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Research Article Clinical Review

Importance of distinguishing between asthma and chronic obstructive

pulmonary disease in primary care
Anthony D. D’Urzo, David Price, Peter Kardos and M. Reza Maleki-Yazdi
Canadian Family Physician September 2021; 67 (9) 661-667; DOI: https://doi.org/10.46747/cfp.6709661

Article Figures & Data eLetters Info & Metrics In this issue

 PDF Canadian Family Physician

Abstract Vol. 67, Issue 9
1 Sep 2021
Table of Contents
Objective To facilitate distinction between asthma and chronic obstructive About the Cover
pulmonary disease (COPD) in day-to-day primary care practice, and provide Index by author

practical treatment strategies using spirometric cases to outline how to

recognize the clinical and spirometric overlap between asthma and COPD.

Sources of information The approaches described here were developed

using evidence-based guidelines and the expertise of the authors, including
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research findings by the authors in the areas of asthma, COPD management,
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and spirometric testing in primary care.
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Main message There are patients with clinical or spirometric features of both  Email Article
asthma and COPD. Both asthma and COPD are associated with some  Citation Tools
degree of inflammation of the respiratory tract, mediated by the increased  Respond to this
article
expression of inflammatory proteins. However, there are clear differences
between asthma and COPD in the pattern of inflammation that occurs in the
lungs. Diagnostic confusion between COPD and asthma is most likely to Related Articles
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arise in older patients with respiratory complaints, particularly against a

background that includes cigarette smoke or workplace exposure. Both Importance de distinguer l’asthme de la maladie
pulmonaire obstructive chronique en première
asthma and COPD are clinical diagnoses based on patient history,
ligne
symptoms, physical examination findings, and objective measures of lung
function. Postbronchodilator spirometry is always needed to confirm a new PubMed Google Scholar

diagnosis of COPD and should also be performed prebronchodilator for the

diagnosis of asthma. However, in many cases, the interpretation of
 Cited By...
:
 spirometry results is not straightforward.
 More in this TOC Section
Conclusion Understanding the nature and extent of the spirometric overlap
 Similar Articles
between asthma and COPD is critical for tailoring a therapeutic strategy that
is based on factors that include medical and family history, signs and
symptoms, and a clear interpretation of spirometry data. This information will
be leveraged differently for individual patients to arrive at the correct clinical
diagnosis and to select the most appropriate therapy.

With an increasing and aging population worldwide, chronic respiratory

diseases (of which chronic obstructive pulmonary disease [COPD] and
asthma are the most common) are becoming important causes of mortality
and morbidity.1,2 The Global Burden of Disease study reported that, in 2015,
asthma was the most prevalent chronic respiratory disease, affecting an
estimated 358.2 million people (an increase in prevalence of 12.6% between
1990 and 2015), with COPD affecting 174.5 million people (an increase in
prevalence of 44.2%).2

When encountering adult patients with respiratory symptoms who have a

history of exposure to noxious particles including cigarette smoke, primary
care physicians are potentially faced with the important task of differentiating
asthma from COPD. Spirometry remains central to the diagnosis, outcome
prediction, and management of both COPD and asthma.3,4 Although there
are differences in pathophysiology, treatment, expected progression, and
outcomes between these 2 conditions,5-8 there is considerable spirometric
and clinical overlap, which makes diagnostic confirmation difficult in day-to-
day practice.

This article attempts to help distinguish between asthma and COPD in day-
to-day primary care practice by using spirometric cases that outline how to
recognize the clinical and spirometric overlap to facilitate a clinical diagnosis.

