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Updated: Feb 19, 2026

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Circulating CXCL10 in cirrhotic portal hypertension might reflect systemic inflammation and predict ACLF and
Jennifer M Lehmann1, Karina Claus1, Christian Jansen1
1Department of Internal Medicine I, University Clinic Bonn, Bonn, Germany.
Insights
In severe portal hypertension, higher circulating CXCL10 levels correlate with decompensation and mortality. A decrease in CXCL10 after transjugular intrahepatic portosystemic shunt (TIPS) indicates better survival.
Area of Science:
- Hepatology
- Immunology
- Vascular Biology
Background:
- Chemokine (C-X-C motif) ligand 10 (CXCL10) role in severe portal hypertension is unknown.
- CXCR% ligands are implicated in hepatic injury, inflammation, and fibrosis.
- CXCL9 and CXCL11 are linked to survival in patients undergoing transjugular intrahepatic portosystemic shunt (TIPS).
Purpose of the Study:
- Investigate the role of CXCL10 in severe portal hypertension.
- Determine if CXCL10 levels predict outcomes in patients receiving TIPS.
- Assess the prognostic value of CXCL10 level changes post-TIPS.
Main Methods:
- Analyzed 89 cirrhotic patients.
- Measured CXCL10 protein levels in portal and hepatic blood pre- and post-TIPS.
- Assessed CXCL10 and IL-8 levels in multiple blood compartments.
- Determined hepatic CXCL10-mRNA via real-time PCR.
Main Results:
- Circulating CXCL10 levels were higher in portal than hepatic veins, suggesting extrahepatic origin.
- Elevated CXCL10 correlated with ascites, higher Child scores, acute decompensation, acute-on-chronic liver failure (ACLF), and mortality.
- Decreased CXCL10 post-TIPS was associated with improved survival.
Conclusions:
- Circulating CXCL10 reflects systemic inflammation in severe portal hypertension.
- CXCL10 predicts survival and complications in TIPS patients.
- A post-TIPS decrease in CXCL10 is a favorable prognostic indicator.
Background & Aims:
CXCR% ligands play an important role in hepatic injury, inflammation and fibrosis. While CXCL9 and CXCL11 are associated with survival in patients receiving transjugular intrahepatic portosystemic shunt (TIPS), the role of CXCL10 in severe portal hypertension remains unknown.
Methods:
A total of 89 cirrhotic patients were analysed. CXCL10 protein levels were measured in portal and hepatic blood at TIPS insertion and 2 weeks later in 24 patients. CXCL10 and IL8 levels were assessed in portal, hepatic, cubital vein and right atrium blood in a further 25 patients at TIPS insertion. Furthermore, real-time PCR determined hepatic CXCL10-mRNA in 40 cirrhotic patients.
Results:
Hepatic CXCL10 showed no association with decompensation. By contrast, circulating CXCL10-levels were higher in portal than in hepatic vein blood, suggesting an extrahepatic source of CXCL10 in cirrhosis. However, CXCL10 protein in blood samples from portal, hepatic, cubital veins and right atrium correlated excellently with each other and with IL-8 levels. Higher CXCL10 circulating levels were associated with presence of ascites and higher Child scores. Higher CXCL10 circulating protein levels were associated with acute decompensation, acute-on-chronic liver failure (ACLF) and independently with mortality. Moreover, a decrease in CXCL10 protein levels after TIPS insertion was associated with better survival in each cohort and analysed together.
Discussion:
Circulating CXCL10 possibly reflects systemic inflammation and it is correlated with acute decompensation, ACLF and complications in patients with severe portal hypertension receiving TIPS. CXCL10 predicts survival in these patients and a decrease in CXCL10 after TIPS may be considered a good prognostic factor.
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