Ilse M. Boudewijn

Less small airway dysfunction in asymptomatic bronchial hyperresponsiveness than in asthma

Bronchial hyperresponsiveness (BHR) can be present in subjects without any respiratory symptoms. Little is known about the role of the small airways in asymptomatic subjects with BHR.

Effects of ageing and smoking on pulmonary computed tomography scans using parametric response mapping.

Chronic obstructive pulmonary disease (COPD) is an obstructive lung disease often caused by cigarette smoke, and characterised by inflammation and abnormalities of the large and small airways (i.e. those with an internal diameter <2 mm), as well as by alveolar destruction (emphysema). Recent evidence suggests that small airway disease precedes emphysema [1] and, therefore, it may be useful to identify the presence and extent of small airway disease and emphysema in early COPD, or preferably, even before the onset of disease. Parametric response mapping can distinguish small airway disease, emphysema and parenchymal disease on pulmonary CT http://ow.ly/Neuw6

Nocturnal dry cough in the first 7 years of life is associated with asthma at school age

Childhood wheeze is an important, well‐known risk factor for asthma, yet little is known about the contribution of nocturnal dry cough. We investigated the association of nocturnal dry cough at ages 1–7 years with doctor‐diagnosed asthma at 8 years of age, both in the presence and absence of wheeze.

Small airway dysfunction in asymptomatic bronchial hyperresponsiveness and asthma

We read with great interest the article by Boudewijn et al. (1), who compared the small airway dysfunction in healthy controls, subjects with asymptomatic airway hyperresponsiveness, and patients with asthma. We are grateful to the authors for their insights into advancing our understandings of the changes in small airway indices prior to and following methacholine bronchial inhalation challenge as well as their relationship with sensation of dyspnea. We respectfully disagree with the way in which the data were presented. First, the small airway dysfunction seemed to be defined as the presence of either of the aberrant small airway indices in the present study. Although the ‘gold criteria’ for defining small airway dysfunction are lacking, a combination of miscellaneous techniques (i.e., interrupter technique, helium–oxygen mixed gas ventilation, biopsy) may be preferred (2), or alternatively, this should be stated as a major limitation of the study. Second, we found that the changes in small airways caliber following methacholine inhalation challenge were better reflected by resonant frequency (Fres) and the area of reactance integrated from 5Hz to Fres (AX), but not R5–R20, in patients with different levels of asthma control (W.-J. Guan and J.-P. Zheng, unpublished data). This suggested that the frequency dependence should be preferentially employed to determine the degree of small airway dysfunction, particularly in those with asymptomatic airway hyperresponsiveness. Third, the changes in forced vital capacity (FVC) should be explicitly stated, for it represented the degree of air trapping or ventilation heterogeneity as a consequence of small airway dysfunction. The readers might be perplexed by the issue as to whether FVC remained normal following inhalation challenge, and if so, the conclusion that a greater change in small airway indices indicated a more pronounced small airway dysfunction could then be safely made. A surrogate approach could be the measurement of residual volume (RV) and the ratio of RV to total lung capacity (TLC) following inhalation challenge, as the authors did at the baseline measurement only. Furthermore, patients with asthma had a mean FEV1 of 101% predicted, suggesting that they had a very limited magnitude of small airway dysfunction. The bronchial inhalation challenge test might have been precluded because those with moderate to severe asthma, who had more pronounced small airway dysfunction, did not meet the eligibility for enrollment. Apart from the aforementioned pitfalls, some other remarks are made. Airway hyperresponsiveness could be, to our knowledge, significantly influenced by the stimuli insults, for instance cigarette smoking. In this cohort, 53% of subjects with asymptomatic airway hyperresponsiveness were current smokers, and this figure was significantly higher than that in patients with asthma (13%) and healthy controls (33%). This was likely to generate a bias toward the small airway dysfunction detected by impulse oscillometry. Moreover, although it would be reasonable to link the changes in small airway indices to the Borg’s score of dyspnea at PC20, the correlation analysis has been, as determined by its inherited demerits, difficult to fully elucidate the causative effects. And the hypothesis that the dyspnea sensation was influenced by small airways was, at least partly, dampened by the observations in patients with asthma who did not yield statistically significant correlations, although several potential confounders have been mentioned in the authors’ discussion. Once these issues have been appropriately addressed, we could explore deeper into the roles that small airways play in the development of asymptomatic airway hyperresponsiveness and the sensation of dyspnea. This is expected to call for further research on the early intervention of mildest form of asthma. A study that compares the utility of different small airway indices on identifying subjects with asymptomatic airway hyperresponsiveness and reflecting the level of asthma control is also necessary.