Growth impairment remains one of the most distinctive and clinically significant complications of paediatric Inflammatory Bowel Disease (IBD). Unlike many other disease outcomes, impaired growth can have consequences that cannot be fully reversed once the window for linear growth has closed. Importantly, growth failure is not simply a reflection of inadequate nutrition: it is an integrated marker of inflammatory burden, nutritional status, treatment exposure and disease control.
Up to 20% of children with IBD, mainly Crohn’s Disease, already have linear growth impairment at diagnosis. Children diagnosed before or during early puberty are at greatest risk, and this is especially true for those with small-bowel involvement (particularly jejunal), persistent inflammatory activity and high cumulative corticosteroid exposure. Diagnostic delay also matters, as prolonged, untreated inflammation can negatively affect the growth trajectory.
The mechanisms are multifactorial. Chronic inflammation, particularly through IL-6 and TNF-α, disrupts the growth hormone–insulin-like growth factor-1 (GH–IGF-1) axis, leading to functional GH resistance and reduced IGF-1 bioactivity. At the same time, reduced food intake, restrictive diets (sometimes self-imposed), malabsorption and micronutrient deficiencies further compromise growth. Corticosteroids add another important component by directly suppressing the growth plate and interfering with GH–IGF-1 signalling.
Therefore, the most effective “growth therapy” is effective control of IBD. Steroid-sparing strategies are particularly important. Exclusive enteral nutrition supports weight gain and short-term linear growth in paediatric CD while avoiding corticosteroid-related growth suppression. More effective therapies, such as anti-TNF therapy, have shown the most consistent benefit for catch-up growth, particularly when introduced early in children with active disease and remaining growth potential. Evidence for newer biologics and small molecules is promising for disease control, but their direct impact on growth remains insufficiently studied.
Nutrition remains an essential partner to anti-inflammatory treatment. Energy and protein intake should be individualised, unnecessary dietary restrictions avoided and deficiencies, particularly of iron, vitamin D and zinc, actively identified and corrected. Bone health also warrants particular attention, especially in children with low BMI or height z-scores, persistent inflammation or significant corticosteroid exposure, all of which are established risk factors for low bone mineral density.
Most importantly, growth should be treated as a target, not merely as an observation. Height, weight, BMI, height velocity and pubertal stage should be systematically assessed, and failure to achieve the expected growth trajectory should prompt reassessment of disease activity, nutrition and treatment effectiveness.
Most children with paediatric IBD can ultimately achieve an adult height close to their genetic potential. Our responsibility is to identify those who are falling behind early enough to ensure that preventable loss of growth potential does not become permanent.
For a more comprehensive overview of this topic, please refer to our recently published review:
Rinawi F, Hussey S, Crowley E, Shouval D, Hojsak I. Growth in paediatric inflammatory bowel disease. JCC Plus 2026;1:e70018.
