Endotoxemia in patients with alcoholic and non-alcoholic cirrhosis and in subjects with no evidence of chronic liver disease following acute alcohol excess.

The presence of endotoxemia in peripheral venous blood was evaluated in 88 patients with alcoholic cirrhosis (AC) and in 42 patients with non-alcoholic cirrhosis (NAC). The two groups did not differ significantly with respect to mean age, liver function tests, and incidence of esophageal varices or ascites. In addition, a group of 24 patients with no evidence of chronic liver disease but with acute exposure to large quantities of alcoholic beverages was investigated. Endotoxin was determined by using the Limulus lysate test. The assays were carried out in the plasma samples by both the dilution technique and the chloroform extraction method. Endotoxemia was found more frequently in patients with AC (67.3%) than in patients with NAC (45.5%, P less than 0.025). The prevalence of endotoxemia was not significantly higher in cirrhotics with ascites or esophageal varices when compared to the subgroup without ascites or esophageal varices. Of the 24 patients with no evidence of chronic liver disease investigated because of acute alcohol excess immediately before admission 11 (45.7%) were found to have endotoxin in the peripheral venous blood. In 7 of these patients a second blood sample was tested 5-8 days later and no endotoxin could be detected. The latter results suggest that heavy alcohol abuse leads to transient endotoxemia even in patients with no signs of chronic liver disease. The findings support the hypothesis that gut-derived endotoxins might play a role in the initiation and aggravation of alcohol-induced liver disease.