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Pentraxin-3 is not related to disease severity in cirrhosis and hepatocellular carcinoma patients

Authors
  • Feder, Susanne1
  • Haberl, Elisabeth M.1
  • Spirk, Marlen1
  • Weiss, Thomas S.1
  • Wiest, Reiner2
  • Buechler, Christa1
  • 1 Regensburg University Hospital,
  • 2 Department of Visceral Surgery and Medicine, University Inselspital, Bern, Switzerland
Type
Published Article
Journal
Clinical and Experimental Medicine
Publisher
Springer International Publishing
Publication Date
Feb 20, 2020
Volume
20
Issue
2
Pages
289–297
Identifiers
DOI: 10.1007/s10238-020-00617-4
PMID: 32078718
PMCID: PMC7181432
Source
PubMed Central
Keywords
License
Unknown

Abstract

The acute-phase protein pentraxin-3 (PTX3) is a component of the innate immune system. Inflammation and tissue injury increased PTX3 in the injured liver, and accordingly, circulating PTX3 was induced in patients with chronic liver diseases. In the present study, PTX3 protein was determined in systemic, hepatic, and portal vein plasma of patients with liver cirrhosis to assess a possible association between hepatic PTX3 release and extent of liver injury. However, PTX3 levels were not related to disease severity. Of note, portal PTX3 levels were higher than concentrations in the hepatic vein. PTX3 in the hepatic and portal veins was negatively correlated with factor V, antithrombin 3, and prothrombin time. PTX3 did neither correlate with C-reactive protein nor galectin-3 or resistin, whereby the latter two proteins are associated with hepatic injury. PTX3 levels were not changed in cirrhosis patients with ascites or varices and did not correlate with the hepatic venous pressure gradient. Likewise, serum PTX3 was not correlated with histological steatosis, inflammation, or fibrosis stage in patients with hepatocellular carcinoma (HCC). Moreover, PTX3 was not associated with tumor node metastasis classification in HCC. Above all, PTX3 increased in hepatic, portal, and systemic blood immediately after transjugular intrahepatic portosystemic shunt (TIPS). Higher PTX3 in portal than hepatic vein plasma and further increase after TIPS suggests that the liver eliminates PTX3 from the circulation. In summary, PTX3 is not of diagnostic value in cirrhosis and HCC patients.

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