Rifaximin reduces gut-derived inflammation in severe acute pancreatitis: an experimental animal model and randomized controlled trial
Abstract
ABSTRACT Severe acute pancreatitis (SAP) is characterized by systemic inflammation and intestinal barrier dysfunction and is often associated with gut microbiota dysbiosis. Rifaximin, a gut-specific non-absorbable antibiotic, is known to modulate the gut microbiota. Here, we investigated rifaximin’s effects and mechanisms in SAP using murine models and a single-center, open-label, randomized controlled trial (Chinese Clinical Trial Registry: ChiCTR2100049794). In mice, rifaximin attenuated pancreatic injury and systemic inflammation and altered gut microbiota composition by decreasing mucin-degrading genera such as Akkermansia (P < 0.05). These protective effects persisted in antibiotic-treated and germ-free mice, suggesting mechanisms not solely dependent on gut microbiota modulation. In patients with predicted SAP (n = 60), rifaximin significantly reduced systemic inflammation compared with controls. WBC decreased from a median of 11.50 × 10⁹/L (IQR 8.76–15.68) to 8.49 × 10⁹/L (6.93–10.20; P = 0.04) and TNF-α from 15.05 pg/mL (12.73–19.75) to 11.00 pg/mL (8.74–15.40; P = 0.009). However, the incidence of culture-confirmed infection did not differ between the rifaximin and control groups (13.3% vs. 13.3%; RR, 1.00; 95% CI, 0.28–3.63). Adverse events were comparable between groups. Metagenomic analyses revealed suppression of mucin-degrading bacteria (e.g., Akkermansia, Bacteroides fragilis, and Hungatella hathewayi) (P < 0.05) and reductions in mucin-degrading…
How strong is the evidence?
Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design. Reported size: 60 participants or records.
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