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Five Blood Markers Linked to IBD Endoscopic Inactivity

Five Blood Markers Linked to IBD Endoscopic Inactivity
10/08/2026

Key Takeaways

  • Among hospitalized adults with ulcerative colitis (UC) or Crohn’s disease (CD) in China, endoscopically inactive groups had significantly lower C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), erythrocyte sedimentation rate (ESR), and platelet counts, and higher albumin, than active groups.
  • The five-marker panel distinguished endoscopic inactivity more strongly than any constituent marker within both disease cohorts.
  • The authors considered the cross-sectional blood-marker findings exploratory and adjunctive to endoscopy, not evidence of treatment-induced healing or a replacement for endoscopy.
For adults with ulcerative colitis (UC) or Crohn’s disease (CD), endoscopic appearance and systemic inflammatory measurements capture different aspects of illness. At a hospital in Shanghai, investigators explored how closely blood measures may align with an inactive-appearing intestinal mucosa at a single visit.

In a retrospective study, Zhou and colleagues evaluated 200 adults with inflammatory bowel disease (IBD) admitted from December 2022 to June 2024 (91 with UC and 109 with CD). Healthy adults served as comparators for blood-marker levels. Fasting blood was drawn within 48 hours of admission, before induction therapy; colonoscopy or ileocolonoscopy occurred on the same day and was scored independently by two endoscopists blinded to blood results. Investigators measured C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), erythrocyte sedimentation rate (ESR), platelet count (PLT), and albumin (ALB). They assessed disease-specific endoscopic inactivity versus activity with the Mayo Endoscopic Score (MES) for UC and the Simplified Endoscopic Score for Crohn’s Disease (SES-CD) for CD.

In both UC and CD, CRP, TNF-α, ESR, and PLT were lower, whereas ALB was higher, among endoscopically inactive versus active patients (p < 0.05). The combined model’s within-cohort AUC for inactivity was 0.922 in UC and 0.904 in CD, exceeding each corresponding single-marker AUC. Relative to healthy controls, patients with either disease had higher inflammatory-marker levels and lower albumin.

After internal bootstrap correction, the combined model’s AUC was 0.906 for UC and 0.886 for CD; this was not independent external validation. The investigators also reported sensitivity and specificity at cutoffs derived within each disease cohort. In both diseases, CRP, ESR, and platelets correlated positively with endoscopic severity, while albumin correlated negatively.

The investigators noted that this retrospective, single-center snapshot could not establish treatment-induced mucosal healing, causation, or prospective performance. Small inactive subgroups prevented adjustment for possible confounding by age, disease duration, and treatment. The cohort-derived cutoffs have no established clinical decision role without independent external validation. Without fecal calprotectin data, the panel could not be compared directly with that marker or assessed for incremental value over it. Endoscopic classification is also unclear: the methods described inactivity as the absence of scored inflammation, while the results used broader inactivity thresholds and activity boundaries inconsistent with the reported mild and moderate categories.

Clinician Questions

Did healthy controls contribute to the five-marker endoscopic inactivity AUCs in ulcerative colitis and Crohn’s disease?

No. The 100 healthy adults supplied blood-marker comparisons against patients with ulcerative colitis and Crohn’s disease; the combined AUCs instead classified inactive versus active endoscopic status within each disease cohort, not patients versus healthy controls.

How many endoscopically inactive UC and CD patients supported the blood-marker models?

The retrospective analysis included 23 endoscopically inactive UC patients and 28 inactive CD patients. Investigators said these small groups prevented adjustment for possible confounders including age, disease duration, and treatment.

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