Cases

Case 1. The patient is a 45-year-old man who has never

been a smoker. He has intermittent bouts of shortness of
breath and chest tightness and normal findings from
cardiovascular workup. His response to asthma therapy
was favourable; thus, the diagnosis is consistent with
asthma. The prebronchodilator and postbronchodilator
forced expiratory volume in 1 second (FEV1) to forced vital
capacity (FVC) ratios are 79.2% and 82.4%, respectively,
while the FEV1 improved from 2.92 L to 3.29 L after
bronchodilation (increase of 370 mL and 13%) (Figure 1).9

Case 2. The patient is a 73-year-old man with a 40 pack-

year smoking history, no allergies to environmental factors,
:
 and a history of progressive shortness of breath over the
past 10 years. His medical and family histories were
otherwise unremarkable for asthma risk factors. The
prebronchodilator and postbronchodilator FEV1-FVC ratios
are 47.8% and 50.3%, respectively. The prebronchodilator
and postbronchodilator FEV1 results are 1.52 L and 1.88 L,
respectively (increase of 360 mL and 24%) (Figure 1).9
Because the postbronchodilator FEV1-FVC ratio remains
below 70% and the FEV1 reversibility criterion is met, the
clinician is led to differentiate asthma from COPD using
historical data, as the spirometric criteria for asthma and
COPD are both met. The historical and spirometric data in
this case are consistent with a clinical diagnosis of COPD.
Case 3. The patient is a 36-year-old woman who has never
been a smoker. She has numerous environmental allergies
and has severe asthma that is well controlled on
maintenance therapy. The prebronchodilator and
postbronchodilator FEV1-FVC ratios are 46.7% and 50.3%,
respectively. The prebronchodilator and postbronchodilator
FEV1 values are 1.65 L and 1.94 L, respectively (increase of
290 mL and 18%) (Figure 1).9
Cases 2 and 3 highlight the spirometric overlap between
asthma and COPD and the limitations of using FEV1
reversibility to help distinguish asthma from COPD.

Case 4. The patient is a 19-year-old boy with a history of

childhood asthma and β2-agonist use increasing over
several months. The prebronchodilator and
postbronchodilator FEV1-FVC ratios are 63.9% and 77.8%,
respectively (Figure 1).9 The prebronchodilator and
postbronchodilator FEV1 values are 2.17 L and 2.74 L,
respectively (increase of 570 mL and 26%). These data
exclude a spirometric diagnosis of COPD based on the
normal postbronchodilator FEV1-FVC ratio, and the
increase in FEV1 is consistent with a spirometric diagnosis
of asthma.
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Spirometric data for case examples
 Acknowledgment
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 Notes
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Sources of information  References
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The approaches described here were developed using evidence-based 

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guidelines and the expertise of the authors, including research findings by 

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the authors in the areas of asthma, COPD management, and spirometric

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testing in primary care.

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Main message

Patients with COPD, asthma, or asthma-COPD overlap (ACO) may present

with similar clinical symptoms.10,11 Furthermore, patients with non–fully
reversible chronic asthma may present with spirometric overlap, making
distinction between the conditions difficult since symptoms such as chronic
cough or sputum production are also frequently reported in patients with
COPD or ACO.12 Once spirometric data have been obtained and considered
in conjunction with other important clinical information, clinical uncertainty
may be reduced and physicians may be better able to arrive at an accurate
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clinical diagnosis.

Definitions and diagnosis. The most recent update by the Global Initiative
for Chronic Obstructive Lung Disease (GOLD)3 defines COPD as a disease
characterized by persistent respiratory symptoms (eg, dyspnea, cough,
sputum production) and airflow limitation stemming from airway or alveolar
abnormalities typically caused by substantial exposure to noxious particles
:
 or gases (eg, tobacco smoke, biomass fuel, air pollution, workplace hazards).
In addition to environmental exposure, the updated definition recognizes the
importance of host factors (eg, genetic abnormalities, abnormal lung
development, accelerated aging) that predispose certain individuals to
develop COPD.3 Unlike asthma, which is often diagnosed earlier in life,
COPD is a progressive condition of declining lung function that typically
appears and is diagnosed after 40 years of age (Table 1).5,6,13

