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sample is thought to be from the larger airways (Keatings, Evans et al. 1997; Nocker, Out et
al. 2000). Induced sputum eosinophilic measures did predict exacerbations better than
bronchoalveolar lavage samples (Nocker, Out et al. 2000). While correlations were identified
between blood eosinophils and serum ECP, and sputum eosinophils and sputum ECp, in a
number of studies it was the sputum ECP that best correlated to bronchial obstruction, and the
sputum ECP and eosinophils that best correlated to methacholine challenge in asthmatics
(Sorva, Metso et al. 1997; Grebski, Wu et al. 1999; Piacentini, Bodini et al. 1999). Sputum
eosinophils and ECP were related to the symptom scores and FEV1, while no relationship was
demonstrated between blood eosinophils and symptom scores (Bacci, Cianchetti et al. 1998).
Finally, the measurement of ECP was easier to do from induced sputum than from blood or
lavage fluid, required less technical input and time and had better correlation to disease
activity (Barck, Lundahl et al. 2005). In a comparison between blood and urine samples, one
study showed a better correlation between lung function and the inflammatory parameters
measured in the urine samples (Labbe, Aublet-cuvelier et al. 2001).
t.7
Chapter summary
So in this introductory outline; the burden of paediatric respiratory disease in New Zealand is
great and asthma in both adults and children is a major cause of morbidity, stimulating my
interest in conducting research in this area. The diagnosis of asthma, particularly in children,
can be difficult with no single diagnostic or prognostic marker. Asthma continues to be a
clinical diagnosis based on history of symptoms, few examination findings and response to
treatment, with possible confirmation from lung function testing in older children. However
the mainstay of treatment is anti-inflammatory medication, which is associated with
significant side effects such as adrenal cortical insufficiency, growth failure, dysphonia and
oral candidiasis for IHCS use, and adrenal insufficiency which may cause devastating
hypoglycaemia, adrenal suppression, growth failure, hypertension, diabetes mellitus,
reduction in bone mineral density, skin atrophy, straie, poor healing, immunosuppression and
cataracts for oral corticosteroid use (GINA 2002; GINA 2005). We do not routinely measure a
marker for inflammation, but rather base decisions and treatment regimes on surrogare
markers such as symptoms, lung function, chest xray appearances, bronchial reactivity - to
determine successful outcomes.
The theory that asthma is an inflammatory disease was first indicated by autopsy studies in
early and mid last century. With the development of bronchoscopy, biopsy studies became
possible and these consolidated the pathogenesis of asthma as an inflammatory disease. This
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