Metabolic Brain Disease

, Volume 28, Issue 2, pp 321–326

Gut microbiota and hepatic encephalopathy

Authors

    • Department of HepatologyPostgraduate Institute of Medical Education and Research
Original Paper

DOI: 10.1007/s11011-013-9388-0

Cite this article as:
Dhiman, R.K. Metab Brain Dis (2013) 28: 321. doi:10.1007/s11011-013-9388-0

Abstract

There is a strong relationship between liver and gut; while the portal venous system receives blood from the gut, and its contents may affect liver functions, liver in turn, affects intestinal functions through bile secretion. There is robust evidence that the pathogenesis of hepatic encephalopathy (HE) is linked to alterations in gut microbiota and their by-products such as ammonia, indoles, oxindoles, endotoxins, etc. In the setting of intestinal barrier and immune dysfunction, these by-products are involved in the pathogenesis of complications of liver cirrhosis including HE and systemic inflammation plays an important role. Prebiotics, probiotics and synbiotics may exhibit efficacy in the treatment of HE by modulating the gut flora. They improve derangement in flora by decreasing the counts of pathogenic bacteria and thus improving the endotoxemia, HE and the liver disease. Current evidence suggest that the trials evaluating the role of probiotics in the treatment of HE are of not high quality and all trials had high risk of bias and high risk of random errors. Therefore, the use of probiotics for patients with HE cannot be currently recommended. Further RCTs are required. This review summarizes the main literature findings about the relationships between gut flora and HE, both in terms of the pathogenesis and the treatment of HE.

Keywords

Gut microbiomeGut microecologyHepatic encephalopathyInflammationProbioticsPrebioticsSynbiotics

Abbreviations

HE

hepatic encephalopathy

MHE

minimal HE

HRQOL

health-related quality of life

PAMPs

pathogen-associated molecular patterns

SIBO

small intestinal bacterial overgrowth

CTP

Child–Turcotte–Pugh

MELD

model for end-stage liver disease

TNF

tumor necrosis factor

Copyright information

© Springer Science+Business Media New York 2013