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1999).In 146 children with asthma and 37 controls, the percentage of eosinophils increased
from a mean of l.S%o in children who had infrequent asthma to2.3Vo with frequent asthma
and to 3.8Vo if they had persisting symptoms, compared to controls at lTo. Similarly, ECp
Ievels increased from l l3ng/ml in infrequent asthma to 220nglml in frequent asthma and
37Snglml in the persistent asthmatics compared to 139ng/ml in the control goup. While there
were significant differences between the asthmatic groups, no difference was demonstrated
between the 'infrequent exacerbation' and 'control' children (Gibson, Simpson et al. 2003).
However, in 27 healthy and 60 asthmatic children, no correlation was seen with any marker of
airway inflammation and asthma severity as measured by lung function (Wilson, Bridge et al.
2000). In addition, in 58 asthmatic children, it was the methacholine challenge rather than the
sputum eosinophil counts or ECP that related to the presence of recent symptoms (Wilson,
James et al. 2001). No correlation was demonstrated between sputum eosinophils and FEVI or
sputum ECP in 25 asthmatic children (piacentini, Bodini et al. 1999). Further, no correlations
were demonstrated in 32 children with stable asthma between ambulatory cough frequency,
sputum inflammatory parameters or FEVI (Li, Irx et al. 2003). In 40 children with difficult
asthma, only nine children had abnormal sputum cytology; six had a predominant sputum
eosinophilia while three had a predominant neutrophilia (Irx, Payne et al. 2005).
Within one hour of arriving in the emergency department with acute asthma, eight children in
one study and 38 in a second took less time to produce an induced sputum sample than when
done during a time of stability. The sputum showed higher numbers of total cells, eosinophils,
neutrophils, basophils and mast cells compared to macrophages which was the dominant cell
during the recuperative phase when the sampling was repeated two weeks later with symptom
resolution (Twaddell, Gibson et al. 1996; Norzila, Fakes et al. 2000). The second study also
demonstrated reductions in ECP, myeloperoxidase, IL5 and IL8 by the recovery sample. The
primary cell of inflammation was either eosinophil or neutrophil or showed a co-dominant
pattern (Norzila, Fakes et al. 2000). Following a treatment with single nebulised
glucocorticoid dose, there was a reduction in eosinophil percentage in 30 asthmatic children
but ECP, IL5, GM-CSF and albumin levels, as well as FEV1, remained unchanged (Oh,I*e et
al.1999).
A number of studies have looked at the inflammation in induced sputum before and after
commencing IHCS treatment for more chronic asthma symptoms. In 14 children reduced
sputum and serum eosinophils and ECP levels were seen after two weeks of IHCS treatment
(Sorva, Metso et al. 1997). And in 60 children, there was reduction in sputum eosinophils
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