Table 1.
View inline | View popup
Usual features of asthma and COPD

The diagnosis of COPD is established by the presence of a

postbronchodilator FEV1-FVC ratio of less than 0.70 (ie, 70%) or the lower
limit of normal; in older patients the 70% cutoff value can overestimate the
obstruction.14 In COPD, airflow obstruction is determined by both irreversible
(eg, alveolar destruction) and partly reversible (eg, smooth muscle
bronchoconstriction) components, among others.15 The updated GOLD
strategy emphasizes the value of spirometry with bronchodilator testing at
initial diagnosis.3 It is important to note that in COPD there are no restrictions
on the magnitude of FEV1 reversibility as long as the FEV1-FVC ratio remains
reduced (Figure 1, case 3).9

The Global Initiative for Asthma (GINA)4 defines asthma as a heterogeneous

disease that is typically characterized by chronic airway inflammation. This
condition is demarcated by the history of respiratory symptoms, such as
wheeze, shortness of breath, chest tightness, and cough, which can vary in
intensity and over time.4 In addition, asthma is characterized by variable
(usually largely reversible) expiratory airflow limitation. Objective evidence of
asthma may include excessive variability in lung function (eg, an increase in
lung function postbronchodilator up to the normal range is frequent but not
always possible; or changes in function between visits); a decrease in lung
function after exercise or during a bronchial provocation test; and variation in
lung function beyond the normal range with repeated measurement.4 In
adults with respiratory symptoms suggestive of asthma, an increase in FEV1
of more than 12% and of more than 200 mL from baseline is usually
accepted as fulfilling the reversibility criteria consistent with asthma (Figure
1, case 1).4,9 However, as noted above, it is important to recognize that many
patients with COPD may also fulfil this criteria as long as the FEV1-FVC ratio
remains below 70% or the lower limit of normal (Figure 1, case 2),9,16-18
resulting in a scenario of lung function overlap where disease
misclassification may result if solely FEV1 reversibility is used to distinguish
between these 2 conditions. However, an important exception is that a
postbronchodilator increase of FEV1-FVC ratio into the normal range
excludes the diagnosis of COPD (Figure 1, case 4).9

There are, however, patients with clinical or spirometric features of both

:
 asthma and COPD. Recently, GINA and GOLD have jointly recommended
that the term asthma–COPD overlap syndrome be abandoned because it has
been used to represent a single disease state or phenotype; the term
asthma–COPD overlap includes patients presenting with objective features of
both asthma and COPD (Figure 1, cases 2 and 3).4,9 Furthermore,
acknowledging that both asthma and COPD are highly heterogeneous
diseases, Reddel reinforced that ACO similarly encompasses different
phenotypes caused by a variety of underlying mechanisms.19

Pathogenesis and pathophysiology. Both asthma and COPD are

associated with some degree of inflammation of the respiratory tract,
mediated by the increased expression of inflammatory proteins such as
cytokines, chemokines, adhesion molecules, and inflammatory enzymes and
receptors. However, there are clear differences between asthma and COPD
in the pattern of inflammation that occurs in the lungs. These differences are
due to the involvement of different inflammatory cells and mediators and,
importantly, to the underlying triggers of inflammation, eg, chronic exposure
to smoke and noxious particles for COPD as opposed to allergens and
infections for asthma (Table 1).20 There is also systemic inflammation in
patients with COPD that is thought to contribute to comorbidities such as
cardiovascular disease, diabetes, and osteoporosis.21 The distinction
between asthma and COPD inflammatory profiles may become blurred in
individuals with severe asthma; in asthma patients who smoke and have a
neutrophilic pattern of inflammation; and during acute exacerbations of both
asthma and COPD, which have similar (mixed) inflammatory features.20

Chronic airway inflammation is a prominent feature of asthma and it is well

known that controlling the inflammation will help reduce symptoms and
exacerbations, and also likely limit the extent of airway remodeling, ie,
structural changes over the course of the disease.22 As such, anti-
inflammatory agents like corticosteroids remain first-line and cornerstone
treatment for asthma (although not all asthma patients respond to inhaled
corticosteroids [ICS]).

