Clinical impact of microbiome in patients with decompensated cirrhosis

Abstract

Cirrhosis is an increasing cause of morbidity and mortality. Recent studies are trying to clarify the role of microbiome in clinical exacerbation of patients with decompensated cirrhosis. Nowadays, it is accepted that patients with cirrhosis have altered salivary and enteric microbiome, characterized by the presence of dysbiosis. This altered microbiome along with small bowel bacterial overgrowth, through translocation across the gut, is associated with the development of decompensating complications. Studies have analyzed the correlation of certain bacterial families with the development of hepatic encephalopathy in cirrhotics. In general, stool and saliva dysbiosis with reduction of autochthonous bacteria in patients with cirrhosis incites changes in bacterial defenses and higher risk for bacterial infections, such as spontaneous bacterial peritonitis, and sepsis. Gut microbiome has even been associated with oncogenic pathways and under circumstances might promote the development of hepatocarcinogenesis. Lately, the existence of the oral-gut-liver axis has been related with the development of decompensating events. This link between the liver and the oral cavity could be via the gut through impaired intestinal permeability that allows direct translocation of bacteria from the oral cavity to the systemic circulation. Overall, the contribution of the microbiome to pathogenesis becomes more pronounced with progressive disease and therefore may represent an important therapeutic target in the management of cirrhosis.

Gut-Liver Axis, Gut Microbiota, and Its Modulation in the Management of Liver Diseases: A Review of the Literature

“…It has been shown that microbiota of the sigmoid colon in liver cirrhosis patients differs in those with HE when compared with patients without HE [51]. Gut dysbiosis in liver cirrhosis also contributes to the development of Spontaneous Bacterial Peritonitis (SBP) through damaged intestinal barrier and a higher degree of microbial translocation [52].…”

Contribution of the Intestinal Microbiome and Gut Barrier to Hepatic Disorders

“…Prolonged liver inflammation results in cirrhosis and end-stage liver disease (ESLD) that places patients at risk for spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), and ultimately hepatocellular carcinoma (HCC). 139 Compared with healthy individuals, patients with cirrhosis have slower intestinal transit time, intestinal bacterial overgrowth, and altered fecal microbial profiles, with enrichment of Proteobacteria and Fusobacteria and reduced Bacteroidetes. [139][140][141][142] Fecal microbial signatures of patients with cirrhosis vary with disease severity (compensated vs uncompensated cirrhosis) and might be used to predict outcomes of hospitalized patients.…”

“…139 Compared with healthy individuals, patients with cirrhosis have slower intestinal transit time, intestinal bacterial overgrowth, and altered fecal microbial profiles, with enrichment of Proteobacteria and Fusobacteria and reduced Bacteroidetes. [139][140][141][142] Fecal microbial signatures of patients with cirrhosis vary with disease severity (compensated vs uncompensated cirrhosis) and might be used to predict outcomes of hospitalized patients. 143 Intriguingly, liver transplantation has been correlated with partial reversal of the gut dysbiosis associated with cirrhosis.…”

Gut microbiota signatures in Schistosoma japonicum infection-induced liver cirrhosis patients

“…Microbiota dysbiosis was often reported in cirrhosis patients: (I) autochthonous/non-autochthonous taxa ratio reduction; (II) Firmicutes/Bacteroidetes ratio inversion; or (III) increased prevalence of potentially pathogenic bacteria [42,43,44]. Interestingly, the liver-gut axis was involved in the physiopathology of cirrhosis: overgrown intestinal bacteria have the potential to translocate across the leaky gut barrier and reach the liver, leading to cirrhosis development or progression [45]. However, few studies explored the gut microbiota in the context of S. japonicum infection-induced liver cirrhosis.…”