To the Editor:
We read with great interest the study by Majid et al describing pulmonary function tests (PFTs) and flow-volume loops in patients with tracheobronchomalacia.1 A central question is whether abnormalities in the PFT results and flow-volume loops are attributable to tracheobronchomalacia or concomitant lung disease (eg, COPD or asthma). A secondary question that remains unaddressed is whether such abnormalities in any way predict differential outcomes with attempts to address the tracheobronchomalacia.
In the study by Majid et al, 64 (71%) of 90 tracheobronchomalacia patients had either COPD or asthma. The PFT results and flow-volume loops from all 90 patients were analyzed in aggregate, irrespective of the presence or absence of additional pulmonary disease.1 Majid et al reported that “Among 76 patients with available flow-volume loops, the most frequent finding was low maximum forced expiratory flow, in 62 (81.6%) subjects, followed by biphasic morphology in 15 (19.7%), notched expiratory loop in 7 (9.2%), and expiratory oscillations in 2 (2.6%). The balance of 13 subjects (17.1%) had no distinctive flow-volume loop abnormality.”1
This study design missed an opportunity to evaluate, through analysis stratified according to comorbid lung pathology, whether tracheobronchomalacia was associated with abnormalities seen on PFT results and flow-volume loops that are independent of the concomitant lung disease. There is currently no clear evidence to support the assumption that tracheobronchomalacia has an independent effect on PFTs and flow-volume loops. Majid et al appropriately point out that central airway collapse from tracheobronchomalacia likely has no effect on expiratory air-flow limitation.1–4 Furthermore, several patients with substantial tracheobronchomalacia from Mounier-Kuhn syndrome, but normal lung parenchyma, are reported to have normal PFT results.5 Flow-volume loops in COPD and asthma can also be characterized by low maximum forced expiratory flow and biphasic morphology. Could this suggest differential patterns of airways obstruction and in turn convey differential responses to interventions intended to address tracheobronchomalacia? Perhaps the biphasic pattern predicts substantial small-airways obstruction and low probability of improvement with such interventions.
It would be informative if Majid et al could provide data on PFT results and flow-volume loops in patients with only tracheobronchomalacia and no other pulmonary disease, and whether any of the reported PFT results and flow-volume loop findings observed prior to central airway stabilization procedures predict improvement in PFT results, flow-volume loops, or a clinically meaningful outcome.
Footnotes
The authors have disclosed no conflicts of interest.
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