In COPD, it is thought to be chronic exposure to noxious particles that, by

insulting the bronchial tree and distal airways, causes inflammation that
culminates in obstruction of predominantly small airways and destruction and
distension of the alveolar walls (ie, bronchitis or emphysema).23 As such,
smoking cessation is the only disease-modifying approach, while
bronchodilators, which improve airflow and reduce hyperinflation (air
trapping), are the cornerstone of COPD management. In contrast to asthma,
benefits from anti-inflammatory ICS are restricted to patients with frequent
exacerbations and some patients with elevated eosinophil levels.3

Differential diagnosis. In certain cases, distinguishing between asthma and

COPD is straightforward; for example, asthma would be diagnosed in an
atopic individual who is younger than 50 years of age, is a non-smoker, has a
history of childhood wheeze, has a family history of asthma, presents with
:
 wheezing, and has substantial or full bronchodilator reversibility at the time of
clinical evaluation (Figure 1, case 1).9

Diagnostic confusion between COPD and asthma is most likely to arise in

older patients with respiratory concerns, particularly against a background of
cigarette smoke or workplace exposure.

In light of the considerable overlap between features of asthma and COPD

(Figure 1, cases 2 and 3),9 differential disease characteristics of asthma,
COPD, and ACO have been summarized in the collaborative report by GOLD
and GINA,24 focusing on the features that are most helpful in identifying and
distinguishing typical asthma or COPD; this report also recommends that a
diagnosis of ACO should be considered if a similar number of features of
both asthma and COPD are present.24 In addition to asthma and ACO, other
potential differential diagnoses for COPD include congestive heart failure,
bronchiectasis, tuberculosis, obliterative bronchiolitis, diffuse panbronchiolitis
(in patients with Asian heritage), and sarcoidosis, although these are usually
easier to distinguish from COPD.3

It is also recommended that targeted testing be carried out for α1-antitrypsin

deficiency (AATD)3 in all newly diagnosed patients with COPD since AATD is
a predisposing genetic cause of pulmonary emphysema.6 Adults diagnosed
with presumed asthma that is not completely reversible after bronchodilator
treatment are also candidates for AATD testing.25,26 Fewer than 10% of
individuals with symptomatic AATD in primary care are appropriately
diagnosed, which may be owing to COPD being underdiagnosed and the
lack of awareness of AATD.25 The lack of awareness of AATD is similar in the
context of patients with asthma or asthmalike symptoms.26

Finally, it should be highlighted that patient history and clinical evaluation

should be taken into account during the differential diagnosis investigations;
for example, many patients with ACO who are 40 years and older have a
long-standing history of atopy or wheezing starting before the age of 40
years27 but they come to the attention of their physicians much later (ie,
when 50 to 70 years of age).7,28

If ACO is the working diagnosis, then treatment must include ICS plus long-
acting bronchodilators to maximize lung function, symptom control, and
other important clinical outcomes. It is safe to say that unlike asthma, where
symptoms are variable over time, including at times within a given day,
COPD progresses in an insidious fashion such that patients may report few
symptoms as a result of lifestyle adjustments designed to minimize the
effects of pulmonary impairment on the sensation of breathlessness.

Role of spirometry in differential diagnosis. Both asthma and COPD are

clinical diagnoses based on patient history, symptoms, physical examination
findings, and objective measures of lung function. Postbronchodilator
spirometry is always needed to confirm a new diagnosis of COPD and should
also be performed prebronchodilator for the diagnosis of asthma. In many
:
 cases, the interpretation of spirometry results is not straightforward for the
following reasons:

A spirometric distinction between COPD and asthma is only seen if the

flow limitation postbronchodilator completely resolves, which is a finding
consistent only with asthma (Figure 1, case 4).9

In cases of normal spirometry findings (normal FEV1, FVC, FEV1-FVC

ratio) but classical clinical data for symptoms and history of asthma the
diagnosis of asthma is still probable,29 and some patients may show
improvements at an FEV1 of more than 200 mL and more than 12% after
bronchodilator challenge (Figure 1, case 1).9

In permanent flow limitation, the higher the extent of postbronchodilator

FEV1 reversibility (> 400 mL) the more likely an asthma diagnosis is, but
this is not a validated assumption.

