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Noninvasive monitoring of airway inflammation.

The management of asthma relies, in large measure, on subjective evaluation of the frequency and severity of symptoms as well as on obtaining objective measurements of airway caliber such as peak expired flow rates (PEFR) or the forced expiratory volume in one second (FE'It). The objective measurements are important because of a lack of sensitivity in asthmatics' perception of airway narrowing, which may be worse in patients with longstanding asthma (1). Frequent assessment of both symptoms and flow rates is often needed because of the need to achieve optimal control of asthma with minimal treatment. A characteristic form of airway inflammation has also been recognized as necessary for the presence of symptomatic asthma. This inflammation consists of activated eosinophils, lymphocytes, and an increased number of mast cells, all of which have been described both in bronchoalveolar lavage (2-4) and airway biopsies from asthmatic subjects (5, 6), as well as characteristic structural changes of the airways (7-9). These inflammatory changes have been described in patients with stable asthma and those who have died from very severe asthma. However, until recently a non-invasive method was not available to evaluate whether an exacerbation of asthma symptoms was associated with increased numbers of activated inflammatory cells in the airways. Evaluating the severity of an exacerbation and the requirement for treatment with corticosteroids has relied on indirect indices to suggest that airway inflammation has worsened. These indices have included increased symptoms, demonstrated worsening airflow obstruction, increased variability of flow rates, and airway hyperresponsiveness.