The potential of lipopolysaccharide-binding protein to predict the severity and prognosis of cirrhotic patients with severe sepsis.

Bacterial translocation and episodic endotoxemia are common phenomena in cirrhotic patients and animals. Lipopolysaccharides (LPSs), which can promote the synthesis of LPS-binding protein (LBP) in the liver, intestine, and lungs, play a central role in the pathophysiology of sepsis. LBP is an acute phase protein that plays an important role in LPS signaling. In cirrhosis, cytokines and LBP levels are increased and responsible for the hyperdynamic circulation. Albillos et al reported that the subset of ascitic cirrhotic patients with marked immune and hemodynamic derangement can be identified by increased LBP levels. High LBP levels have also been found to be predictive of severe bacterial infections in cirrhotic patients with ascites. Previous studies suggested that the serum level of cytokines including LBP can serve as surrogate markers for the prognosis of cirrhosis. It has been reported that elevated LBP levels may be related to bacterial passage from the gut to the circulation without overt infection in cirrhotic patients with ascites. A recent study including 286 cirrhotic patients and 100 controls discovered that cirrhotic patients with increased serum LBP levels were four times more likely to have severe bacterial infection during follow-up than cirrhotic patients with normal LBP. In this issue of the Journal of the Chinese Medical Association, Chen and colleagues evaluated the serum LBP, inflammatory cytokines, and the relationship between LBP concentrations, liver function reserve, and outcome in 58 critically ill cirrhotic patients with severe sepsis. Their study concluded that the concentration of LBP is inversely associated with disease severity scores and 28-day outcomes in critically ill cirrhotic patients with severe sepsis. A previous similar study reported that increased LBP levels inhibited LPS-mediated cytokine release and prevented hepatic failure, resulting in a significantly improved survival rate of experimental mice. Thus, it has been suggested that low or constitutive levels of LBP facilitate the recognition of LPS and early activation of immune cells, whereas acute phase elevated LBP levels serve to neutralize LPS to prevent overstimulation of the immune system. Another investigation similar to the Chen et al study reported that high concentrations of LBP in serum of patients with severe sepsis or septic shock inhibit the LPS response in human monocyte. Using isolated