In permanent flow limitation, FEV1 reversibility (> 12% and > 200 mL)
may be compatible with both asthma and COPD (Figure 1, cases 2 and
3).9 In these cases, clinical and historical factors and follow-up visits are
needed to establish a clinical diagnosis.

While a thorough description of the performance of a correct maximal

breathing maneuver is beyond the scope of this article, selection of the most
appropriate test results and correct interpretation of the data are essential.30
A recent systematic scoping review suggests that in primary care COPD
misdiagnosis is attributable to factors related to spirometric testing.31

Spirometric overlap between asthma and COPD is highlighted in an analysis

examining acute bronchodilator responsiveness (using 3 criteria) in a large
cohort with moderate to very severe COPD.32 The UPLIFT (Understanding
Potential Long-term Impacts on Function with Tiotropium) trial found that
53.9% of patients had 12% or greater and 200 mL or greater improvement in
FEV1 over baseline, 65.6% had 15% or greater improvement in FEV1 over
baseline, and 38.6% had 10% or greater absolute increase in FEV1
percentage of predicted value.32 This study demonstrated substantial acute
bronchodilator reversibility in COPD patients who had no other features of
asthma, regardless of the criteria used to define reversibility.32 In the most
recent reports, the prevalence of bronchodilator reversibility, expressed as
increase in FEV1 of 12% or greater and 200 mL or greater, was 17.3% and
18.4% among participants with asthma and COPD, respectively,33,34
underscoring that FEV1 reversibility is of limited value for distinguishing
asthma from COPD.

In asthma, spirometry results at a single visit do not always confirm a

diagnosis; results must be considered in the context of the clinical
presentation and whether treatment has been started (see Box 5-3 in the
2021 GINA report).4

The spirometric overlap between asthma and COPD was also recently
highlighted in the Effect of Indacaterol/Glycopyronium versus
Fluticasone/Salmeterol on COPD Exacerbations (FLAME) study,34 which
:
 compared the effectiveness of the long-acting β2-agonist (LABA) indacaterol
plus the long-acting antimuscarinic glycopyrronium once daily with the
LABA-ICS combination of salmeterol–fluticasone propionate twice daily for
preventing exacerbations in patients with COPD. The mean reversibility of the
FLAME study population met the FEV1 reversibility required for asthma. The
FLAME protocol nevertheless applied stringent asthma exclusion criteria
(excluding all COPD patients with a history of concomitant allergic rhinitis,
asthma, or very pronounced blood eosinophils [> 600 cells/μL]) and lung
function reversibility was performed using methods adopted in most
bronchodilator studies in COPD. The FLAME study importantly demonstrated
COPD patients with a history of exacerbations benefited more from an ICS-
free dual bronchodilation with indacaterol-glycopyrronium than from a LABA-
ICS combination for the prevention of further exacerbations, a finding that
would not be expected in an asthma-rich population.34

Conclusion

The clinical and spirometric overlap between asthma and COPD presents
important challenges for primary care physicians who are often faced with
considerable time constraints in day-to-day clinical practice. Understanding
the nature and extent of this overlap is critical for tailoring a therapeutic
strategy that is based on factors that include medical and family history,
signs and symptoms, and a clear interpretation of spirometry data. This
information will be leveraged differently for individual patients to determine
the correct clinical diagnosis and the appropriate therapy.

Acknowledgment

The preparation of this manuscript was funded by Novartis Pharmaceuticals

Canada Inc. No funding or sponsorship was received for the publication of
this article. The authors thank Farid Khalfi, PhD, and Ian Wright, PhD (both
from Novartis Ireland Ltd), for providing medical writing support in
accordance with the 2015 Good Publication Practice (GPP3) guidelines
(http://www.ismpp.org/gpp3).

Notes

Editor’s key points

▸ The clinical and spirometric overlap between asthma and chronic

obstructive pulmonary disease (COPD) presents important challenges for
primary care physicians, who are often faced with substantial time
constraints in day-to-day clinical practice.

