http://www.nejm.org/doi/full/10.1056/nejmra1411863.

The AsthmaCOPD Overlap

Syndrome

https://www.nature.com/articles/npjpcrm201684 Identifying possible asthmaCOPD overlap

syndrome in patients with a new diagnosis of COPD in primary care

http://thorax.bmj.com/content/thoraxjnl/64/8/728.full.pdf. The overlap syndrome of asthma

and COPD: what are its features and how important is it?

https://copdrp.biomedcentral.com/articles/10.1186/s40749-015-0012-z. The asthma-COPD

overlap syndrome: a new entity?
Review

Open Access

The asthma-COPD overlap syndrome: a new entity?

Miriam Barrecheguren,
Cristina Esquinas and
Marc MiravitllesEmail author

COPD Research and Practice20151:8

https://doi.org/10.1186/s40749-015-0012-z

Barrecheguren et al. 2015

Received: 25 May 2015

Accepted: 24 August 2015

Published: 22 October 2015

Summary

Asthma and COPD are the most frequent chronic respiratory diseases. Although they have
different characteristics, some individuals share features of both diseases, which has been
called the asthma-COPD overlap syndrome (ACOS). Although there is not a universally
accepted definition for ACOS, it was initially defined as symptoms of increased variability of
airflow in association with an incompletely reversible airflow obstruction. The most recent
COPD guidelines include this phenotype and its diagnostic features.

Patients with ACOS are usually characterized by increased reversibility of airflow

obstruction, eosinophilic bronchial and systemic inflammation, and increased response to
inhaled corticosteroids, compared with COPD patients. The relevance of the ACOS is the
need to identify patients with COPD who may have underlying eosinophilic inflammation
that responds better to inhaled corticosteroids. Until new diagnostic tools are developed, a
previous diagnosis of asthma in a patient with COPD can be a reliable criterion to suspect
ACOS in a patient with COPD but a comprehensive approach may be required in most cases
for a definitive diagnosis of ACOS.

Keywords
COPD Asthma ACOS Phenotypes Treatment

Introduction

Chronic obstructive pulmonary disease (COPD) is an underdiagnosed disease with a high

morbidity and mortality and is a very significant public health problem. In Europe the
estimated prevalence varies from 2.1 % and 26.1 % between countries [1]. Given its high
prevalence, COPD entails a high burden in all the levels of care.

In recent years, there has been a growing interest in defining and characterising COPD
patients into different phenotypes that share clinical features, similar response to the available
treatments and that may have prognostic implications [2, 3]. Among these, the asthma-COPD
overlap syndrome (ACOS) is a clear example that fulfils all the criteria and is currently
kindling great interest.

COPD and asthma have clear differences, but some patients may present with a mixture of
both diseases. ACOS may be a manifestation of characteristics of the asthma and COPD that
the patient is suffering from. Clinically, the ACOS usually corresponds to asthmatic smokers
who develop non-fully reversible airway obstruction, however, when the previous history of
asthma is unknown, the diagnosis of ACOS may be difficult due to the lack of specific
biomarkers. In many cases the correct diagnosis of ACOS will require a comprehensive
approach including clinical manifestations, spirometry with bronchodilator test, identification
of eosinophilic inflammation, lung volumes and carbon monoxide diffusion capacity and
even CT scan, and such diagnosis should be made by a specialist [4].

The interest in recognizing these individuals lies in their better response to inhaled
corticosteroids (ICS) compared to those with COPD. This specific and differential treatment
justifies the efforts to differentiate the subgroup of patients with ACOS from the large
population of COPD patients.

Definition and clinical features

From a COPD perspective, the identification of ACOS is relevant to describe a subgroup of

smokers with COPD that share some pathogenic and inflammatory characteristics with
asthma. Patients with ACOS are also more likely to be frequent exacerbators (defined as the
presence of 2 or more exacerbations per year), to have reduced physical activity, worse
quality of life and more respiratory symptoms, particularly dyspnoea and wheezing, than
patients with COPD alone [5, 6].

ACOS has been defined as symptoms of increased variability of airflow in association with
incompletely reversible airflow obstruction [7]. More recently, Louie et al. [8] defined ACOS
as asthma with partially reversible airflow obstruction, with or without emphysema or
reduced carbon monoxide diffusing capacity (DLCO) to <80 % predicted, and COPD with
emphysema accompanied by reversible or partially reversible airflow obstruction, with or
without environmental allergies or reduced DLCO. Izquierdo-Alonso et al. [9] identified
ACOS as patients with COPD (more than 10 pack-years of smoking and post-bronchodilator
FEV1/FVC<0.7) and a personal history of asthma before the age of 40, with the addition of
normal carbon monoxide (CO) diffusing capacity and the absence of pulmonary emphysema
demonstrated by imaging techniques.

