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Serum ECP levels and methacholine challenge in infants with recurrent wheezing
Janine Reichenbach1, Andrea Jarisch, Saima Khan
1University Children's Hospital Frankfurt am Main, Germany.
Insights
Serum eosinophil cationic protein (sECP) does not correlate with bronchial hyperreactivity (BHR) in infants with recurrent wheezing. These findings suggest independent pathways in childhood asthma development.
Area of Science:
- Pediatric Pulmonology
- Allergy and Immunology
- Biochemistry
Background:
- Serum eosinophil cationic protein (sECP) is a marker for eosinophilic airway inflammation and a predictor of childhood asthma.
- Bronchial hyperreactivity (BHR) is thought to result from inflammatory mediator release.
Purpose of the Study:
- To investigate the correlation between eosinophilic inflammation (sECP levels) and BHR in infants with recurrent wheezing.
- To assess if sECP is a predictor of BHR in this population.
Main Methods:
- 72 infants (12-30 months) with recurrent wheezing underwent methacholine challenge tests to assess BHR.
- Serum ECP levels were measured and infants were categorized into low, medium, and high sECP groups.
- BHR was compared against sECP levels across the three groups.
Main Results:
- Mean sECP levels were 6.6 ± 2.3 μg/L (low), 14.3 ± 2.8 μg/L (medium), and 34.5 ± 9.5 μg/L (high).
- Mean provocative methacholine concentrations were 350.9 ± 258.3 μg (low), 340.7 ± 226.3 μg (medium), and 301.3 ± 189.8 μg (high).
- No significant correlation was found between sECP levels and BHR (r = -0.076, P = 0.6).
Conclusions:
- sECP levels and BHR appear to be independent factors in the development of childhood asthma.
- These findings suggest distinct pathogenic mechanisms contribute to asthma etiology.
- Further research may be needed to elucidate the interplay of these factors.
Background:
High levels of serum eosinophil cationic protein (sECP) as a marker of eosinophilic airway inflammation have been described as a predictor of childhood asthma. Bronchial hyperreactivity (BHR) appears to be secondary to the release of inflammatory mediators.
Objective:
We investigated the possible correlation between eosinophilic inflammation and BHR in 72 infants with recurrent wheezing.
Methods:
To determine bronchial reactivity, lung function measurements with methacholine challenge were performed in 72 infants, aged 12 to 30 months, and the degree of BHR to methacholine was compared with sECP values. Patients were grouped according to low (group 1, <10 microg/L, n = 22), medium (group 2, 10 to 20 microg/L, n = 23), and high (group 3, >20 microg/L, n = 27) sECP values.
Results:
In group 1, sECP levels ranged from 3.1 to 9.9 microg/L, mean 6.6 microg/L +/- standard deviation [SD] 2.3, in group 2, from 10.3 to 19.8 microg/L, mean 14.3 microg/L +/- SD 2.8, and in group 3 from 23.0 to 66.7 microg/L, mean 34.5 microg/L +/- SD 9.5. Distribution of provocative methacholine concentration among groups was as follows: group 1, 30 to 976 microg, mean 350.9 microg +/- SD 258.3; group 2, 36 to 752 microg, mean 340.7 microg +/- SD 226.3; group 3, 41 to 848 microg, mean 301.3 microg +/- SD 189.8 methacholine.
Conclusion:
There was no significant correlation between sECP levels and bronchial reactivity in all groups (r = -0.076, P = 0.6), indicating that these parameters reflect two independent pathogenic mechanisms in the etiology of childhood asthma.