Search

Background and Aim: Treatment with antitumour necrosis factor-α therapy such as infliximab may improve growth in children with Crohn disease (CD), but the extent of improvement in growth and its relation to pubertal progress and glucocorticoid (GC) therapy are unclear. This is a retrospective study of growth, puberty, and disease activity during the 6 months before starting infliximab (T - 6), at baseline (T0), and for the following 6 months (T + 6) and 12 months (T + 12) in children with CD., Patients and Methods: The growth and treatment details of 28 children (male, 17) who were given infliximab at a median (10th, 90th) age of 13.1 years (10.0, 15.7) were reviewed. Data on disease markers (C-reactive protein, erythrocyte sedimentation rate, and albumin), total alkaline phosphatase, and a physician's global assessment were also collected. Results are expressed as median (10th, 90th)., Results: Of the 28 cases, 21 (75%) demonstrated a clinical response to infliximab treatment. Overall, height velocity (HV) increased from 3.6 cm/y (0.4-7.8) at T0 to 5.5 cm/y (2.1-9.2) at T + 6 (P = 0.003). In infliximab responders, HV increased from 2 cm/y (0.3-7.1) to 6.4 cm/y (2.3-9.1) (P = 0.004) and in the nonresponders, HV remained static at 4.3 cm/y (2.5-8.6) at T0 and 3.0 cm/y (2.0-11.3) (P = 0.701) at T + 6. HV also increased in the subgroup of 13 children who had remained prepubertal from 4.5 cm/y (0.4-8) to 5.5 cm/y (3.3-8.4) (P = 0.050). In the subgroup of 11 children who had a reduction (n = 2) or cessation in GC (n = 9), HV increased from 1.8 cm/y (0.3-8.3) at T0 to 5.6 cm/y (2.2-9.2) at T + 6 (P = 0.14), whereas those children who did not receive GC during the 12 months had an increase from 3.7 cm/y (0.6-6.5) to 6.4 cm/y (2.9-9.0) (P < 0.05). HV at T0 and T + 6 showed a significant association with the average alkaline phosphatase during the prior 6 months (r = 0.39, P < 0.05). HV did not show any association with individual markers of disease activity., Conclusions: Clinical response to infliximab therapy is associated with an improvement in linear growth in the short term in children with CD. This increase in height may not be simply due to progress in pubertal status or reduction in GC dose.

Childhood inflammatory bowel disease (IBD) especially those with Crohn disease is commonly complicated by faltering growth and pubertal delay. Pro-inflammatory cytokines are often elevated in IBD and may affect linear growth and puberty either systemically or at the level of the growth plate. Further study of the underlying mechanisms of the deleterious effects of cytokines on the growth plate may improve management of faltering growth in childhood IBD. Well-controlled clinical studies of the respective effect of nutritional support, immunomodulatory therapy, biological agents and growth and puberty promoting agents on managing faltering growth also require further attention.