It is important to recognise that the presence of chronic non-fully reversible airflow

obstruction in a subject with asthma is not necessarily ACOS. It is well known that severe
asthma patients may develop non-reversible airflow limitation without any characteristics of
COPD [10].

The definition of ACOS is also included in some of the latest guidelines. The Spanish
guidelines of COPD identify ACOS patients based on some diagnostic criteria: A) Major
criteria: very positive bronchodilator response (>400 ml and >15 % in FEV1), sputum
eosinophilia or previous diagnosis of asthma. B) Minor criteria: increased total serum IgE,
previous history of atopy or positive bronchodilator test (>200 mL and >12 % in FEV1) on at
least two occasions [11, 12]. To be diagnosed with ACOS, a patient must fulfil two major or
one major and two minor criteria. The recent Czech Republic and Finnish guidelines also
include ACOS with its own diagnostic criteria. In the Czech Republic diagnostic guidelines
major criteria include a strong bronchodilator test positivity (FEV1>15 % and>400 ml),
positive bronchial challenge test, FeNO>4550 ppb and/or sputum eosinophilia 3 % and a
previous histoy of asthma, and as minor criteria: mild bronchodilator test positivity
(FEV1>12 % and>200 ml), increased total IgE and history of atopy [13]. The main Finnish
diagnostic criteria are also a significant bronchodilatory effect (FEV1>15 % and>400 ml),
sputum eosinophilia or elevated ENO (>50 ppb) and previous asthma symptoms (starting
before the age of 40). As additional criteria they include an elevated total IgE, atopy, repeated
significant bronchodilatory response (FEV1>12 % and >200 ml) and a PEF-follow up
typical of asthma [14]. For both guidelines, a patient must fulfil two major (or main) criteria
or one major and two minor (or additional) criteria.

A recent GOLD-GINA document about ACOS describes this syndrome as persistent airflow
limitation with several features usually associated with asthma and several features usually
associated with COPD [15].

Diagnosis: current and future strategies

In asthma the term endotype has been introduced to identify subtypes of patients defined by a
distinct functional of pathophysiological mechanism [16]. It is possible that different
mechanisms in patients suffering from asthma or COPD could lead to the clinical expression
that we now define as ACOS. Most studies define ACOS as a phenotype of COPD. There is
no unified definition of ACOS but some main features can help us to identify this phenotype.
In patients with COPD, increased reversibility is one of the key differential aspects of
individuals with ACOS, but it can be misleading if taken alone. Significant reversibility in
COPD is common and observed frequently in clinical practice and in series of patients
included in clinical trials [17]. Somewhat more than 50 % of the patients with moderate-to-
very-severe COPD in the UPLIFT clinical trial met the most commonly used criteria for
acute bronchodilator responsiveness [18]. Related to this bronchodilator response, bronchial
hyperresponsiveness (BHR) is observed in almost all patients with asthma, especially in those
with active symptoms and in up to two-thirds of COPD patients [19]. Furthermore, BHR is
observed in aproximately 10 % to 20 % of the general population and has shown to be a risk
factor of developing asthma and COPD [8]. In patients with established asthma or COPD,
more severe BHR is associated with more severe symptoms and a more rapid decline in
FEV1 [20]. Nevertheless, in a population of COPD patients without significant comorbidities,
individuals with high levels of reversibility presented better long-term outcomes [21]. These
controversial results underscore the need of a specialised approach to the diagnosis and
assessment of the patients with ACOS.

Possibly the most important diagnostic feature of ACOS in COPD is the presence of sputum
eosinophilia. Inflammation in asthma patients is considered to be mainly eosinophilic and
mediated by CD4+ T lymphocytes while in COPD it is neutrophillic and driven by CD8+.
Papi et al. [22] observed that peripheral eosinophilic counts and sputum eosinophil counts
were significantly higher in stable COPD patients with partial reversibility of airflow
limitation compared to COPD patients without reversibility. Since sputum eosinophilia is not
routinely performed in clinical practice, indirect markers of this type of inflammation have
been investigated. Chou et al. [23] demonstrated higher levels of exhaled nitric oxide (eNO)
in patients with COPD and eosinophilic airway inflammation (>3 % eosinophils in induced
sputum), with a cut off of 23.5 ppb of eNO having a sensitivity of 62.1 % and a specificity of
70.5 % for the identification of eosinophilic inflammation. Interestingly, patients with COPD
and peripheral eosinophilic inflammation treated with ICS present fewer exacerbations
compared to those with lower blood count levels [24].

