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Since its initial descriptions in 1946,1 the measurement of airway responsiveness with inhaled bronchoconstrictor stimuli such as methacholine or histamine has become routine practice in the diagnosis and follow up of asthmatic patients. Practically, this involves the patient inhaling increasing doses or concentrations of a stimulus until a given level of bronchoconstriction is achieved, typically a 20% fall in forced expired volume in one second (FEV1). Airway responsiveness is then expressed as the provocative dose or concentration of the stimulus required to achieve this degree of bronchoconstriction (PD20 and PC20, respectively). The term “airway responsiveness” is preferred when discussing PD20 and PC20 measurements as this is a non-specific term that encompasses the underlying mechanisms that may be responsible for differences in these measurements either between individuals or within an individual over time2. This is best illustrated in fig 1 where it can be seen that a decrease in PC20 may be due to a steeper dose-response curve (hyperreactivity) or to a shift in the curve to the left (hypersensitivity), or both. Thus, when an individual displays a decreased PC20 it is usually not known whether this is due to hyperreactivity or hypersensitivity although it is certainly one, the other, or both—all of which are covered by the term airway “hyperresponsiveness”. Figure 1 Changes in FEV1 induced by increasing doses of a bronchoconstrictor stimulus such as histamine or methacholine. Bronchial hyperresponsiveness, defined as the dose causing a 20% fall in FEV1, can be induced by airway hypersensitivity (shift to the left of the dose-response curve) or airway hyperreactivity (steeper slope of the dose-response curve). This figure illustrates how either of these two different mechanisms may result in the same degree of hyperresponsiveness (as measured by a shift in PC …