Growth impairment and associated pubertal delay are common complications of pediatric inflammatory bowel disease (IBD), particularly Crohn’s disease (CD). Chronic undernutrition (related primarily to inadequate intake) and pro-inflammatory cytokines are the two major and interrelated contributory factors. Pathogenic mechanisms include interference with growth hormone/insulin-like growth factor-1 axis, with gonadotropin-releasing hormone secretion patterns, and direct cytokine effects on growing bone. Chronic corticosteroid therapy compounds disease-related causes of growth impairment. The influence on growth of polymorphisms in IBD susceptibility or modifier genes is under study. Accurate recognition of impaired growth requires appreciation of normal growth. Pre-illness standard deviation scores (SDS) for height should be obtained and compared with height SDS at diagnosis, so that the impact of disease on growth can be fully appreciated. The greater the deficit prior to recognition of IBD, the greater is the demand for catch-up growth. Height velocity should be regularly monitored and its adequacy for age and pubertal stage assessed. Restoration and maintenance of pre-illness growth pattern indicate success of therapy. Current treatment regimens limit use of corticosteroids, via optimization of immunomodulatory drugs, use of enteral nutrition in CD, and, if necessary, surgery for ulcerative colitis and for intestinal complications of localized CD. Biologic agents with the potential for mucosal healing hold promise of growth enhancement even among children, whose growth with previously available therapies remained compromised. For all therapies, there is a window of opportunity to achieve normal growth before puberty is too advanced.

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