Other plasma and sputum biomarkers of ACOS are currently being studied. Iwamoto et al.
[25] investigated four potential biomarkers in COPD (surfactant protein A (SP-A), soluble
receptor for advanced glycation end products (sRAGE), myeloperoxidades (MPO) and
neutrophil gelatinase associated lipocalin (NGAL)). Compared with asthma patients, sputum
MPO and plasma SP-A were significantly elevated in ACOS, while only sputum NGAL was
significantly increased compared to COPD. Fu et al. [26] examined the levels of the systemic
inflammation markers PCR and IL-6 in asthma, COPD and ACOS patients and identified
potential clinical characteristics that were associated with these biomarkers. They found a
high prevalence of systemic inflammation in older people with ACOS and an elevated IL-6
compared with asthma patients. Age, Charlson comorbidity index and IL-6 were
independently associated with ACOS while IL-6 was independently associated with airflow
obstruction and cardiovascular disease suggesting that it may be involved in these two
processes and may therefore be an independent treatment target [26].

There is a growing interest in the identification of genetic determinants for ACOS. Genetic analysis of
the COPD gene cohort identified several variants associated with ACOS, which may demonstrate
distinct genetic risk factors [27]. Christenson et al. [28] investigated whether asthma-associated gene
signatures were increased in a subgroup of COPD patients and associated with asthma-related
features, consisting in eosinophilia and type 2 (TH2) inflammation. In their study, the investigators
developed a 100 gene signature of the Th2-related gene expression, the T2S score that correlated well
with Th2-associated clinical characteristics in asthmatic patients and found that approximately 20 %
of their COPD patients had increased expression of T2S. They next investigated the association of
T2S with clinical parameters in the GLUCOLD cohort of patients with COPD. T2S was significantly
associated with increased tissue eosinophil numbers, increased serum eosinophil percentage and
increased bronchodilator responsiveness (Fig. 1). Interestingly, a higher T2S was associated with
greater reduction in hyperinflation after ICS (with or without LABA) treatment versus placebo at
30 months [28]. Nevertheless, albeit promising, these techniques are not available in every centre and
cannot yet be used as a diagnostic tool in clinical practice.

Fig 1

Clinical expression of the asthma-COPD overlap syndrome (ACOS). The ACOS usually
corresponds to a smoker asthmatic patient that develops non fully reversible airway
obstruction and/or a COPD individual (with or without a known history of asthma) with a
Th2 signature (increased blood and lung eosinophilia, increased airway hyper-
responsiveness, and better response to ICS). Reproduced with permission from ref. [43]

Epidemiology of ACOS

Data derived from large population studies have revealed that a high proportion of adult
patients with respiratory symptoms are commonly diagnosed with more than one obstructive
lung disease, especially elderly individuals [29].

More interesting is the prevalence of ACOS observed among populations of patients diagnosed with
COPD. This prevalence can be estimated from research databases or clinical studies. The prevalence
of ACOS derived from clinical studies is usually lower compared with the analysis of databases, due
to the use of more restrictive diagnostic criteria. Using the criteria established by the Spanish National
Consensus Conference (Table 1), in a cross sectional study with 279 COPD patients Miravitlles et al.
[30] observed a prevalence of ACOS of 5 %. A larger survey in 3125 COPD patients using the same
criteria observed a prevalence of ACOS of 3.9 %. However, this prevalence increased to 15.9 % when
using the criterion of a previous diagnosis of asthma [31]. In a retrospective observational study of
499 patients with COPD Golpe et al. [32] observed a similar prevalence (5 %) in smoking-related
COPD patients but with a higher frequency of ACOS in COPD patients caused by inhalation of
biomass smoke (21.2 %). Following modified criteria from the Spanish consensus that included a
normal diffusion capacity for carbon monoxide (DLCO), Izquierdo-Alonso et al. [9] detected a
prevalence of ACOS of 12 % in an observational, multicentre study performed in 331 COPD patients
recruited in pulmonology outpatient services. Similar frequencies have been described in studies
performed in other countries [5, 8]. In the COPD Gene study, Hardin and colleges found that 13 % of
subjects with COPD also reported physician-diagnosed asthma [5]. In epidemiological studies such as
the PLATINO study performed in Latin America, a prevalence of 11.6 % was described using a
postbronchodilator FEV1/FVC<0.7 and asthma diagnosis as ACOS criteria [33]. In the Spanish
EPISCAN epidemiological study, including patients with COPD and previous diagnosis of asthma
before the age of 40, a prevalence of 17.4 % of ACOS was observed among the COPD population
[34].

