BACKGROUND/AIMS: Plasma endotoxin levels commonly increase in patients with liver cirrhosis. We purposed to identify change of intestinal permeability and frequency of endotoxemia in patients with viral liver cirrhosis. Additionally, we studied the relationship between plasma endotoxin levels and failure of gut barrier function. METHODOLOGY: Subjects included 27 patients with viral liver cirrhosis (LC) and 45 volunteers as healthy control (HC). Intestinal permeability index was determined by the level of urinary excretion of polyethylene-glycol after oral administration and plasma endotoxin levels by using quantitative Limulus assay. Grades of liver dysfunction were categorized by Child-Pugh classification and MELD score. RESULTS: Intestinal permeability indexes were higher in LC than in HC (1.48±0.56%, n=27 vs. 0.93±0.50%, n=45, p=0.019). Plasma endotoxin levels were higher in LC than in HC (0.35±0.17EU/ mL vs. 0.11±0.14EU/mL, p<0.001). In LC, plasma endotoxin levels progressively increased in relation to severity of liver dysfunction (Child-Pugh class A (0.31±0.17EU/mL), B (0.37±0.14EU/mL) and C (0.42±0.23EU/mL), p=0.013, MELD category 1/2/3/4=0.27±0.14/0.39±0.17/0.32±0.21/0.47±0.28E U/mL, p=0.043). LC with/without portal hypertension (1.47±0.55%, p<0.01/1.29±0.59%, p<0.05) had higher intestinal permeability indexes than HC (0.93±0.50%). CONCLUSIONS: Severity of liver dysfunction was associated with endotoxemia. Although gut barrier function did not show a significant relationship with endotoxemia, increased intestinal permeability may be a significant finding that at least in part is associated with the pathophysiology of viral liver cirrhosis.
BACKGROUND/AIMS: Plasma endotoxin levels commonly increase in patients with liver cirrhosis. We purposed to identify change of intestinal permeability and frequency of endotoxemia in patients with viral liver cirrhosis. Additionally, we studied the relationship between plasma endotoxin levels and failure of gut barrier function. METHODOLOGY: Subjects included 27 patients with viral liver cirrhosis (LC) and 45 volunteers as healthy control (HC). Intestinal permeability index was determined by the level of urinary excretion of polyethylene-glycol after oral administration and plasma endotoxin levels by using quantitative Limulus assay. Grades of liver dysfunction were categorized by Child-Pugh classification and MELD score. RESULTS: Intestinal permeability indexes were higher in LC than in HC (1.48±0.56%, n=27 vs. 0.93±0.50%, n=45, p=0.019). Plasma endotoxin levels were higher in LC than in HC (0.35±0.17EU/ mL vs. 0.11±0.14EU/mL, p<0.001). In LC, plasma endotoxin levels progressively increased in relation to severity of liver dysfunction (Child-Pugh class A (0.31±0.17EU/mL), B (0.37±0.14EU/mL) and C (0.42±0.23EU/mL), p=0.013, MELD category 1/2/3/4=0.27±0.14/0.39±0.17/0.32±0.21/0.47±0.28E U/mL, p=0.043). LC with/without portal hypertension (1.47±0.55%, p<0.01/1.29±0.59%, p<0.05) had higher intestinal permeability indexes than HC (0.93±0.50%). CONCLUSIONS: Severity of liver dysfunction was associated with endotoxemia. Although gut barrier function did not show a significant relationship with endotoxemia, increased intestinal permeability may be a significant finding that at least in part is associated with the pathophysiology of viral liver cirrhosis.