{"doi":"10.1080/07853890.2026.2650232","title":"The role of systemic inflammation in hepatic encephalopathy: advances in inflammatory mechanisms, prevention and treatment research","abstract":null,"journal":"Annals of Medicine","year":2026,"id":625361,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":275211,"name":"Ying Wen","orcid":"0000-0003-0867-3958","position":1,"is_corresponding":false},{"id":1001134,"name":"Wen Wang","orcid":"0000-0001-8392-3457","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"The role of systemic inflammation in hepatic encephalopathy: advances in inflammatory mechanisms, prevention and treatment research","abstract":"OBJECTIVES: This review synthesizes current evidence establishing systemic inflammation as a key pathogenic driver in hepatic encephalopathy (HE) beyond hyperammonemia. It does not replace the ammonia hypothesis but rather acts as a critical synergistic factor, modulating and amplifying ammonia neurotoxicity. It further evaluates the mechanisms linking inflammation to HE and the therapeutic advances in inflammation-targeted prevention and treatment strategies. METHODS: A comprehensive narrative literature review was conducted, analyzing relevant preclinical models and clinical studies. The search and synthesis focused on inflammatory mechanisms in chronic liver disease, gut-liver-brain axis dysfunction, cirrhosis-associated immune dysfunction (CAID), and resulting neuroinflammatory pathways. RESULTS: Systemic inflammation, driven by gut dysbiosis, barrier failure, and CAID, amplifies ammonia neurotoxicity and independently contributes to neuroinflammation, blood-brain barrier disruption, and cerebral metabolic dysfunction in HE. Key inflammatory markers, such as IL-6, correlate with disease severity. Therapies targeting inflammation - particularly gut microbiota modulation with rifaximin and fecal microbiota transplantation (FMT) - demonstrate significant efficacy in reducing HE recurrence, lowering systemic inflammation, and improving cognitive outcomes. Other approaches, including albumin infusion, also show promise. CONCLUSIONS: Systemic inflammation is a pivotal and synergistic factor in HE pathogenesis. Combining anti-inflammatory strategies that target the gut-liver-brain axis with traditional ammonia-lowering therapies offers a more comprehensive and effective treatment paradigm. Future research should prioritize protocol optimization, long-term safety assessment, and the development of personalized treatment approaches.","is_dataset_classified":null,"base_score":0.0,"endowment":0.0,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"41904644","pmcid":"PMC13034708","openalex_id":"https://openalex.org/W7142622771","authors":[],"funders":[],"total_grants":0,"fwci":0.0,"citation_percentile":0.33442777,"influential_citations":0,"citation_trend":[],"oa_status":"gold","license":"cc-by-nc","oa_locations":[{"url":"https://www.tandfonline.com/doi/pdf/10.1080/07853890.2026.2650232?needAccess=true","host_type":"journal"},{"url":"https://www.tandfonline.com/doi/pdf/10.1080/07853890.2026.2650232?needAccess=true","host_type":"publisher"},{"url":"https://www.tandfonline.com/doi/pdf/10.1080/07853890.2026.2650232","host_type":"publisher"},{"url":"https://doi.org/10.1080/07853890.2026.2650232","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/41904644","host_type":"repository"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13034708/","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC13034708","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC13034708?pdf=render","host_type":"Europe_PMC"}],"fields_of_study":["Liver Disease and Transplantation","Organ Transplantation Techniques and Outcomes","Liver Diseases and Immunity","Humans","Hepatic Encephalopathy","Inflammation","Animals","Fecal Microbiota Transplantation","Gastrointestinal Microbiome","Ammonia","Rifaximin","Dysbiosis","Liver Cirrhosis","Hyperammonemia","Blood-Brain Barrier"],"mesh_terms":["Gastrointestinal Microbiome","Fecal Microbiota Transplantation","Rifaximin","Ammonia","Animals","Blood-Brain Barrier","Hepatic Encephalopathy","Humans","Inflammation","Liver Cirrhosis","Hyperammonemia","Dysbiosis"],"keywords":["Inflammation","Systemic inflammation","Systemic therapy","Clinical research","Clinical trial","Protocol (science)","Risk factor","Systemic inflammatory response syndrome","hepatic encephalopathy","Rifaximin","Fecal Microbiota Transplantation","Gastrointestinal Microbiome"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-04T06:33:21.954643Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}