Table 1

Asthma-COPD overlap syndrome, definitions and diagnostic criteria

Asthma and COPD (symptoms of increased variability of

Gibson P, Simpson J [7], 2009
COPD gene [5],2011
Spanish consensus [11], 2012
(patients must fulfill 2 major
criteria or 1 major and 2 minor)
Czech Republic guidelines [13],
2013 (patients must fulfill 2 major Histoy of asthma
criteria or 1 major and 2 minor)
Louie S et al. [8], 2013
Menezes M et al. [30], 2013
airflow and incompletely reversible airflow obstruction)
Patients with COPD and a diagnosis of asthma before the
age of 40
Major criteria
Very positive bronchodilator response (>400 ml and
>15 % in FEV1)
Sputum eosinophilia
Previous diagnosis of asthma
Minor criteria
Increased total serum IgE
Previous history of atopy
Positive bronchodilator test (>200 mL and >12 % in
FEV1) on at least two occasions
Major criteria
Strong bronchodilator test positivity (FEV1>15 %
and>400 ml)
Positive bronchial challenge test
FeNO>4550 ppb and/or sputum eosinophilia 3 %
Minor criteria
Mild bronchodilator test positivity (FEV1>12 %
and>200 ml)
Increased total IgE
History of atopy
-Asthma with partially reversible airflow obstruction
with/without emphysema or reduction of DLCO <80 %
predicted.
-COPD with emphysema accompanied by reversible or
partially reversible airflow obstruction, with or without
environmental allergies or reduced DLCO
FEV1/FVC <0.7 and medical diagnosis of asthma or
 wheezing+positive bronchodilator test (>200 mL and
>12 % in FEV1)
COPD (more than 10 pack-years and post bronchodilator
FEV1/FVC<0.7)
History of asthma before the age of 40
Izquierdo-Alonso et al. [9] (2013)
Normal carbon monoxide (CO) diffusion capacity and
absence of pulmonary emphysema demonstrated by
imaging techniques
Persistent airflow limitation with several features usually
GOLD-GINA document [15]
associated with asthma and several features usually
(2014)
associated with COPD
Main criteria
Significant bronchodilatory effect (FEV1>15 %
and>400 ml)
Sputum eosinophilia or elevated ENO (>50 ppb)
Previous asthma symptoms (starting before the age of
Finish guidelines [14] (2014) 40)
(patients must fulfill 2 main criteria
Additional criteria
or 1 main and 2 additional)
Elevated total IgE
Atopy
Repeated significant bronchodilatory response
(FEV1>12 % and >200 ml)
PEF-follow up typical of asthma

Treatment

There is little information about the response of ACOS patients to most of the current
pharmacological therapies as they have been systematically excluded from both COPD and
asthma pharmacological trials. The only clinical trial performed to date in patients with
ACOS studied the effects of tiotropium in 472 individuals with concomitant COPD and
asthma. Improvements in lung function and a reduction in rescue medication were observed
with tiotropium [35]. However, the main interest in differentiating ACOS from COPD lies in
the different response to ICS. Some studies demonstrate that patients with COPD and
eosinophilic inflammation treated with ICS present a significant improvement in bronchial
inflammation together with clinical and spirometric improvement [36, 37]. Two small,
randomised trials have demonstrated that prescribing corticosteroids (oral or inhaled)
according to the intensity of bronchial eosinophilic inflammation in patients with COPD was
significantly superior in preventing exacerbations and improving health-related quality of life
compared with the prescription of ICS according to current guidelines [38, 39].

Already in 2007 the Canadian guidelines specified that: if the asthma component (in COPD)
is prominent, earlier introduction of ICS may be justified [40]. Later, in 2010, the Japanese
guidelines of COPD dedicated a chapter to Treatment of COPD complicated by asthma
[41] and indicate that ICS combined with long-acting beta-2 agonists (LABA) would be the
first choice treatment irrespective of the level of airflow obstruction. More recently, the
Spanish guidelines of COPD, the Czech Republic guidelines and the Finnish guidelines
address the indication of ICS in the patients with ACOS in all stages of severity [13, 14].

