RESUMO

1. Pulmonary Function Laboratory and Respiratory Investigation Unit, Division of Respirology, Kingston Health Science Center & Queen’s University, Kingston (ON) Canada. 2. Unidade de Fisiologia Pulmonar, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre (RS) Brasil.

BACKGROUND
 
Asthma and COPD are the commonest respiratory diseases followed by pulmonologists. Due to shared clinical features, discriminating between the two diseases can be challenging; moreover, there might be asthma-COPD overlap (ACO).(1) Symptomatic patients are often referred for pulmonary function tests (PFTs), because their physicians hope that such tests will provide clear-cut diagnostic information.
 
OVERVIEW
 
Patient “A” was a 61-year-old woman, former smoker (18 pack-years), who was referred for PFTs “to confirm asthma,” because a previous spirometry had shown a large FEV1 response (0.55 L) to bronchodilator. Repeated PFTs showed a moderate and proportional decrease in FEV1 and FVC (FEV1/FVC = 0.72) with a large post-bronchodilator volume response (ΔFVC = 0.81 L), leading to a commensurate increase in FEV1, that is, pre- and post-bronchodilator FEV1/FVC ratios were similar. Gas trapping was detected on body plethysmography (RV/TLC = 0.59), with preserved TLC; of note, DLCO, carbon monoxide transfer coefficient (KCO), and alveolar ventilation (VA)/TLC ratio were all moderately reduced. These results combined were more consistent with COPD than asthma; in fact, a chest CT showed moderate-to-severe centrilobular emphysema and diffuse airway thickening. Patient “B” was a 73-year-old gentleman previously diagnosed with COPD, on the basis of a heavy smoking history and airflow limitation on remote spirometry. Repeated PFTs confirmed moderate airflow limitation (FEV1/FVC = 0.58; FEV1 = 64% of the predicted value). Following the use of inhaled bronchodilator, FEV1 and mid-expiratory flows normalized. Lung volumes, DLCO, KCO and VA/TLC ratio were within normal limits, as was a chest CT. Collectively, these data were deemed more consistent with asthma than COPD.
 
The list of scenarios in which PFTs are ambiguous about the presence of asthma or COPD (Table 1) is considerably larger than is that describing the few “diagnostic” situations provided above. For instance, even if a large increase in post-bronchodilator FEV1 (ΔFEV1  ≥ 20% and ≥ 400 mL) is more commonly associated with asthma, this is not necessarily the case when the increase in FEV1 is largely driven by volume recruitment (Patient “A”; Table 1, scenario 6). In practice, no cutoff value has provided excellent performance to differentiate asthma from COPD clearly. (1) The spirometric pattern designated Preserved Ratio Impaired Spirometry, also seen in Patient “A,” has been described in both diseases.(2) Low DLCO and KCO speak against asthma (Patient “A”), but low DLCO may occur in non-anemic patients with asthma if VA is a low fraction of TLC.(3) Conversely, preserved (or increased) DLCO is more consistent with asthma, but it may occur in COPD patients with a predominance of chronic bronchitis (Table 1, scenario 10).(4) Establishing the presence of ACO is even more challenging. Given the seven definitions of ACO,(5) spirometry-based criteria were the least reliable and stable over time.

 
CLINICAL MESSAGE
 
In various circumstances, PFTs alone are unable to definitively establish asthma and/or COPD (Table 1). Relating functional data with additional clinical information (pre-test likelihood of disease, potentially including eosinophil counts) is crucial to this endeavor. A cautious, noncommittal approach is recommended: even if the results do suggest one of the diseases, it is safer (and more honest) to state that “in the right clinical context,” the results are “consistent with” asthma and/or COPD.

1. Sin DD, Miravitlles M, Mannino DM, Soriano JB, Price D, Celli BR, et al. What is asthma-COPD overlap syndrome? Towards a consensus definition from a round table discussion. Eur Respir J. 2016;48(3):664-673. https://doi.org/10.1183/13993003.00436-2016


2. Stringer WW, Porszasz J, Bhatt SP, McCormack MC, Make BJ, Casaburi R. Physiologic Insights from the COPD Genetic Epidemiology Study. Chronic Obstr Pulm Dis. 2019;6(3):256-266. https://doi.org/10.15326/jcopdf.6.3.2019.0128


3. Neder JA, Berton DC, Muller PT, O’Donnell DE. Incorporating Lung Diffusing Capacity for Carbon Monoxide in Clinical Decision Making in Chest Medicine. Clin Chest Med. 2019;40(2):285-305. https://doi.org/10.1016/j.ccm.2019.02.005


4. Clausen JL. The diagnosis of emphysema, chronic bronchitis, and asthma. Clin Chest Med. 1990;11(3):405-416.


5. Barrecheguren M, Pinto L, Mostafavi-Pour-Manshadi SM, Tan WC, Li PZ, Aaron SD, et al. Identification and definition of asthma-COPD overlap: The CanCOLD study. Respirology. 2020;25(8):836-849. https://doi.org/10.1111/resp.13780