BACKGROUND Hepatic encephalopathy (HE) can be considered a result of dysregulated gut-liver-brain axis function, where cognitive impairment can be reversed or prevented by the beneficial effects induced by "gut-centric" therapies, such as the administration of nonabsorbable disaccharides, nonabsorbable antibiotics, probiotics and prebiotics. AIM To assess the short-term efficacy and safety of the probiotic Escherichia coli Nissle (EcN) 1917 strain compared to lactulose and rifaximin in patients with minimal/mild HE. METHODS From January 2017 to March 2020, a total of 45 patients with HE were enrolled in this prospective, single-centre, open-label, randomized study. Participants were randomly assigned at a ratio of 1:1:1 to one of the treatment groups: The EcN group ( n = 15), lactulose group ( n = 15) or rifaximin group ( n = 15) for a 1 mo intervention period. The main primary outcomes of the study were changes in serum ammonia and Stroop test score. The secondary outcomes were markers of a chronic systemic inflammatory response (ІL-6, ІL-8, and IFN-γ) and bacteriology of the stool flora evaluated by specialized nonculture techniques after a 1 mo intervention period. RESULTS Patients who were given rifaximin or EcN showed a more significant reduction in serum ammonia and normalization of Bifidobacteria and Lactobacilli abundance compared to the lactulose group. However, the most pronounced restoration of the symbiotic microflora was associated with EcN administration and characterized by the absence of E. coli with altered properties and pathogenic enterobacteria in patient faeces. In the primary outcome analysis, improvements in the Stroop test parameters in all intervention groups were observed. Moreover, EcN-treated patients performed 15% faster on the Stroop test than the lactulose group patients ( P = 0.017). Both EcN and rifaximin produced similar significant reductions in the proinflammatory cytokines INF-γ, IL-6 and IL-8. EcN was more efficient than lactulose in reducing proinflammatory cytokine levels. CONCLUSION The use of the probiotic EcN strain was safe and quite efficient for HE treatment. The probiotic reduced the ammonia content and the level of serum proinflammatory cytokines, normalized the gut microbiota composition and improved the cognitive function of patients with HE. The application of the EcN strain was more effective than lactulose treatment.

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Background: The pathophysiology of hepatic encephalopathy is incompletely understood. It remains illusive how the contributing factors of neuronal ammonia accumulation, cell swelling and inflammation interact. Objective: Correlation of neuronal autoantibody levels to the degree of hepatic encephalopathy as first indication of immune mediated pathogenesis. Methods: We investigated serum autoantibody levels of representative brain proteins in patients with hepatic encephalopathy as well as in an experimental rat model with cirrhosis and hepatic encephalopathy after carbon tetrachloride exposure. They were examined in relation to presence of hepatic encephalopathy and the degree of neurological impaiment evaluated by quantitative scores. Results: In hepatic encephalopathy an increase of all of the examined antibodies was observed in serum. The grade of antibody elevation correlated to the degree of encephalopathy registered by quantitative evaluation of brain dysfunction. Conclusion: The degree of hepatic encephalopathy parallels neuronal autoantibody elevation. In case a causal relationship could finally be established, it adds to the understanding of hepatic encephalopathy and may open a new perspective for treatment of this handicaping condition by immunosuppressive strategies.

Introduction. The work is devoted to problem of gastrointestinal tract functioning due to chronic problem in kidneys. The initial recognition of kidney disease as independent from other medical conditions is widely attributed to Richard Bright’s 1827 book “Reports of Medical Cases,” which detailed the features and consequences of kidney disease. The CKD influence GIT by Disruption of the colonic microbiome and its attendant as a result of which there is loss of gut barrier integrity and increased generation of uremic toxins resulting in disruption of GIT normal functioning. Goal. To study the causes of clinical manifestations of chronic kidney disease and how it affects GIT. Materials and Methods. Review of modern and foreign literary sources; methods – description, analysis, abstracting. Results and discussion. CKD is common in US and in adults over 30 the reason behind that is Diabetes leading to kidney disease. Both: type 1 and type 2 diabetes. But also heart disease and obesity can contribute to the damage that causes kidneys to fail. Research suggests that gene GPX1, GSTO1, GSTO2, UMOD, and MGP genes are associated with CKD. The pathophysiology of CKD has a lot to contribute in GIT malfunctioning. Conclusions. The link between GIT malfunctioning and kidney pathology can be explained by the pathophysiology of CKD and its outcomes affecting GIT.