New treatments targeting a reduction in eosinophilic concentrations are being developed.

Among them, the anti-IL5 benralizumab has not proven to reduce exacerbations in COPD
patients with peripheral eosinophilia, but patients with the highest eosinophilic count showed
improvements in FEV1 and a reduction in the exacerbations rate, which support further
investigation [42].

Conclusion

Patients with ACOS show 3 characteristic features that help us to identify them: enhanced
bronchial and systemic eosinophilic inflammation, increased reversibility of airflow and
increased response to ICS compared with patients with COPD alone. Whether one believes in
the existence of ACOS or just in the coexistence of these two different diseases in the same
individual, it is clear that patients with ACOS are different from those with asthma and
COPD. Although these patients share features with both asthma and COPD, they have some
different clinical characteristics and prognosis and what it more important, a better response
to ICS.

Abbreviations
ACOS:

Asthma-COPD overlap disease

COPD:

Chronic obstructive pulmonary disease

ICS:

inhaled corticosteroids

BHR:

bronchial hyperresponsiveness

LABA:

long acting 2 agonist

DLCO:

carbon monoxide diffusing capacity

CO:

carbon monoxide
SP-A:

surfactant protein A

sRAGE:

soluble receptor for advanced glycation end products

MPO:

mieloperoxidase

NGAL:

neutrophil gelatinase associated lipocalin

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution
4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits
unrestricted use, distribution, and reproduction in any medium, provided you give appropriate
credit to the original author(s) and the source, provide a link to the Creative Commons
license, and indicate if changes were made. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data
made available in this article, unless otherwise stated.

Competing interests

Marc Miravitlles has received speaker fees from Almirall, Boehringer Ingelheim, Pfizer,
AstraZeneca, Chiesi, Esteve, GlaxoSmithKline, Menarini, Grifols, Nycomed, and Novartis,
and consulting fees from Almirall, Boehringer Ingelheim, Pfizer, GlaxoSmithKline, Gebro
Pharma, CLS Behring, MediImmune, Novartis, Grifols and Nycomed. Miriam Barrecheguren
and Cristina Esquinas have no conflict of interest to disclose.

Authors contributions

All authors wrote, read and approved the final manuscript.

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http://www.healthline.com/health/asthma/asthma-copd-overlap-syndrome#causes-and-risk-factors3

Everything You Need to Know About Asthma-COPD Overlap

Syndrome

Symptoms
Causes and risk factors
Diagnosis
Treatment
Tips
Outlook
Prevention

Overview

Asthma-COPD overlap syndrome (ACOS) is when you have symptoms of both asthma and
chronic obstructive pulmonary disease (COPD).

Asthma is a chronic lung disease that causes reversible airway narrowing, inflammation in
the airways, and mucus production. Some symptoms of asthma are shortness of breath,
tightening in the chest, and wheezing.

Most people with asthma have exacerbations, or flare-ups. These are times when their
symptoms are worse than usual. There are also times when they have few or no symptoms.
Emphysema and chronic bronchitis are the two main conditions that fall under the COPD
umbrella. COPD can cause shortness of breath, chest tightening, mucus production, and an
ongoing cough. COPD is a progressive disease. People with COPD have regular symptoms
and also experience flares.

Asthma and COPD are the most commonly diagnosed chronic lung diseases. They both
involve inflammation of the airways, obstruction of airflow, and some other common
symptoms.

Read on to learn more about asthma and COPD, and what it means to live with both
conditions.

Symptoms

What are the symptoms?

Symptoms of ACOS are likely to include:

labored breathing
wheezing
coughing, with or without mucus
tightness in the chest

Symptoms vary from day to day and typically includes flare-ups. There are also key
differences between the symptoms of asthma and COPD.

If you only have asthma, symptoms change often and you can be symptom-free for a long
time. Asthma often involves symptom triggers like exercise, exposure to allergens, or a
respiratory illness. It can start in adulthood, but asthma usually begins in childhood. People
with asthma often have allergies and the skin condition eczema.

If you only have COPD, symptoms usually start after age 40. Symptoms can vary from day to
day, but theyre chronic and progressive, even with treatment. Most people with COPD also
have a history of smoking or smoke exposure.

ACOS shares characteristics of both COPD and asthma. People with ACOS experience some
type of ongoing airway obstruction.

They also experience wheezing, or breathing difficulties, that often respond to

bronchodilators. Bronchodilators are medications that open the airway.

