# The role of GH/IGF-1 axis dysfunction and inflammatory cytokines in pediatric short stature

## TL;DR

This study explores how growth hormone signaling and inflammation contribute to short stature in children.

## Contribution

The study identifies a link between GH/IGF-1 axis dysfunction, elevated inflammatory cytokines, and GHR gene mutations in children with short stature.

## Key findings

- Children with short stature had significantly lower GH and IGF-1 levels and higher IL-6 and IL-8 levels.
- A negative correlation between IL-6 and IGF-1 suggests inflammation may impair growth signaling.
- GHR gene mutations were more common in children with short stature and linked to lower IGF-1 levels.

## Abstract

Short stature in children is a common clinical condition frequently associated with abnormalities in the GH/IGF-1 axis. Emerging evidence points to the involvement of inflammatory cytokines and serum markers in modulating this dysfunction. This study aims to investigate the molecular pathways underlying GH/IGF-1 axis impairment and assess the levels of inflammatory cytokines and other related biomarkers in children with short stature.

A total of 150 children diagnosed with short stature were recruited from the endocrinology department of a tertiary care hospital. An ageand sex-matched group of 150 healthy children served as controls for comparison. Serum concentrations of growth hormone (GH), insulin-like growth factor-1 (IGF-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and other relevant biomarkers were measured using enzyme-linked immunosorbent assay (ELISA). Genetic testing was performed to detect mutations in genes involved in the GH/IGF-1 signalling pathway. Data analysis was conducted using SPSS software, with statistical significance set at p< 0.05.

Children with short stature showed significantly reduced GH and IGF-1 levels (p< 0.001) and elevated IL-6 and IL-8 levels (p< 0.01). A moderate negative correlation was found between IL-6 and IGF-1 levels (r=-0.45, p< 0.001), suggesting that inflammation may impair growth signalling. GHR gene mutations were significantly more common in the short stature group (14.7% vs. 2.7%, p< 0.001) and were associated with lower IGF-1 levels.

This findings of the study suggest that impaired GH/IGF-1 signalling, increased inflammatory cytokines, and a higher prevalence of GHR gene mutations collectively contribute to the pathophysiology of pediatric short stature. These results highlight the need for integrative diagnostic approaches and future therapeutic strategies that target both endocrine and inflammatory pathways.