Segment-level prediction of endoscopic activity in ulcerative colitis using magnetic resonance enterography and fecal calprotectin: a Bayesian multilevel study
How much can MR enterography and fecal calprotectin tell us about endoscopic activity in individual colonic segments?
Background
Treat-to-target strategies in UC, codified by the STRIDE-II consensus, require repeated objective confirmation of mucosal healing. In practice, this demand defaults to colonoscopy, an invasive, resource-intensive procedure that is difficult to justify at the frequency modern monitoring protocols require.
Non-invasive surrogates have improved but remain incomplete. Fecal calprotectin (FC) offers a validated and accessible index of mucosal inflammation, but it is a patient-level summary: it says something is wrong somewhere, not where, and not with what probability. Intestinal ultrasound (IUS) has emerged as a strong bedside tool for real-time assessment across most colonic segments and is now embedded in ECCO guidance (Kucharzik et al. 2025). Its principal limitation is the rectum, where sonographic windows are unreliable, and the structural detail it provides is inherently less rich than cross-sectional imaging.
MR enterography occupies a different position. Its strength in luminal Crohn’s disease is well established, and the transmural, segment-level imaging it provides across the entire colon makes it conceptually well suited to UC monitoring. What has been missing is evidence that MRE features carry independent predictive value for endoscopic disease activity at the segment level, and a modelling framework that translates those features into an interpretable risk estimate rather than a forced active/inactive classification.
This prospective, single-centre study included 49 adults with UC, contributing 245 segment-matched MRE and colonoscopy observations, alongside 30 controls.
The Model
The outcome variable in this study is the Mayo Endoscopic Subscore (MES), scored 0 to 3 per colonic segment. This scale is ordered and ranked, but the steps between categories are not equal in clinical or statistical terms. Collapsing it to a binary active/inactive threshold would discard information and, more importantly, would force a false certainty on the distinction between MES 1 and MES 2, which is precisely the most contested and clinically consequential boundary in UC endoscopy. An ordered logistic regression model preserves the ranked structure of the outcome and estimates separate thresholds between adjacent categories.
The multilevel structure follows from the study design. Each patient contributes five segments, and those segments share the patient’s biology, treatment history, and systemic inflammatory burden. Treating 245 segments as 245 independent observations would underestimate uncertainty in the segment-level predictions and produce overconfident interval estimates. A multilevel ordinal model with a patient random intercept explicitly accounts for this within-patient correlation and captures unmeasured individual-level heterogeneity.
Inference was conducted in a Bayesian framework. The practical consequence is that the model returns a posterior probability distribution over MES 0–3 rather than only a point classification. The primary threshold was MES ≥2. For triage, a predicted probability below 0.387 was assigned GREEN, a probability of 0.766 or above was assigned RED, and intermediate values were assigned YELLOW. These are risk strata for further clinical assessment, not automatic decisions about colonoscopy or treatment.
Predictors entered the model at two levels. At the segment level: bowel wall thickness, length of affected segment as a proportion of total segment length, and presence of arterial enhancement on MRE. At the patient level, shared across all five of that patient’s segments: fecal calprotectin.
What It Shows
Across 49 adults with UC and 245 colonic segments, bowel wall thickness was the clearest imaging predictor of higher MES. Affected segment length and arterial hyperenhancement also contributed, while fecal calprotectin retained an independent association. That combination is useful because calprotectin supplies patient-level inflammatory context and MRE supplies local, segment-level information.
Three discrimination estimates are reported for MES ≥2, and the distinction between them is not a technicality. The marginal AUC was 0.782: this uses the measured predictors without a known patient-specific random effect and is the relevant estimate for a new patient. Grouped 10-fold cross-validation, with every patient’s segments kept in the same fold, produced an AUC of 0.765. This is internal validation rather than evidence of performance at another centre. The conditional AUC was 0.930, but it incorporates the estimated patient random effect and therefore describes within-cohort discrimination when patient-level information is available; it should not be read as new-patient performance.
Discrimination was also threshold-dependent: the marginal AUC was 0.835 for MES ≥1 and 0.868 for MES 3. The MES 1/2 distinction was the weakest boundary. Under the three-tier scheme, GREEN and RED together accounted for 131 of 245 segments (53.5%); the remaining segments were YELLOW. The intermediate tier is useful precisely because it preserves uncertainty where the model is least decisive. RED does not by itself mean treatment escalation, and none of the tiers should be interpreted as replacing colonoscopy.
Why It Matters
The study shows how segment-level MRE features and a patient-level biomarker can be combined without pretending that segments from the same person are independent. Its practical contribution is a calibrated, probabilistic account of activity and uncertainty. The findings support further external validation; they do not establish MRE as a substitute for colonoscopy.
First-author study, in collaboration with Motilent Ltd. (London). Oral presentation at ESGAR 2026, Montpellier. Manuscript in final co-author review before submission to Alimentary Pharmacology & Therapeutics.