Summary Background Progressive gut milieu (microbiota) changes occur in patients with cirrhosis and are associated with complications [e.g. hepatic encephalopathy (HE)]. Aim To examine the role of rifaximin in the management of HE and other complications of cirrhosis, including potential mechanisms of action and the need for future studies. Methods A literature search was conducted using the keywords ‘rifaximin’, ‘hepatic encephalopathy’, ‘ascites’, ‘variceal bleeding’, ‘peritonitis’, ‘portal hypertension’, ‘portopulmonary hypertension’ and ‘hepatorenal syndrome’. Results The nonsystemic agent rifaximin reduces the risk of HE recurrence and HE‐related hospitalisations in cirrhosis. In patients with cirrhosis, rifaximin modulates the bacterial composition of the gut microbiota without a consistent effect on overall faecal microbiota composition. However, rifaximin can impact the function or activities of the gut microbiota. For example, rifaximin significantly increased serum levels of long‐chain fatty acids and carbohydrate metabolism intermediates in patients with minimal HE. Rifaximin also favourably affects serum proinflammatory cytokine and faecal secondary bile acid levels. Conclusions The gut microenvironment and associated microbiota play an important role in the pathogenesis of HE and other cirrhosis‐related complications. Rifaximin's clinical activity may be attributed to effects on metabolic function of the gut microbiota, rather than a change in the relative bacterial abundance.
serum and urinary samples. The investigators should have measured and compared serum and urinary metabolites with other biomarkers including neutrophil gelatinase-associated lipocalin (NGAL). Serum concentrations of NGAL increase before those of sCr and help in the early detection of AKI in cirrhosis. (2) Increase in metabolites (e.g., kynurenate, tripeptides, and tetrapeptides) is not specific for patients with liver diseases and renal dysfunction. (3) It is not clear how the cutoff was set for determination of mean decrease in accuracy (MDA). For example, urinary kynurenate has an MDA of 30 in patients with AKI and 21 in those requiring dialysis. Whether a difference in MDAs has any correlation with disease state needs further investigation.The study should be more focused in patient selection by including only those with a high risk of developing severe and irreversible AKI and need for dialysis. These include patients with acute-onchronic liver failure, bacterial sepsis, complicated ascites, and acute variceal bleed. (4) Response to AKI determines need for dialysis. The clinical outcomes of patients with volume responsive mild prerenal AKI related to diuretic use are vastly different from those of patients with nonresponsive hepatorenal syndrome. Thus, we need to determine the relationship of serum and urinary metabolites with the type and severity of AKI as well as response of AKI. Timing of dialysis in the study was also not uniform across the centers. Finally, it would be interesting to know whether metabolomics-related outcomes are applicable for incident AKI in patients with cirrhosis and underlying chronic kidney disease.Author Contributions: A.J. was responsible for writing the manuscript and critical analysis. S.S. was responsible for critical analysis.
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