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Front Physiol. 2021 Jun 11;12:649668. doi: 10.3389/fphys.2021.649668. eCollection 2021.

Divergences in Macrophage Activation Markers Soluble CD163 and Mannose Receptor in Patients With Non-cirrhotic and Cirrhotic Portal Hypertension.

Frontiers in physiology

Nikolaj Worm Ørntoft, Michel Blé, Anna Baiges, Jose Ferrusquia, Virginia Hernández-Gea, Fanny Turon, Marta Magaz, Søren Møller, Holger Jon Møller, Juan Carlos Garcia-Pagan, Henning Gronbaek

Affiliations

  1. Department of Hepatology and Gastroenterology, European Reference Network on Hepatological Diseases (ERN RARE-LIVER), Aarhus University Hospital, Aarhus, Denmark.
  2. Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (CIBEREHD), European Reference Network on Hepatological Diseases (ERN RARE-LIVER), Institut de Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
  3. Center of Functional and Diagnostic Imaging and Research, Department of Clinical Physiology and Nuclear Medicine 260, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark.
  4. Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.

PMID: 34177608 PMCID: PMC8231705 DOI: 10.3389/fphys.2021.649668

Abstract

INTRODUCTION: Macrophages are involved in development and progression of chronic liver disease and portal hypertension. The macrophage activation markers soluble (s)CD163 and soluble mannose receptor (sMR), are associated with portal hypertension in patient with liver cirrhosis but never investigated in patients with non-cirrhotic portal hypertension. We hypothesized higher levels in cirrhotic patients with portal hypertension than patients with non-cirrhotic portal hypertension. We investigated sCD163 and sMR levels in patients with portal hypertension due to idiopathic portal hypertension (IPH) and portal vein thrombosis (PVT) in patients

METHODS: We studied plasma sCD163 and sMR levels in patients with IPH (

RESULTS: Median sCD163 concentration was 1.51 (95% CI: 1.24-1.83) mg/L in healthy controls, 1.96 (95% CI: 1.49-2.56) in patients with non-cirrhotic PVT and 2.16 (95% CI: 1.75-2.66) in patients with IPH. There was no difference between non-cirrhotic PVT patients and healthy controls, whereas IPH patients had significantly higher levels than controls (

CONCLUSION: Soluble CD163 and sMR levels are elevated in patients with IPH and patients with cirrhosis, but normal in patients with non-cirrhotic PVT. This suggests that hepatic macrophage activation is more driven by the underlying liver disease with cirrhosis than portal hypertension.

Copyright © 2021 Ørntoft, Blé, Baiges, Ferrusquia, Hernández-Gea, Turon, Magaz, Møller, Møller, Garcia-Pagan and Gronbaek.

Keywords: biomarker; cirrhosis; macrophages; non-cirrhotic portal hypertension; portal hypertension

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

  1. Dig Dis Sci. 2018 Nov;63(11):3153-3157 - PubMed
  2. J Viral Hepat. 2015 Apr;22(4):427-32 - PubMed
  3. Liver Int. 2020 Jun;40(6):1408-1414 - PubMed
  4. Aliment Pharmacol Ther. 2012 Nov;36(9):875-85 - PubMed
  5. J Hepatol. 2014 Jan;60(1):197-209 - PubMed
  6. Hepatology. 2014 Aug;60(2):521-30 - PubMed
  7. Hepatology. 2014 Jun;59(6):2276-85 - PubMed
  8. Aliment Pharmacol Ther. 2016 Nov;44(10):1062-1070 - PubMed
  9. Nature. 2001 Jan 11;409(6817):198-201 - PubMed
  10. J Hepatol. 2007 Aug;47(2):228-38 - PubMed
  11. Gut. 2011 Oct;60(10):1389-93 - PubMed
  12. J Hepatol. 2007 Nov;47(5):671-6 - PubMed
  13. Clin Res Hepatol Gastroenterol. 2014 Oct;38(5):564-9 - PubMed
  14. J Hepatol. 2016 Apr;64(4):813-22 - PubMed
  15. J Gastroenterol Hepatol. 2021 Jan;36(1):240-248 - PubMed
  16. Hepatology. 2018 Dec;68(6):2413-2423 - PubMed
  17. Gut. 2013 Aug;62(8):1231-2 - PubMed
  18. Lab Invest. 2010 Jul;90(7):1024-32 - PubMed
  19. Gut. 2011 Oct;60(10):1307-8 - PubMed
  20. Clin Chem Lab Med. 2014 Mar;52(3):453-61 - PubMed
  21. J Hepatol. 2020 Dec;73(6):1586-1588 - PubMed
  22. Clin Transl Gastroenterol. 2021 Mar 1;12(3):e00315 - PubMed
  23. J Leukoc Biol. 2012 Dec;92(6):1177-86 - PubMed
  24. Aliment Pharmacol Ther. 2012 Jul;36(2):173-80 - PubMed
  25. Liver Int. 2016 Oct;36(10):1549-57 - PubMed
  26. Aliment Pharmacol Ther. 2012 Jun;35(12):1424-33 - PubMed
  27. PLoS One. 2017 Dec 13;12(12):e0189345 - PubMed
  28. Scand J Clin Lab Invest. 2002;62(4):293-9 - PubMed
  29. J Hepatol. 2013 May;58(5):956-61 - PubMed
  30. J Gastroenterol Hepatol. 2018 Feb;33(2):484-491 - PubMed
  31. Shock. 2010 Apr;33(4):412-8 - PubMed
  32. J Viral Hepat. 2020 Jan;27(1):28-35 - PubMed
  33. Hepatology. 1990 May;11(5):787-97 - PubMed
  34. Am J Gastroenterol. 2014 Nov;109(11):1749-56 - PubMed
  35. Hepatology. 2005 Mar;41(3):422-33 - PubMed
  36. Scand J Gastroenterol. 2004 Jun;39(6):594-9 - PubMed
  37. Nat Rev Dis Primers. 2018 Aug 16;4(1):16 - PubMed
  38. J Gastroenterol Hepatol. 2015 Aug;30(8):1293-300 - PubMed
  39. Liver Int. 2017 Apr;37(4):569-575 - PubMed
  40. J Gastroenterol. 2005 Jan;40(1):52-6 - PubMed
  41. Scand J Clin Lab Invest. 2012 Feb;72(1):1-13 - PubMed

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