Investigating BMI at Pediatric IBD Diagnosis

Key Takeaways
- Among children newly diagnosed with IBD at two pediatric referral centers, 23% were underweight, 68% had normal BMI, and 9% were overweight at diagnosis.
- Growth failure was observed in 7% at diagnosis and 5.3% at 36 months.
- Underweight was more common in Crohn’s disease than ulcerative colitis, at 30% versus 15%, a statistically significant difference.
- Most children who were underweight when IBD was diagnosed later attained a normal or elevated BMI.
Investigators retrospectively evaluated a multicenter pediatric IBD cohort of 128 children diagnosed at two pediatric referral centers, including 69 with Crohn’s disease and 59 with ulcerative colitis. They collected clinical, biochemical, and anthropometric data at diagnosis and during follow-up. Underweight was defined as a BMI z-score ≤ −2; growth failure, also described as stunting, was defined as a height-for-age z-score ≤ −2. The definitions distinguished weight status from linear growth.
Underweight was more frequent in Crohn’s disease than ulcerative colitis (p = 0.022), as was stunting. Biologic therapy was initiated more often in underweight children than in their non-underweight peers, although the difference was not statistically significant. The adjusted odds ratio (OR) and its confidence interval (CI) did not demonstrate increased relapse odds with baseline underweight (adjusted OR 0.52, 95% CI 0.19–1.30). The treatment comparison does not establish an effect of biologic therapy on nutritional status or relapse.
At a mean follow-up of 29.4 months, 86% (25/29) of children initially classified as underweight had reached a normal or elevated BMI. This change in weight category describes nutritional status during follow-up rather than a treatment effect. The adjusted hazard ratio (HR) for time to relapse likewise did not demonstrate increased risk with baseline underweight (adjusted HR 0.60, 95% CI 0.28–1.29). Neither adjusted measure established baseline underweight as an independent predictor of subsequent relapse.
The retrospective design permits assessment of associations but cannot establish that nutritional status causes differences in disease course. The later observation on linear growth applies only to children with measurements available at that time; it does not describe a complete matched cohort followed from diagnosis.
The authors associated malnutrition at pediatric IBD diagnosis, particularly in Crohn’s disease, with greater inflammatory burden.