▸ Patients with COPD, asthma or asthma-COPD overlap may present

with similar clinical symptoms. Furthermore, patients with non–fully
reversible chronic asthma may present with spirometric overlap, making
distinction of each condition difficult since symptoms such as chronic
cough or sputum production are also frequently reported in patients with
:
 COPD or asthma-COPD overlap.

▸ Once spirometric data have been obtained and considered in

conjunction with other important clinical information, such as patient
history and physical examination findings, clinical uncertainty may be
reduced and physicians may be better able to arrive at an accurate
clinical diagnosis and appropriate treatment.

Footnotes

Contributors

All authors contributed to the content of this manuscript and approved

the final version for submission.

Competing interests

Dr Anthony D. D’Urzo has received research, consulting, and lecturing

fees from Almirall, Altana, AstraZeneca, Boehringer Ingelheim (Canada)
Ltd, Forest Laboratories, GlaxoSmithKline, KOS Pharmaceuticals, Merck
Canada, Methapharm, Novartis Canada/USA, Ono Pharma, Pfizer
Canada, Schering Plough, Sepracor, SkyePharma, and Teva Canada. Dr
David Price has board membership with Amgen, AstraZeneca,
Boehringer Ingelheim, Chiesi, Circassia, Mylan, Mundipharma, Novartis,
Regeneron Pharmaceuticals, Sanofi Genzyme, Teva Pharmaceuticals,
and Thermo Fisher; consultancy agreements with Amgen, AstraZeneca,
Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Mylan, Mundipharma,
Novartis, Pfizer, Teva Pharmaceuticals, and Theravance; grants and
unrestricted funding for investigator-initiated studies (conducted through
Observational and Pragmatic Research Institute) from AstraZeneca,
Boehringer Ingelheim, Chiesi, Circassia, Mylan, Mundipharma, Novartis,
Pfizer, Regeneron Pharmaceuticals, Respiratory Effectiveness Group,
Sanofi Genzyme, Teva Pharmaceuticals, Theravance, and the UK
National Health Service; payment for lectures and speaking engagements
from AstraZeneca, Boehringer Ingelheim, Chiesi, Cipla, GlaxoSmithKline,
Kyorin, Mylan, Mundipharma, Novartis, Regeneron Pharmaceuticals,
Sanofi Genzyme, and Teva Pharmaceuticals; payment for the
development of educational materials from Mundipharma and Novartis;
payment for travel, accommodation, and meeting expenses from
AstraZeneca, Boehringer Ingelheim, Mundipharma, Mylan, Novartis, and
Thermo Fisher; funding for patient enrolment or completion of research
from Novartis; stock and stock options from AKL Research and
Development Ltd, which produces phytopharmaceuticals; owns 74% of
the social enterprise Optimum Patient Care Ltd (Australia and United
Kingdom) and 74% of Observational and Pragmatic Research Institute
(Singapore); is a peer reviewer for grant committees of the Efficacy and
Mechanism Evaluation Programme and Health Technology Assessment;
and was an expert witness for GlaxoSmithKline. Dr Peter Kardos has
received honoraria from AstraZeneca, Chiesi, GlaxoSmithKline,
Klosterfrau, MSD, Novartis, Sanofi, and Willmar Schwabe. Dr M. Reza
Maleki-Yazdi has received speaker’s bureau and honoraria and
consultancy fees from AstraZeneca, Boehringer Ingelheim,
GlaxoSmithKline, Merck, Nycomed, Novartis, and Pfizer, and research
grants from AstraZeneca, Boehringer Ingelheim, Forest Pharmaceuticals,
GlaxoSmithKline, Merck, Nycomed, Novartis, Ono Pharmaceuticals, and
Pfizer.

This article is eligible for Mainpro+ certified Self-Learning credits. To earn

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 credits, go to www.cfp.ca and click on the Mainpro+ link.

This article has been peer reviewed.

La traduction en français de cet article se trouve à www.cfp.ca dans la

table des matières du numéro de septembre 2021 à la page e240.

Copyright © the College of Family Physicians of Canada

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