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Acute inflammation in young children inhibits C-type natriuretic peptide
Timothy C R Prickett1, James Hector-Taylor, Robert C Olney
1Department of Medicine, University of Otago, Christchurch, New Zealand. tim.prickett@otago.ac.nz
Insights
Acute illness in children significantly reduces C-type natriuretic peptide (CNP) levels, impacting growth velocity. This finding is crucial for assessing growth disorders in pediatric patients.
Area of Science:
- Pediatric Endocrinology
- Biochemistry
- Inflammation Research
Background:
- C-type natriuretic peptide (CNP) is a key paracrine growth factor in endochondral bone development.
- Amino-terminal CNP (NTproCNP) in plasma reflects growth-plate activity and pediatric growth velocity.
- Adult inflammation elevates CNP; pediatric acute illness effects were unexplored.
Purpose of the Study:
- To investigate the relationship between acute illness, inflammation markers, and CNP peptide levels in young children.
- To determine if acute inflammation affects CNP production in pediatric patients.
Main Methods:
- Studied 42 acutely ill children (2 months to 5 years) and 15 healthy controls.
- Measured venous concentrations of NTproCNP and CNP.
- Assessed inflammatory markers: body temperature, C-reactive protein (CRP), and white blood cell count.
Main Results:
- Acutely ill children showed significantly suppressed NTproCNP and CNP standard deviation scores (SDSs) compared to controls.
- NTproCNP SDS was inversely correlated with body temperature (r = -0.42) and CRP levels (r = -0.56).
Conclusions:
- Acute inflammation in young children markedly reduces CNP production.
- Reduced CNP during illness must be considered when evaluating growth disorders.
- Inflammatory cytokines may contribute to impaired skeletal growth via decreased CNP.
Background:
C-type natriuretic peptide (CNP) is a paracrine growth factor critical in endochondral bone growth. Amino-terminal CNP (NTproCNP), measurable in plasma, correlates with growth-plate activity and can be used as a biomarker of growth velocity in children. Because severe inflammation in adults increases CNP, we studied CNP peptides and inflammatory markers in children with acute illness.
Methods:
Forty-two children aged 2 mo to 5 y with acute illness warranting admission to an acute assessment unit were studied. Fifteen age-matched healthy children attending an outpatient clinic served as controls. Venous CNP concentrations were measured at admission, along with markers of acute inflammation (body temperature, C-reactive protein (CRP), and white blood cell count) in children with acute illness.
Results:
NTproCNP and CNP SD scores (SDSs) in the acutely ill group were significantly suppressed (P < 0.001) as compared with those of healthy children or healthy population norms. NTproCNP SDS was significantly inversely related to body temperature (r = -0.42, P < 0.01) and CRP (r = -0.56, P < 0.001).
Conclusion:
Acute inflammation in young children potently reduces CNP production, which needs to be considered when screening for growth disorders. Our data raise the possibility that the adverse effects of inflammatory cytokines on skeletal growth may be mediated in part by reduced CNP.
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