The pathogenic mechanisms implicated in the failure of intestinal barrier in cirrhosis have not been fully elucidated as yet and remains to be investigated.
A research article to be published on 28 June 20008, in the World Journal of Gastroenterology addresses this question. The research team led by Dr. Shin and Dr. Lee investigated whether intestinal macromolecular permeability is altered in patients liver cirrhosis and its relationship with the serum TNF-α level and nitric oxide (NO) metabolite level in urine to clarify the role of intestinal macromolecular permeability, the serum TNF-α level and nitrite level in urine to the development of liver cirrhosis with ascites. The results suggest that increased intestinal macromolecular permeability and NO are probably of importance in the pathophysiology and progression of liver cirrhosis with ascites, and furthermore, increased intestinal permeability may be a contributory factor in the development of encephalopathy in liver cirrhosis.
In this study, there were no concomitant infections and a significantly higher TNF-α level in cirrhotic patients without ascites than healthy control subjects or patients with liver cirrhosis (LC) with ascites was seen; thus, there was a tendency for a negative correlation between the TNF-α level and Child-Pugh class in the advanced stage of LC. In advanced cirrhosis, hepatic damage and inflammation are reduced due to a decreased liver reserve and marked fibrosis, and consequently, ALT levels decrease. Additionally, diminished amounts of cytokine-producing cells such as hepatocytes and Kupffer cells may lead to a decrease of TNF-α production. In the current study, intestinal permeability index (%) and urinary nitrite excretion were significantly higher in patients with LC with ascites as compared to patients with LC without ascites or healthy control subjects, with a significant correlation.