| Abstract [eng] |
Aim of the study. To conduct a literature review and summarize current knowledge on hepatic encephalopathy by analyzing scientific studies from 2015 to 2025 that investigate the links between hepatic encephalopathy and the gut microbiota. Objectives of the study. To define the concept, clinical manifestations, classification, epidemiology, pathophysiological mechanisms, and treatment strategies of hepatic encephalopathy. To evaluate changes in the taxonomic composition of the gut microbiota in patients with hepatic encephalopathy and the effects of lactulose, probiotics, rifaximin, and fecal microbiota transplantation on the gut microbiota and clinical outcomes. Materials and methods. The literature search was conducted in the PubMed database. The MeSH terms "hepatic encephalopathy" and "gastrointestinal microbiome" were used, along with the keywords "microbiota," "microbiome," "dysbiosis," "gut-liver axis," and "gut-liver-brain axis." The literature review included 25 publications published between 2015 and 2025 that met the established inclusion and exclusion criteria. An additional 32 publications were included in the general section of the literature review. Results and conclusions. The clinical presentation of hepatic encephalopathy is characterized by a wide spectrum of cognitive impairments. The severity of symptoms ranges from clinically imperceptible changes detected by cognitive and neurophysiological tests to impaired consciousness, marked disorientation, and coma. Hepatic encephalopathy is classified according to four axes: etiology, severity of symptoms, temporal course, and precipitating factors. Hepatic encephalopathy most commonly occurs in patients with liver cirrhosis, and its onset indicates that the cirrhosis is decompensated. An analysis of epidemiological data reveals a steadily increasing prevalence of decompensated liver cirrhosis and, consequently, hepatic encephalopathy. Neurotoxicity caused by hyperammonemia remains the primary theory regarding the pathogenesis of hepatic encephalopathy; however, recent scientific literature emphasizes the importance of dysbiosis, systemic inflammation, and a compromised intestinal barrier. Studies indicate that patients with hepatic encephalopathy exhibit reduced diversity and abundance of the gut microbiota. Hepatic encephalopathy, across its various stages, is characterized by specific dysbiosis, as well as distinct concentrations of bacterial taxa and metabolites. These changes are associated with the development and progression of hepatic encephalopathy and poorer clinical outcomes; however, causal relationships have not been established or confirmed. Currently, standard treatment for hepatic encephalopathy includes lactulose and rifaximin; oral branched-chain amino acids, L-ornithine L-aspartate, neomycin, or metronidazole may also be prescribed. The studies reviewed emphasize that, in the context of lactulose treatment, patients’ baseline gut microbiota may determine the response to treatment, and an increase in the abundance of potentially beneficial bacteria is associated with better clinical outcomes. An analysis of rifaximin’s effects found that it reduces systemic inflammation and improves clinical outcomes. When evaluating the prophylactic effects of this drug and treatment with lower doses, positive results and better clinical outcomes are observed. Studies evaluating new, non-routinely approved treatment methods indicate that probiotics are well-tolerated by patients with liver cirrhosis and hepatic encephalopathy, and that the prophylactic administration of probiotics may improve clinical outcomes. Fecal microbiota transplantation also improves clinical outcomes, and its effectiveness depends on the characteristics of the donor and recipient as well as the establishment of the microbiota. |
