Longitudinal Growth in Children and Adolescents with Inflammatory Bowel Disease

Hildebrand, Hans; Karlberg, Johan; Kristiansson, Bengt

doi:10.1097/00005176-199402000-00008

Cited by 179 publications

(127 citation statements)

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“…For example, Crohn's disease, characterized by transmural inflammation of the gastrointestinal tract (1), severely inhibits growth in approximately one third of affected children (2)(3)(4)(5). A significant proportion of children with Crohn's disease become short adults (6,7). Despite repeated clinical reports over seven decades (8), the basis of this observation has not been fully explained.…”

mentioning

confidence: 99%

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Sawczenko

Azooz

Paraszczuk

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

111

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Inflammatory diseases frequently impair linear growth. Crohn's disease inhibits growth in up to one third of affected children. In rats with trinitrobenzenesulphonic acid-induced colitis, 40% of growth impairment is attributable to inflammation, with the rest being due to undernutrition. In transgenic mice without inflammation, raised IL-6 retards growth, suppressing insulin-like growth factor (IGF)-I. We hypothesized that IL-6, induced by intestinal inflammation, suppresses growth and inhibits IGF-I expression. Therefore, an anti-IL-6 Ab was given to rats with trinitrobenzenesulphonic acid colitis. The Ab did not improve nutrient intake or decrease inflammation compared with untreated disease controls, but it significantly restored linear growth (P ‫؍‬ 0.023) and increased IGF-I (P ‫؍‬ 0.05). In humans, the IL-6 ؊174 G͞C promoter polymorphism affects IL-6 transcription, with the GG genotype inducing the greatest IL-6 levels. Because IL-6 is increased in Crohn's disease, we further hypothesized that growth failure would vary with the IL-6 ؊174 genotype. At diagnosis, among 153 children with Crohn's disease, those with the IL-6 GG genotype were more growthretarded than those with the GC or CC genotypes (height SD score, ؊0.51 vs. ؊0.10; P ‫؍‬ 0.031). Also, the patients with the IL-6 GG genotype had higher circulating levels of C-reactive protein, an IL-6-induced product (36 vs. 18 mg͞dl, P ‫؍‬ 0.028). However, their risk of developing Crohn's disease was similar to other genotypes when compared with 351 healthy controls (P ‫؍‬ 0.7). Thus, the IL-6 ؊174 genotype mediates growth failure in children with Crohn's disease.Crohn's disease ͉ height ͉ insulin-like growth factor I ͉ C-reactive protein ͉ food intake

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mentioning

confidence: 99%

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Sawczenko

Azooz

Paraszczuk

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

111

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“…The rate of growth impairment in pediatric IBD at diagnosis varies with the type of disease (CD vs. ulcerative colitis [UC]), gender, and the time of diagnosis [3][4][5][6][7][8][9][10][11]. Apparently, the age and pubertal stage at diagnosis are key factors for growth potential.…”

Section: Definition and Prevalencementioning

confidence: 99%

“…Furthermore, growth impairment in children with CD was found to be a predictor for more disabling disease [22]. The association between disease severity and growth impairment is mainly seen in CD, as it is found in only 3-10% of pediatric UC patients at diagnosis [7,8]. Data on final height in pediatric UC patients is limited but it is evident that it is less frequently affected [21].…”

Section: Definition and Prevalencementioning

confidence: 99%

Impact of Therapeutic Strategies on Growth in Pediatric Inflammatory Bowel Disease

Shamir¹

2014

J Clin Cell Immunol

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Growth retardation is a common complication of pediatric inflammatory bowel disease (IBD), which may have long term effects on final adult height and carries significant social and psychological implications. Etiology may be multifactorial including undernutrition, metabolic dysregulation, inflammatory impact on hormonal growth axis and the effect of drugs such as glucocorticoids. Control of disease activity and minimizing the need for corticosteroid therapy are necessary measures in order to facilitate normal growth. However, in many cases these strategies are not sufficient. Currently, there is inconsistent evidence regarding the efficacy of available therapeutic agents to induce long-term effect on growth. The new era of biologic therapies which carries a greater potential to achieve mucosal healing, holds promise for better growth even in children with severe growth impairment. It becomes apparent that prompt recognition of growth impairment combined with aggressive tailored therapeutic approach may offer the best chance for catch-up growth. This review will discuss the definition, prevalence and mechanism of growth retardation in children with IBD and highlight the specific benefits of current therapeutic strategies.

