Linear growth and bone metabolism in pediatric patients with inflammatory bowel disease

• Autor(a) principal: Ferreira,Paloma Velez de Andrade Lima Simões
• Data de Publicação: 2019
• Outros Autores: Cavalcanti,André de Souza, Silva,Giselia Alves Pontes da
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Jornal de Pediatria (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0021-75572019000300008
• topic: Inflammatory bowel disease; Growth failure; Low bone mineral density

Abstract Objective: To review the pathophysiology and evaluation methods of linear growth and bone mineral density in children and adolescents diagnosed with inflammatory bowel disease. Source of data: Narrative review carried out in the PubMed and Scopus databases through an active search of the terms: inflammatory bowel disease, growth, failure to thrive, bone health, bone mineral density, and children and adolescents, related to the last ten years, searching in the title, abstract, or keyword fields. Synthesis of findings: Inflammatory bowel diseases of childhood onset may present as part of the clinical picture of delayed linear growth in addition to low bone mineral density. The presence of a chronic inflammatory process with elevated serum levels of inflammatory cytokines negatively interferes with the growth rate and bone metabolism regulation, in addition to increasing energy expenditure, compromising nutrient absorption, and favoring intestinal protein losses. Another important factor is the chronic use of glucocorticoids, which decreases the secretion of growth hormone and the gonadotrophin pulses, causing pubertal and growth spurt delay. In addition to these effects, they inhibit the replication of osteoblastic lineage cells and stimulate osteoclastogenesis. Conclusion: Insufficient growth and low bone mineral density in pediatric patients with inflammatory bowel disease are complex problems that result from multiple factors including chronic inflammation, malnutrition, decreased physical activity, late puberty, genetic susceptibility, and immunosuppressive therapies, such as glucocorticoids.