Endogenous endotoxemia in patients with liver cirrhosis--a quantitative analysis of endotoxin in portal and peripheral blood.

In order to investigate the mechanism of endogenous endotoxemia (that is, endotoxemia observed in the absence of infection) in patients with liver cirrhosis, the concentration of endotoxin in the portal (PO-Et) and peripheral blood (PE-Et) from fifty three patients undergoing abdominal surgery was simultaneously measured by a quantitative endotoxin assay. The PE-Et of the patients with liver cirrhosis (19.8 +/- 20.2 pg/ml, n = 23) was significantly elevated, when compared with that of the patients without liver cirrhosis (9.2 +/- 5.1 pg/ml, n = 30), and was close to the normal range of PE-Et obtained from thirty healthy volunteers (7.2 +/- 4.1 pg/ml, n = 30). The PO-Et was also higher in the patients with liver cirrhosis than in the patients without liver cirrhosis. Moreover, PO-Et was significantly higher than PE-Et in all the patients (p less than 0.05). The per cent difference in the endotoxin concentration between the portal and peripheral blood (percentage of delta Et) was significantly decreased in the cirrhotic patients, especially in those with esophageal varices, which was well correlated with the phagocytic activity of the reticuloendothelial system (RES) determined by the clearance of iron colloid. The endogenous endotoxemia is thus likely to be due to the impaired clearance of endogenous endotoxin in portal blood, resulting from both the decreased phagocytic activity of RES in the liver and the coexisting porta-systemic bypass.