Research Square
Transient Gut Microbiota Modulation and Baseline Bacteroides Abundance Predict Constipation Recurrence in Children With Cerebral Palsy: A 4‑Year Longitudinal Cohort Study
By Li X, Yang W, Wang P and 2 others.
Abstract
Abstract Introduction : Cerebral palsy (CP) is frequently complicated by chronic constipation, yet the long-term sustainability of gut microbiota modulation and predictors of recurrence remain unclear. This study evaluated whether synbiotic-induced microbiota changes are sustained 4 years post-intervention and whether baseline gut microbial features predict constipation recurrence in children with CP. Methods This longitudinal observational cohort study included 25 children with CP and chronic constipation who received a 6‑month synbiotic intervention (probiotics plus psyllium husk fiber). Fecal 16S rRNA sequencing was performed at baseline, 6 months, and 48 months post-intervention. Constipation recurrence was defined using Rome IV criteria. Alpha diversity was assessed via the Shannon index, and functional pathways were predicted using PICRUSt2. Logistic regression with bootstrap resampling (1,000 replicates) was used to evaluate predictors of recurrence. Results Shannon diversity increased at 6 months versus baseline (Δ = 1.2, q = 0.019) but regressed to baseline levels at 48 months (q = 0.008 vs M6). Baseline Bacteroides abundance > 0.1% was associated with non-recurrence (OR = 3.2; 95% CI: 1.5–6.8; bootstrap 95% CI: 1.3–7.1; AUC = 0.78; p = 0.009). Recurrent cases (n = 4) showed persistent enrichment of predicted branched-chain amino acid and aromatic amino acid biosynthesis pathways at 48 months (q < 0.05), whereas non-recurrent children exhibited upregulation of tryptophan biosynthesis. All functional inferences are derived from 16S rRNA-based computational predictions and require metabolomic validation. Conclusions Synbiotic-induced gut microbiota benefits are transient after treatment cessation. Baseline Bacteroides abundance may inform personalized risk stratification, though this hypothesis‑generating threshold requires validation in larger prospective cohorts and confirmation through targeted metabolomics and immune profiling.



