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Progressive systemic inflammation precedes decompensation in compensated cirrhosis
Rubén Sánchez-Aldehuelo1,2, Càndid Villanueva2,3, Joan Genescà2,4
1Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
JHEP Reports : Innovation in Hepatology
|January 24, 2025
Summary
Systemic inflammation and bacterial products are present in compensated cirrhosis patients with significant portal hypertension. Worsening inflammation indicates a higher risk of decompensation.
Area of Science:
- Hepatology
- Gastroenterology
- Immunology
Background:
- Systemic inflammation is a known driver of decompensation in advanced cirrhosis.
- Its role in compensated cirrhosis, particularly concerning bacterial translocation, remains less understood.
Purpose of the Study:
- To evaluate inflammation and bacterial translocation markers in compensated cirrhosis.
- To analyze the dynamics of these markers in relation to the first decompensation event.
Main Methods:
- Biomarkers (IL-6, TNF-alpha, vWF, CRP, CD14, CD163, FABP, haptoglobin, LPS) were measured in compensated cirrhosis patients (n=164) over 2 years.
- Patients were stratified by the presence of clinically significant portal hypertension (CSPH) and decompensation development.
- Included patients with subclinical portal hypertension (n=54) and controls (n=35).
Main Results:
- Patients with CSPH showed higher baseline IL-6, CD163, FABP, and LPS levels compared to controls.
- IL-6 and LPS levels increased at 1 year in patients with CSPH, with a more pronounced IL-6 rise preceding decompensation.
- Elevated CD163 and FABP, and lower haptoglobin, were associated with decompensation across time points.
Conclusions:
- Compensated cirrhosis with CSPH is characterized by systemic inflammation and bacterial product presence.
- Progressive systemic inflammation precedes the first clinical decompensation in these patients.
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