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“…60 In addition to the usual symptoms of diarrhea, abdominal pain, weight loss, anemia, and rectal bleeding, children may exhibit growth failure years before disease diagnosis. 61,62 Anorexia, malabsorption, and increased metabolic demands all contribute to poor growth. Small bowel disease may impair absorption of iron, zinc, folate, and vitamin B 12 .…”

Section: Crohn Diseasementioning

confidence: 99%

Glucocorticoid-Induced Osteoporosis in Children: Impact of the Underlying Disease

Leonard

2007

Pediatrics

110

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Glucocorticoids inhibit osteoblasts through multiple mechanisms, which results in significant reductions in bone formation. The growing skeleton may be especially vulnerable to adverse glucocorticoid effects on bone formation, which could possibly compromise trabecular and cortical bone accretion. Although decreased bone mineral density has been described in various pediatric disorders that require glucocorticoids, and a population-based study reported increased fracture risk in children who require Ͼ4 courses of glucocorticoids, some of the detrimental bone effects attributed to glucocorticoids may be caused by the underlying inflammatory disease. For example, inflammatory cytokines that are elevated in chronic disease, such as tumor necrosis factor ␣, suppress bone formation and promote bone resorption through mechanisms similar to glucocorticoid-induced osteoporosis. Summarized in this review are changes in bone density and dimensions during growth, the effects of glucocorticoids and cytokines on bone cells, the potential confounding effects of the underlying inflammatory-disease process, and the challenges in interpreting dual-energy x-ray absorptiometry results in children with altered growth and development in the setting of glucocorticoid therapy. Two recent studies of children treated with chronic glucocorticoids highlight the differences in the effect of underlying disease, as well as the importance of associated alterations in growth and development. S166LEONARD by guest on May 10, 2018 http://pediatrics.aappublications.org/ Downloaded from D URING CHILDHOOD AND adolescence, skeletal development is characterized by gender-, maturation-, and race-specific increases in cortical dimensions and trabecular density. The 2000 National Institutes of Health Osteoporosis Prevention, Diagnosis, and Therapy Consensus Development Conference identified bone accrual during childhood as a critical determinant of lifelong skeletal health. The authors of the resulting consensus statement 1 specifically called for research to determine the impact of chronic diseases and glucocorticoid therapy on bone accrual in children.Glucocorticoid-induced osteoporosis (GIO) is the most common cause of secondary osteoporosis in adults and is the result of profound effects of glucocorticoids on bone cells. 2 Glucocorticoids inhibit osteoblastogenesis and promote osteoblast apoptosis, which results in significant reductions in bone formation. 3 Studies in adults have demonstrated that glucocorticoids cause rapid, dose-dependent bone loss and increased fracture risk. 4 The growing skeleton may be especially vulnerable to adverse glucocorticoid effects on bone formation, which could possibly compromise trabecular and cortical bone accretion.Glucocorticoids are used in myriad pediatric diseases. Decreased bone mineral density (BMD) has been described in various pediatric disorders that require glucocorticoids, including asthma, juvenile rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and organ trans...

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Longitudinal Growth in Children and Adolescents with Inflammatory Bowel Disease

Cited by 179 publications

References 0 publications

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Impact of Therapeutic Strategies on Growth in Pediatric Inflammatory Bowel Disease

Glucocorticoid-Induced Osteoporosis in Children: Impact of the Underlying Disease

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