J Vis Exp. 2026 Sep 1;(235). doi: 10.3791/73747.

ABSTRACT

Liver resection and liver transplantation remain cornerstone treatments for many hepatobiliary diseases, yet postoperative infection, impaired liver regeneration, and post-hepatectomy liver failure (PHLF) remain serious complications. Perioperative stressors can disrupt the gut-liver axis by altering the intestinal microbiota, epithelial barrier integrity, microbial metabolites, bile acid signaling, and host immunity. This review examines how these alterations relate to clinical outcomes and evaluates evidence for microbiota-targeted interventions, including probiotics, synbiotics, nutritional optimization, antibiotic stewardship, bile acid modulation, and emerging multiomics strategies. We distinguish liver resection from living-donor and deceased-donor liver transplantation because the patient populations, graft or remnant anatomy, ischemia-reperfusion exposures, immune status, and outcome definitions differ. Clinical evidence most consistently supports selected pro-/synbiotic strategies for reducing postoperative infection in higher-risk settings, whereas microbiome-based prediction of PHLF, fecal microbiota transplantation (FMT), bile acid-directed therapy, and precision multiomics-guided pathways remain investigational. Future work should use transparent literature identification, standardized perioperative protocols, risk-defined populations, external validation, and prospective multicenter trials. A better understanding of gut-liver interactions may help preserve beneficial host-microbial signals while limiting translocation and inflammation during recovery.

PMID:42683887 | DOI:10.3791/73747

Int J Gen Med. 2026 Mar 24;19:590621. doi: 10.2147/IJGM.S590621. eCollection 2026.

ABSTRACT

Inflammatory bowel disease (IBD) involves chronic intestinal inflammation driven by gut-brain axis imbalance, fostering complications through an "inflammation-neuro-coagulation" triad. Current staging systems inadequately capture the dynamics of this multidimensional network. Therefore, integrated multi-omics analyses-including metagenomics, metabolomics, and single-cell transcriptomics-are essential to construct dynamic models that monitor coagulation, microbiome, and metabolism for precise assessment of disease activity and thrombotic or bleeding risks. Interventions targeting gut-brain axis nodes, such as eliminating tissue factor-positive (TF⁺) T cells or modulating vagal activity, show potential to disrupt the inflammation-coagulation cycle, although rigorous randomized trials are still needed. Artificial intelligence (AI)-assisted systems that integrate real-time biomarker monitoring with multi-omics predictions represent a novel paradigm for managing IBD-related coagulation dysfunction. Key challenges include elucidating gut-brain-liver axis regulation of coagulation and characterizing platelet functional heterogeneity. Future efforts must prioritize ethically compliant multi-omics platforms and racially stratified risk models to advance personalized coagulation management in IBD.

PMID:41913906 | PMC:PMC13033200 | DOI:10.2147/IJGM.S590621