammation and catecholamine metabolites. Additionally, the source of MOPEG sulfate is difficult to determine, because it is not only a metabolite of norepinephrine but also of epinephrine.4 Epinephrine is important, because it is the main agonist for beta-2 adrenoceptors,5 with unselective beta-blockers being beneficial in patients with advanced liver disease and portal hypertension.6 To further assess a potential interplay between autocrine/paracrine catecholamine production by immune cells and immune activation, we analysed mononuclear immune cells from peripheral blood and ascites from patients with decompensated cirrhosis.

Ascites and peripheral blood were collected from 12 patients with decompensated cirrhosis, details of which are given in online supplemental table 1. In short, expression of cell markers and adrenoreceptor beta 2 …

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  • Contributors AF and PL included patients and collected specimen; AG, BK, CN, CM, FS and HDN performed the experiments; CN, HDN and PL analysed the data; and AF, CS, HDN, JN and PL wrote and critically revised the manuscript.

  • Funding CN received funding from the Association for the Promotion of Internal Medicine, University Hospital Bonn. HDN, FS and CM were funded by Deutsche Krebshilfe (70114349).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.