Obesity Linked to Higher CRP and ESR in IBD Cohorts
Key Takeaways
- Among adults with Crohn’s disease and ulcerative colitis in US healthcare systems, obesity was associated with significantly higher baseline CRP and ESR than healthy weight.
- Obesity was also associated with significant baseline CRP and ESR elevations in psoriasis and psoriatic arthritis, with descriptively larger point estimates.
- Overweight accompanied by high-risk comorbidity was associated with intermediate, significant elevations in both markers across the conditions.
Participants needed two separated diagnoses of the same condition, BMI measurements at baseline and follow-up, and continuing annual healthcare activity; separately analyzed disease cohorts could overlap. Investigators compared standard healthy-weight, overweight and obesity BMI categories, along with a separate overweight-plus-high-risk-comorbidity group, against healthy weight. CRP, ESR and ferritin measurements were assessed when available at baseline and during follow-up. Disease-specific mixed-effects models used patient random intercepts, BMI-by-time terms and inverse-probability weighting, with adjustment for demographics, comorbidity, changing BMI, and biologic and corticosteroid use. Bowel disease models also adjusted for 5-aminosalicylic acid (5-ASA) use.
At baseline in Crohn’s disease, obesity versus healthy weight was associated with adjusted CRP levels 49% higher (95% confidence interval [CI] 34%–66%) and ESR levels 24% higher (95% CI 16%–34%).
In ulcerative colitis, adjusted baseline CRP was 59% higher (95% CI 40%–80%) and ESR was 42% higher (95% CI 29%–55%) with obesity than with healthy weight; all four bowel disease estimates were statistically significant. Baseline CRP and ESR elevations with obesity were also significant in psoriasis and psoriatic arthritis, with descriptively larger point estimates than in the bowel disease cohorts. Overweight with high-risk comorbidity was associated with intermediate, significant elevations in both markers. CRP and ESR associations generally weakened but persisted in most cohorts at the final follow-up. Ferritin associations were generally near null; neither bowel disease cohort showed a significant obesity–ferritin association at any measured time point.
The investigators proposed shared adiposity-related inflammation as a possible explanation. Required continuing healthcare contact excluded many initially eligible adults, while nonprotocol laboratory ordering and different reasons for ferritin testing in bowel and psoriatic disease complicate comparisons.
BMI does not describe fat distribution, and cardiometabolic illness complicates attribution in the overweight subgroup. Treatment adjustment cannot replace direct measures of bowel, skin or joint disease activity. Without a comparator free of immune-mediated disease or a reported formal between-disease interaction test, descriptive differences cannot establish disease specificity. Observational confounding also precludes inferring validated BMI-adjusted thresholds, changes in clinical management or a measured benefit of weight loss.
Clinician Questions
Why might ferritin track BMI differently from CRP and ESR in Crohn’s disease and ulcerative colitis?
Investigators proposed that ferritin in Crohn’s disease and ulcerative colitis reflects iron storage as well as inflammation, with iron status and hepcidin-mediated handling influencing its levels. CRP responds primarily to interleukin-6, while ESR reflects fibrinogen and immunoglobulins.
Do the BMI and inflammatory-marker findings in Crohn’s disease and ulcerative colitis apply to children or patients outside US healthcare systems?
The Crohn’s disease and ulcerative colitis analysis included adults aged 18–79 receiving care in US healthcare organizations. The authors cautioned against assuming its BMI–inflammatory-marker associations generalize to children, international populations or people with less consistent healthcare-system contact.