Abstract
This review briefly describes the most common chronic inflammatory diseases in childhood, such as cystic fibrosis (CF), inflammatory bowel diseases (IBDs), juvenile idiopathic arthritis (JIA), and intrauterine growth restriction (IUGR) that can be considered, as such, for the changes reported in the placenta and cord blood of these subjects. Changes in growth hormone (GH) secretion, GH resistance, and changes in the insulin-like growth factor (IGF) system are described mainly in relationship with the increase in nuclear factor-κB (NF-κB) and pro-inflammatory cytokines. Changes in the growth plate are also reported as well as a potential role for microRNAs (miRNAs) and thus epigenetic changes in chronic inflammation. Many mechanisms leading to growth failure are currently known; however, it is clear that further research in the field is still warranted.
Highlights
Most chronic inflammatory diseases in childhood are characterised by impaired growth
This review briefly describes the most common chronic inflammatory diseases in childhood, such as cystic fibrosis (CF), inflammatory bowel diseases (IBDs), juvenile idiopathic arthritis (JIA), and intrauterine growth restriction (IUGR) that can be considered, as such, for the changes reported in the placenta and cord blood of these subjects
The mechanism underlying the pathophysiology of this process is not clearly understood yet, it is a complex phenomenon which comprises of chronic inflammation itself, prolonged use of glucocorticoids, and suboptimal nutrition [1,2]
Summary
Most chronic inflammatory diseases in childhood are characterised by impaired growth. The mechanism underlying the pathophysiology of this process is not clearly understood yet, it is a complex phenomenon which comprises of chronic inflammation itself, prolonged use of glucocorticoids, and suboptimal nutrition [1,2]. The GH–IGF axis and IGF system in children with chronic inflammation may be altered by several mechanisms, such as GH/IGF-1 insufficiency, GH/IGF-1 resistance, down-regulation of GH/IGF receptors, disruption in downstream GH/IGF signalling pathways, or dysregulation of IGF binding proteins (IGFBPs) [1]. Many studies over the last decade clearly demonstrate huge interactions between pro-inflammatory cytokines and the IGF system. The aim of this review is to give an overview of the main mechanisms underlying the onset of growth impairment in chronic inflammatory disease in childhood
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