ROLE OF GUT MICROBIOME DYSBIOSIS IN TRIGGERING RECURRENT ACUTE PANCREATITIS IN NON-ALCOHOLIC PATIENTS

Recurrent acute pancreatitis (RAP) remains a clinical challenge,particularly in non-alcoholic patients where 20–30% of cases are idiopathic despite extensive evaluation.Recent studies highlight a potential role for gut microbiome dysbiosis in triggering and perpetuating recurrent pancreatic injury. This review summarizes the current evidence linking gut microbiome dysbiosis with RAP in non-alcoholic patients, explores underlying mechanisms, and discusses emerging diagnostic and therapeutic strategies.RAP arises from a complex interplay of ductal obstruction,genetic predisposition, metabolic risk factors, and immune dysregulation. Growing evidence indicates that guts microbiome disturbances—characterized by reduced microbial diversity, overgrowth of pathobionts such as Enterococcus and Escherichia/Shigella,and depletion of beneficial commensals like Lactobacillus—may amplify inflammation and lower the threshold for recurrence. Dysbiosis contributes to intestinal barrier dysfunction, bacterial translocation, and activation of innate immune pathways,including toll-like receptors and the NLRP3 inflammasome.Microbiome-derived biomarkers, including diversity indices, metabolite profiles (e.g., short-chain fatty acids, diaminopimelic acid), and surrogate markers of barrier dysfunction, show promise for predicting RAP risk. Therapeutic approaches aimed at restoring eubiosis,such as prebiotics,probiotics,and fecal microbiota transplantation,are under investigation,although clinical data remain heterogeneous. Gut microbiome dysbiosis likely plays a pathogenic role in non-alcoholic RAP through multiple overlapping mechanisms.Future research should focus on longitudinal human studies and randomized controlled trials to establish causality and refine microbiome-based interventions.Precision medicine approaches that integrate microbial,genetic,and immune profiling may ultimately transform prevention and management of RAP.