• Respiratory measurement

Cisneros et al1 report associations between scores on the Asthma Quality of Life Questionnaire (AQLQ) and three indices of bronchial reactivity (dose–response slope (DRS), continuous index of responsiveness (CIR) and bronchial reactivity index (BRI)), which they suggest are qualitatively different from sensitivity, measured by PD₂₀FEV₁. This conclusion is questionable.

First, there are no meaningful differences between DRS, CIR and BRI. All are calculated using the final percentage fall in the forced expiratory volume in 1 s (FEV₁) and final cumulative dose. The only difference between them is the mathematical transformation applied to the data. Any differences in the associations between AQLQ and DRS, CIR or BRI can only be due to differences in the shape or linearity of the mathematical functions describing their relationships with AQLQ.

Secondly, the information provided by PD₂₀ is not qualitatively different from that provided by DRS. PD₂₀ is calculated by interpolation from standard dose–response curves plotted on a semi-log scale. The same data plotted on a linear dose axis appear as a straight line, the slope of which is the DRS. In subjects with a PD₂₀, there is a close correlation between DRS and PD₂₀.2 Figure 1 shows the relationship between logPD₂₀ and logDRS (r=−0.97, p<0.0001) in 41 subjects with asthma with airway hyper-responsiveness (AHR) to histamine, from a clinical trial in our laboratory.3 Cisneros et al1 do not state the correlation between PD₂₀ and their indices of ‘reactivity’, but a close correlation would argue against any meaningful differences in the interpretation of PD₂₀ and ‘reactivity’.

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Figure 1

Log dose–response slope and logPD₂₀FEV₁ in 41 subjects with asthma after histamine challenge (r=−0.97, p<0.0001). Data from these subjects have been reported previously.2

Thirdly, there are inconsistencies in the data in their figure 2.1 Seven subjects have PD₂₀ values close to zero (possibly 0.1 μmol?), and therefore should have DRS values of ∼200 (ie, 20% fall/0.1 μmol) and CIR values of ∼2.3 (ie, log 200). These subjects do not appear in figure 2B,C. Furthermore, the distribution of AQLQ differs between figure 2A and B.

The advantage of a continuous measure of airway responsiveness such as DRS, rather than PD₂₀, is not that DRS provides qualitatively different information but rather that it yields an estimate of airway responsiveness in all subjects, not just the subset with AHR. Airway responsiveness is a continuum, with the cut-off point for AHR defined arbitrarily. However, AHR can be normalised with inhaled corticosteroid therapy,3 and subjects with asthma can move in and out of the abnormal range. A more appropriate interpretation of the difference between PD₂₀ and ‘reactivity’ in their relationships with AQLQ reported by Cisneros et al1 would be that quality of life is worse in subjects with AHR, but does not worsen with increasing severity of AHR.