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Editorial
. 2018 Sep 14;24(34):3813-3820.
doi: 10.3748/wjg.v24.i34.3813.

Clinical impact of microbiome in patients with decompensated cirrhosis

Affiliations
Editorial

Clinical impact of microbiome in patients with decompensated cirrhosis

Theodora Oikonomou et al. World J Gastroenterol. .

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.

Keywords: Decompensated cirrhosis; Dysbiosis; Hepatic encephalopathy; Liver carcinoma; Microbiome; Oral-gut-liver axis.

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Conflict of interest statement

Conflict-of-interest statement: No potential conflicts of interest. No financial support.

Figures

Figure 1
Figure 1
Pathophysiological mechanism showing the role of microbiome over the oral-gut-liver axis. (Arrows imply the successive steps over the pathophysiology of complications.) PH: Portal hypertension; HE: Hepatic encephalopathy; SBP: Spontaneous bacterial peritonitis; ACLF: Acute-on-chronic liver failure; HCC: Hepatocellular carcinoma.

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