Magnetic resonance imaging‐quantified small bowel motility is a sensitive marker of response to medical therapy in Crohn's disease

Summary Background Magnetic resonance enterography ( MRE ) can measure small bowel motility, reduction in which reflects inflammatory burden in Crohn's Disease ( CD ). However, it is unknown if motility improves with successful treatment. Aim To determine if changes in segmental small bowel motility reflect response to anti‐ TNF α therapy after induction and longer term. Methods A total of 46 patients (median 29 years, 19 females) underwent MRE before anti‐ TNF α treatment; 35 identified retrospectively underwent repeat MRE after median 55 weeks of treatment and 11 recruited prospectively after median 12 weeks. Therapeutic response was defined by physician global assessment (retrospective group) or a ≥3 point drop in the Harvey–Bradshaw Index (prospective group), C‐reactive protein ( CRP ) and the Ma RIA score. Two independent radiologists measured motility using an MRE image‐registration algorithm. We compared motility changes in responders and nonresponders using the Mann–Whitney test. Results Anti‐ TNF α responders had significantly greater improvements in motility (median = 73.4% increase from baseline) than nonresponders (median = 25% reduction, P  < 0.001). Improved MRI ‐measured motility was 93.1% sensitive (95% CI : 78.0–98.1%) and 76.5% specific (95% CI : 52.7–90.4%) for anti‐ TNF α response. Patients with CRP normalisation (<5 mg/L) had significantly greater improvements in motility (median = 73.4% increase) than those with persistently elevated CRP (median = 5.1%, P  = 0.035). Individuals with post‐treatment MaRIA scores of <11 had greater motility improvements (median = 94.7% increase) than those with post‐treatment MaRIA score >11 (median 15.2% increase, P  = 0.017). Conclusions Improved MRI ‐measured small bowel motility accurately detects response to anti‐ TNF α therapy for Crohn's disease, even as early as 12 weeks. Motility MRI may permit early identification of nonresponse to anti‐ TNF α agents, allowing personalised treatment.