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In the first paragraph of most reviews we are reminded that ‘asthma is an inflammatory disease characterised by … ’. This perspective has been influenced by—and, in turn, has driven—a great deal of respiratory research over the last 20 years. In the clinical sphere, studies based on factor analysis inform us that airway inflammation is an independent domain of the asthma syndrome, distinct from airways hyper-responsiveness, abnormal lung function and symptoms.1 2 Established treatments (notably inhaled corticosteroids and antileukotrienes) as well as potential new therapies are directed towards modifying the underlying inflammatory process rather than just providing symptom relief. For all of these reasons, actually measuring airway inflammation ought to be a regular feature in the management of asthma. In that regard, the renowned passion of Professor Freddie Hargreave and colleagues for using induced sputum analysis in the routine assessment of airways disease is entirely logical and is to be applauded.3 The strength of induced sputum analysis is that inflammatory cell characteristics (eosinophil predominance or not) may be used to interpret the aetiology of a patient's symptoms, anticipate the short to medium-term prognosis and, most importantly, the likelihood of response to treatment with corticosteroid.4–6 Unfortunately, 15 years on, for pragmatic reasons, the approach he encouraged is not routine except in a few centres.
Against this background, the measurement of nitric oxide as the fraction in exhaled air (FeNO) came on the scene and interest in its clinical applications has grown.7 Chief among these, for reasons we have referred to, has been its role as a surrogate measurement of eosinophilic airway inflammation. This appeared to be very convenient, given the desirability of measuring airway inflammation by a less time-consuming and well-validated …
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