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Inflammation induces stunting by lowering bone mass via GH/IGF-1 inhibition in very preterm infants
Eduardo Cuestas1, Macarena Hillman2, Silvia Galetto2
1Department of Pediatrics and Neonatology, Hospital Privado Universitario de Córdoba, Instituto Universitario de Ciencias Biomédicas de Córdoba, Córdoba, Argentina. ecuestas@hospitalprivadosa.com.ar.
Insights
Sustained systemic inflammation in very preterm infants (VPI) leads to stunted growth and lower bone mass. This is linked to inhibited growth hormone/insulin-like growth factor-1 axis, impacting VPI development.
Area of Science:
- Neonatology
- Pediatric Endocrinology
- Inflammatory Medicine
Background:
- Sustained systemic inflammatory response (SIR) is linked to poor postnatal growth in very preterm infants (VPI).
- The hypothesis is that SIR in VPI leads to linear growth retardation due to reduced bone mass accrual, mediated by Growth Hormone/Insulin-like Growth Factor-1 (GH/IGF-1) axis inhibition at term corrected age (CA).
Purpose of the Study:
- To investigate the association between sustained SIR and linear growth, bone mass, and GH/IGF-1 axis function in VPI at term CA.
- To explore the role of inflammatory markers in VPI growth and body composition.
Main Methods:
- Prospective data collection on inflammatory markers (CRP, PCT), GH, IGF-1, and anthropometric/nutritional data in 23 VPI (<32 weeks GA).
- Body composition analysis using dual-energy X-ray absorptiometry (DEXA) at term CA.
- Multiple linear regression models were used for analysis.
Main Results:
- VPI with sustained SIR (n=11) showed significantly lower IGF-1, length z-score (LZS), bone mineral content (BMC), and lean mass (LM) compared to those without SIR (n=12).
- Infants with SIR also exhibited higher GH and fat mass (FM).
- LZS correlated with PCT; BMC with IGF-1; FM and LM with CRP; GH with bronchopulmonary dysplasia and CRP; and IGF-1 with invasive mechanical ventilation, CRP, and PCT.
Conclusions:
- Sustained SIR in VPI contributes to linear growth failure and reduced bone mass accrual.
- This is associated with elevated GH and suppressed IGF-1 levels, indicating GH/IGF-1 axis inhibition.
- SIR may explain non-nutritional factors affecting VPI growth and body composition, highlighting the need to minimize inflammatory stress for improved outcomes.
Background:
Sustained systemic inflammatory response (SIR) was associated with poor postnatal growth in very preterm infants (VPI). We hypothesize that VPI with sustained SIR will exhibit linear growth retardation related to lower bone mass accrual mediated by GH/IGF-1 axis inhibition at term corrected age (CA).
Methods:
C-reactive protein (CRP), procalcitonin (PCT), growth hormone (GH), insulin-like growth factor 1 (IGF-1), calcium, phosphorus, alkaline phosphatase, anthropometric, nutritional, neonatal and maternal data were collected prospectively in 23 infants <32 weeks gestational age. Body composition using dual-energy X-ray absorptiometry was performed at term CA. Analysis was undertaken with multiple linear regression models.
Results:
At term CA 11 infants with sustained SIR compared with 12 infants without sustained SIR present significantly lower IGF-1, length z-score (LZS), bone mineral content (BMC) and lean mass (LM), and higher GH and fat mass (FM). LZS was associated significantly with PCT, BMC with IGF-1, FM and LM with CRP, GH with bronchopulmonary dysplasia and CRP, and IGF-1 with invasive mechanical ventilation, CRP and PCT.
Conclusions:
In addition to the known effect on linear growth failure, sustained SIR induces lower bone mass accrual related to higher GH and lower IGF-1 levels in VPI.
Impact:
Very preterm infants (VPI) with sustained systemic inflammatory response (SIR) compared with VPI without SIR present stunting, lower bone mass, higher GH and lower IGF-1 levels at term corrected age. SIR may help to explain the influence of non-nutritional factors on growth and body composition in VPI. SIR induces postnatal stunting related to lower bone mass accrual via GH/IGF-1 axis inhibition in VPI. VPI with SIR need special attention to minimize inflammatory stress, which could result in improved postnatal growth. Research on inflammatory-endocrine interactions involved in the pathophysiology of postnatal stunting is needed as a basis for new interventional approaches.
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