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Inflammatory Diseases and Growth: Effects on the GH-IGF Axis and on Growth Plate
Francesca Cirillo1, Pietro Lazzeroni2, Chiara Sartori3
1Division of Paediatric Endocrinology and Diabetology, Department of Obstetrics, Gynaecology and Paediatrics, Azienda AUSL-IRCCS, Viale Risorgimento, 80, 42123 Reggio Emilia, Italy. francesca.cirillo@ausl.re.it.
Insights
Chronic inflammatory diseases in children, including cystic fibrosis and IBDs, impact growth via placental and cord blood changes. These conditions affect growth hormone and IGF systems, highlighting the need for further research into growth failure mechanisms.
Area of Science:
- Pediatric Endocrinology
- Immunology
- Developmental Biology
Background:
- Chronic inflammatory diseases in childhood, such as cystic fibrosis (CF), inflammatory bowel diseases (IBDs), juvenile idiopathic arthritis (JIA), and intrauterine growth restriction (IUGR), are associated with significant physiological changes.
- These conditions can manifest alterations in the placenta and cord blood, suggesting an early impact on fetal development and subsequent growth.
Purpose of the Study:
- To review the common chronic inflammatory diseases in childhood.
- To describe the associated changes in the placenta and cord blood.
- To elucidate the mechanisms linking inflammation to growth failure, including hormonal and epigenetic factors.
Main Methods:
- Literature review of studies on childhood chronic inflammatory diseases.
- Analysis of reported changes in placental and cord blood parameters.
- Examination of the roles of growth hormone (GH), insulin-like growth factor (IGF) system, nuclear factor-κB (NF-κB), pro-inflammatory cytokines, growth plate, and microRNAs (miRNAs).
Main Results:
- Chronic inflammation in childhood is linked to alterations in GH secretion, GH resistance, and the IGF system.
- Increased nuclear factor-κB (NF-κB) and pro-inflammatory cytokines are implicated in these growth-related changes.
- Changes in the growth plate and a potential role for microRNAs (miRNAs) in epigenetic modifications associated with chronic inflammation were observed.
Conclusions:
- Multiple mechanisms contribute to growth failure in children with chronic inflammatory diseases.
- The interplay between inflammation, hormonal regulation, and epigenetic factors is crucial.
- Further research is warranted to fully understand and address growth impairment in these pediatric conditions.
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.
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