Elucidation of the gut-liver axis is crucial for the management of liver cirrhosis. Various researches focussing on the changes of intestinal functions form the core of investigation in this field. Majority of earlier studies concluded small intestinal dysmotility in their patients with liver cirrhosis whereas remarkable changes in the contraction pattern were seen in early manometric studies. Multiple investigations correlated to the severity of the liver disease (e.g., Child-Pugh class), the presence of small intestinal bacterial overgrowth (SIBO) and hepatic encephalopathy (HE) along with the history of spontaneous bacterial peritonitis revealed that the orocecal transit time, predominantly small intestinal transit is prolonged in these patients. Moreover, bacteriologically proven SIBO in proximal jejunal aspiration has been found to be present in up to 59% of cirrhotic patients and is related to systemic endotoxemia.

Clinical and experimental studies showed that delayed small bowel transit in liver cirrhosis might lead to SIBO, which plays an important role in the development of symptoms of abdominal pain and diarrhea. SIBO itself may delay intestinal transit in cirrhotic patients along with autonomic neuropathy, metabolic derangements and diabetic state. Various researches have also demonstrated that the gut microbiota is altered in cirrhotic patients and especially those with HE. Besides, authors have also highlighted a quantitative change in Bacteroides/Firmicutes ratio, with a prevalence of potentially pathogenic bacteria such as Enterobacteriaceae and reduction in specific commensals like Lachnospiraceae.

Patients with liver cirrhosis showed structural and functional changes in the intestinal mucosa, which stimulates an increase in intestinal permeability for bacteria and their products, these alterations act as a key pathogenetic factor for several complications. The mechanism responsible for intestinal barrier dysfunction in cirrhosis is multifactorial that involves alcohol, portal hypertension (vascular congestion and dysregulation), endotoxemia, SIBO, local inflammation and immunological factors and medications. 

Thus, the present review showed evidence of major achievements in relation to intestinal dysfunction in cirrhosis, which in turn, will contribute significantly in future gastroenterology research. However, further studies are required to ascertain whether this intestinal barrier dysfunction is supplemented and/or at least partially caused by structural and functional changes in the epithelial tight junction proteins. Furthermore, authors also highlighted the importance of an imperative need to develop new therapeutic strategies to modulate gut-liver interaction.

Source: Fukui H, Wiest R. Changes of Intestinal Functions in Liver Cirrhosis. Inflamm Intest Dis. 2016 Apr;1(1):24-40.