Enterococcus faecium (EF) DNA plays a significant role in acute decompensated liver cirrhosis, particularly in cases of acute-on-chronic liver failure (ACLF). Cirrhosis, a severe liver condition, causes over 2 million deaths annually, with ACLF being the most critical stage due to systemic inflammation and multi-organ failure.
Enterococcus faecium (EF) DNA plays a significant role in acute decompensated liver cirrhosis, particularly in cases of acute-on-chronic liver failure (ACLF). Cirrhosis, a severe liver condition, causes over 2 million deaths annually, with ACLF being the most critical stage due to systemic inflammation and multi-organ failure. EF DNA was detected in 26% of cirrhosis patients, compared to only 1.3% of healthy individuals, highlighting its strong association with the disease.
EF DNA is linked to systemic inflammation, as evidenced by elevated levels of inflammatory markers like leukocytes, C-reactive protein (CRP), and interleukin-6 (IL-6). EF-positive patients, especially those with ACLF, exhibited worse liver function (higher bilirubin and AST levels) and kidney dysfunction (elevated serum creatinine), suggesting a connection to hepatorenal syndrome. EF DNA also correlates with portal hypertension, indicating that bacterial translocation worsens intestinal permeability, a key factor in inflammation and disease progression.
Molecular detection using RT-qPCR is highly effective in identifying EF DNA, outperforming traditional culture methods. Clinical biomarkers such as IL-6, CRP, and creatinine can help monitor EF-associated inflammation. Overall, EF DNA serves as a promising biomarker of gut barrier dysfunction, systemic inflammation, and kidney injury in decompensated cirrhosis and ACLF, offering potential for early diagnosis and targeted treatment.
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