A retrospective cohort evaluates oral calcium butyrate's clinical impact in inflammatory bowel disease, suggesting beneficial effects.
Background Reduced microbial production of butyrate is implicated in mucosal barrier dysfunction and immune dysregulation in inflammatory bowel disease (IBD)(1,2). Oral butyrate supplementation may support mucosal healing; however, real-world data remain scarce.To evaluate one-year safety, tolerability, and clinical, biochemical, intestinal ultrasound (IUS), and endoscopic outcomes of adjunctive oral calcium butyrate in IBD patients receiving advanced therapies. Methods A retrospective, single-center cohort was conducted between December 2024 and November 2025. Adult patients with ulcerative colitis (UC) or Crohn’s disease (CD) received oral calcium butyrate 900 mg/day (450 mg twice daily) as adjunct therapy while remaining on stable background treatment: Anti-TNF: 48% (infliximab /adalimumab) Ustekinumab: 32% Vedolizumab: 12% Upadacitinib: 8% Clinical activity scores, fecal calprotectin (FCP), CRP, ESR, IUS (bowel wall thickness [BWT], Limberg Doppler), and endoscopic assessments (Mayo Endoscopic Score, SES-CD) were recorded at baseline and 12 months. Missing data (FCP 22%, IUS 12%, endoscopy 28%) were addressed using multiple imputation. Results Fifty patients were included (25 UC, 25 CD), mean age 37 ± 11 years, mean disease duration 5.9 ± 4.3 years.Safety and tolerability: treatment persistence 78%; good/very good tolerability 82%; mild gastrointestinal adverse events 16%; no serious adverse events.Clinical outcomes: clinical response 70%; clinical remission 48%; steroid-free remission 36%.Biochemical & IUS changes: median FCP Δ − 260 µg/g, CRP Δ − 3.5 mg/L, ESR Δ − 8 mm/hr; BWT Δ − 1.0 ± 0.9 mm, Doppler improvement 41%, transmural healing 18%.Endoscopy (subset): UC mucosal healing (MES 0–1) 58%; CD endoscopic response (SES-CD ≥50% reduction) 41%; endoscopic remission 18%. Conclusion Adjunctive oral calcium butyrate 900 mg/day was safe, well tolerated, and associated with improvements across clinical, biomarker, IUS, and endoscopic outcomes in a real-world cohort treated with biologics and JAK inhibitors. Findings support further controlled evaluation of butyrate as a microbiota-targeted therapeutic option in IBD. References: 1. Chapman, M. A., et al. “Butyrate oxidation is impaired in the colonic mucosa of sufferers of quiescent ulcerative colitis.” Gut 35.1 (1994): 73-76. 2. Jangi, Sushrut, et al. “Microbial butyrate capacity is reduced in inflamed mucosa in patients with ulcerative colitis.” Scientific Reports 14.1 (2024): 3479. Conflict of interest: Karakan, Tarkan: None Kilic, Guner: No conflict of interest Karataş, Ali: No conflict of interest Cindoruk, Mehmet: No conflict of interest
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