Related Experiment Video
Updated: May 6, 2026

Cecal Ligation Puncture Procedure
Published on: May 7, 2011
Lipopolysaccharide binding protein in cirrhotic patients with severe sepsis
Yi-Yuan Chen1, Jau-Min Lien1, Yun-Shing Peng2
1Division of Gastroenterology, Chang Gung Memorial Hospital, Taipei, Taiwan, ROC; Chang Gung University, College of Medicine, Tao-Yuan, Taiwan, ROC.
Background:
Lipopolysaccharide binding protein (LBP) is an acute-phase protein produced by the liver. It has been shown that LBP plays an important role in the inflammatory response to sepsis. LBP has also been shown to protect animals from endotoxin challenge by facilitating the removal of endotoxin from the blood circulation. Cirrhotic patients are susceptible to bacterial infection. It is unknown whether pre-existing liver dysfunction impacts the LBP levels and thus the prognosis in severe sepsis.
Methods:
We evaluated the serum LBP, inflammatory cytokines, and the relationship between LBP concentrations, functional liver reserve and outcomes in 58 critically ill cirrhotic patients with severe sepsis.
Results:
The serum LBP levels were significantly higher in 28-day survivors, while the interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels were significantly higher in non-survivors. We analyzed the receiver operating characteristic (ROC) curve to determine the cut-off point for LBP to predict 28-day mortality. The cumulative rates at 28 days were 58.3% versus 16.7% for the high LBP group (>46 ng/mL) and low LBP group (<46 ng/mL) (p < 0.001). The high-LBP group had significantly lower INR, Child-Pugh, Model for End-stage Liver Disease (MELD) scores and TNF-α level. Meanwhile, the LBP levels were inversely correlated with INR, and Child-Pugh, MELD and sequential organ failure assessment (SOFA) scores.
Conclusion:
The concentration of LBP is associated inversely with disease severity scores and outcomes in critically ill cirrhotic patients with severe sepsis.
More Related Videos
Related Concept Videos
Formation of Lipopolysaccharides
Cirrhosis II: Pathophysiology

