S1465 Gut Microbiome Dysbiosis as a Diagnostic Signature in Early Inflammatory Bowel Disease

Introduction: Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn’s disease (CD), is a persistent inflammatory condition of the digestive tract that is increasing in prevalence worldwide. Early diagnosis remains a challenge, limiting timely intervention. Growing research indicates that gut microbial dysbiosis may precede clinical onset, offering promise as a non-invasive biomarker. This review aims to assess microbiome alterations during early or preclinical IBD. Methods: We conducted a systematic review on the basis of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. As part of this process, we thoroughly searched 3 major databases-Embase, PubMed, and the Cochrane library for studies that were published between 2018 and 2024. Included studies examined gut microbiota in early or newly diagnosed IBD patients compared to healthy controls. We individually analysed the studies, collected relevant information, and evaluated their quality utilizing the Newcastle-Ottawa Scale and the Cochrane Risk of Bias tool. Results: Twenty studies involving 4,689 participants (2,713 IBD patients, 1,976 controls) met inclusion criteria. Seventeen studies reported significantly reduced alpha diversity in early IBD, with one meta-analysis noting a combined mean difference of −0.45 (95% CI: −0.65 to −0.29; P < 0.001). Beta diversity analyses revealed distinct microbial community structures in IBD groups (P < 0.01 in 12 studies). Taxonomic analyses showed consistent depletion of beneficial commensals, including Faecalibacterium prausnitzii, Roseburia, and Bacteroidetes, in ≥14 studies. Fourteen studies reported enrichment of potentially pathogenic taxa such as Escherichia coli and Ruminococcus gnavus. Furthermore, twelve studies observed a decreased presence of Blautia and Coprococcus, which yield short-chain fatty acids (SCFAs), in early Crohn’s disease, with statistical significance (P < 0.05). Conclusion: This review highlights consistent patterns of microbial dysbiosis in early IBD. The reduction in alpha diversity, loss of anti-inflammatory taxa, and increase in pathobionts precede symptom onset, suggesting their utility as early diagnostic markers. Identifying these microbial signatures offers potential for non-invasive, preclinical screening and risk stratification strategies. Additional longitudinal research is necessary to confirm these biomarkers and incorporate microbiome profiling into individualized preventive healthcare.