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Updated: Aug 5, 2026
Investigating Intestinal Inflammation in DSS-induced Model of IBD
Published on: February 1, 2012
Inflammatory marker profiles vary by BMI across Crohn's disease, ulcerative colitis, psoriasis, and psoriatic
Stephen A Shields1, Ann Von Holle1, Ruthvik Padival2
1Research & Analytics Department, AMGA (American Medical Group Association), Alexandria, VA, United States.
Background:
Obesity represents a state of chronic low-grade inflammation, yet comprehensive comparative analyses examining systemic inflammatory markers across multiple immune-mediated inflammatory diseases (IMIDs) in relation to body mass index (BMI) categories remain limited. We evaluated how obesity-associated inflammatory burden manifests longitudinally across immunologically distinct conditions.
Methods:
We conducted a longitudinal cohort study using de-identified electronic health record data from the Optum Labs Data Warehouse, selecting adult patients with Crohn's disease (CD), ulcerative colitis (UC), psoriasis (PsO), or psoriatic arthritis (PsA) with at least two BMI measurements over five years. Using generalized mixed effects regression models, we estimated associations between BMI categories (healthy weight, <25 kg/m²; overweight, 25.0-29.9 kg/m²; obesity, ≥30 kg/m²) and C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and ferritin. We compared patients with obesity and patients with overweight plus a high-risk comorbidity to the healthy-weight referent.
Results:
Across all four conditions, patients with obesity demonstrated significantly elevated CRP (49-83% higher) and ESR (24-48% higher) at baseline compared to healthy-weight counterparts. Patients with overweight plus high-risk comorbidities showed intermediate elevations (CRP 34-55% higher, ESR 13-30% higher). These patterns attenuated over time but remained statistically significant through year 5 in nearly all cohorts. Ferritin demonstrated near null associations across all conditions.
Conclusion:
Consistent CRP and ESR elevations across four immunologically distinct IMIDs, combined with null ferritin associations, suggest that excess adiposity may contribute to systemic inflammatory burden regardless of underlying disease mechanism, warranting further investigation of weight optimization as part of comprehensive IMID management.
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