title: Mechanisms of growth retardation, drug therapy, and nutritional support in pediatric inflammatory bowel disease: a workshop sponsored by the north american and European societies for pediatric gastroenterology and nutrition.
abstract: : Growth retardation is common in children with inflammatory bowel disease (IBD). The most sensitive measure of impaired growth, growth velocity, is abnormal in 65% of children with Crohn's disease. With treatment, growth velocity may return to normal, but catch-up growth is often incomplete and ultimate height lower than predicted. In some patients delayed puberty may compensate for poor growth earlier in life, and there is good evidence that even after menarche, significant growth can occur. Surgery may have a favorable impact on growth in the short term, but final height often remains reduced. The mechanism for growth failure in IBD is thought to be related to both prolonged periods of suboptimal nutritional intake and persistent inflammation. Growth throughout childhood is dependent on growth hormone and insulin-like growth factors (IGF). At puberty, androgens and estrogens also play a significant role in normal growth. Both malnutrition and inflammatory bowel disease result in low levels of IGF-1. With recovery, levels return to normal. Although little work has been done to measure the effects of chronic maintenance drug therapy on growth, it is known that children taking alternate-day prednisone grow normally and can exhibit catch-up growth. Nutritional therapy with tube feeding of elemental diets also improves nutrition and decreases inflammation. Children with either small-bowel Crohn's or Crohn's ileocolitis respond to tube feedings of both elemental or semielemental diets.
authors.affiliation: Department of Pediatrics, Texas Children's Hospital, Houston, Texas, U.S.A.; *Paediatric Gastroenterology and Nutrition, Academisch Medisch Centrum, Amsterdam, The Netherlands.
authors.forename: G D
authors.initials: GD
authors.lastname: Ferry
authors.forename: H A
authors.initials: HA
authors.lastname: Büller