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Review Article
This review examines perioperative alterations in the gut–liver axis in liver surgery and their effects on postoperative outcomes. It evaluates microbiota-targeted interventions, highlighting stronger evidence for pro-/synbiotics in reducing infections, while microbiome biomarkers, bile acid therapies, fecal microbiota transplantation, and multiomics approaches remain investigational and require further clinical validation.
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.
Liver surgery remains a major treatment for hepatocellular carcinoma, cholangiocarcinoma, metastatic tumors, benign hepatobiliary disease, and end-stage liver disease. Modern anesthesia, parenchymal-sparing techniques, transplant care, and Enhanced Recovery After Surgery (ERAS) pathways have made these operations safer. Postoperative infection, delayed functional recovery, and PHLF remain serious complications1,2,3,4,5,6. Some of this risk begins in the intestine. Signals ....
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Mechanistic basis of perioperative gut-liver axis disruption
Under ordinary conditions, the liver receives a steady flow of microbial and metabolic signals from the gut. Low-grade exposure helps maintain hepatic immune tolerance without preventing a response to pathogens. Surgery can disturb that balance. Anesthesia, tissue trauma, hypoperfusion, antibiotics, and reduced availability of enteral substrates can reduce microbial diversity, weaken tight junctions, and increase intestinal permeability3,4,7. When the barrier fails, lipop....
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Perioperative stressors can cause detrimental alterations in the gut-liver axis, including dysbiosis, barrier dysfunction, altered microbial metabolites, and disturbed bile acid signaling, which may contribute to infection, systemic inflammation, and impaired regeneration after liver surgery. The most reproducible clinical signal is lower postoperative infection with selected pro-synbiotic regimens in high-risk hepatobiliary surgery and transplantation, but heterogeneity prevents a universal protocol. Evidence for PHLF p.......
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The authors declare that they have no conflicts of interest.
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