People with ACOS also seem to be younger and experience more shortness of breath than
people with COPD alone. However, because this condition is still being studied, experts do
not yet agree on a single way to define the syndrome.

Causes and risk factors

What are the causes of and risk factors for ACOS?

Because ACOS means you have both asthma and COPD, its important to look at each
condition.

Researchers dont know exactly why some people develop asthma. You might be more likely
to have it if you:

have a family history of allergies or asthma

you smoke or are regularly exposed to irritants such as tobacco smoke
have a personal history of allergies, especially if they developed in early childhood
had respiratory infections as a child

COPD is caused by long-term exposure to lung irritants. In the United States, the most
common cause is cigarette smoke. Cigar smoke, pipe smoke, and secondhand smoke can
cause COPD, too. So can chemical fumes, cooking fumes, and air pollution. Certain genetic
mutations may make you more susceptible to COPD, but this is less common.

Having asthma doesnt mean youll develop COPD. But children with severe, persistent
asthma are 32 times more likely to develop COPD later in life.

ACOS has only recently been identified as a syndrome, so its not yet clear how many people
are affected.

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Diagnosis

How is ACOS diagnosed?

ACOS means you have symptoms of both asthma and COPD. Your doctor may diagnose
asthma, COPD, or ACOS.

ACOS is a fairly new term. Exact guidelines for diagnosing ACOS havent been established.
ACOS generally involves these three features compared with people who have COPD alone:

more of a response to inhaled bronchodilators

increased reversibility of airflow
bronchial and systemic inflammation from eosinophils, a type of white blood cell

To reach a diagnosis, your doctor will perform a physical examination and review your
clinical history. Imaging tests such as X-ray, CT scans, or MRI may be necessary. Its likely
youll also need a noninvasive test called spirometry, also known as a pulmonary function
test, to measure your lung function.

Treatment

Whats the treatment for ACOS?

Because asthma causes inflammation, youll still need asthma treatment. This may include:
 allergen avoidance
allergy medications
inhaled corticosteroids
short-acting bronchodilators
long-acting bronchodilators
preventive vaccines, such as flu, pneumonia, and whooping cough

Youll also need to manage symptoms of COPD to maintain lung function. This may involve:

disease management training

pulmonary rehabilitation
avoiding smoke and other pollutants
healthy eating and nutrition education
long-acting bronchodilator combinations or combination bronchodilator or inhaled
corticosteroids
preventive vaccines, such as flu, pneumonia, and whooping cough
oxygen therapy
surgery to remove damaged lung tissue or air sacs (bullae)

Treatment for ACOS will be tailored to your symptoms and preferences. ACOS requires
careful management and adherence to therapy. These are some of the people you might have
on your healthcare team:

doctors
nurses
respiratory therapist
physical therapist or exercise expert
dietitian or nutritionist

Check out: COPD and allergies, avoiding pollutants and allergens

Tips

Tips for managing ACOS

After a diagnosis of ACOS, your doctor will instruct you on how best to manage your
condition. Take medication as prescribed and follow up regularly.

Here are some other tips for managing ACOS:

Maintain a healthy diet. Eating well can help you keep up your strength and improve your
health. Ask your doctor if you have nutritional requirements and if you should take dietary
supplements. Consider working with a dietician or nutritionist.
Get vaccinated. Additional respiratory illnesses can become dangerous. To lower your risk
of contracting influenza, pneumonia, and whooping cough, talk to your doctor about
vaccinations for these and other illnesses.
Avoid smoke and other pollutants that can irritate your lungs and make symptoms worse.
Exercise. Physical activity is important to your health. But you dont want to overdo it either.
Consult your doctor so you know what activities are safe for you. Ask your doctor about
pulmonary rehabilitation and other exercise programs for people with lung disease.
 Seek support. Whether its friends and family, psychological counseling, or a support group,
its important to reach out for support. Also make sure those closest to you know about your
condition and what to do in an emergency.

For more information about support groups, check out the American Lung Association Better
Breather's Club.

Always contact your doctor if you experience sudden worsening of symptoms, fever, or if
you feel ill.

Learn more: 6 tips for running with exercise-induced asthma (EIA)

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Outlook

Outlook

Theres no cure for ACOS. According to a 2015 systemic review and meta analysis, people
with ACOS tend to have more hospitalizations, higher healthcare costs, and poorer quality of
life than those who have only asthma or COPD.

ACOS is chronic and progressive, meaning it worsens over time. Treatment and disease
management can help keep symptoms under control.

Your doctor can offer more detailed outlook information based on your age, symptoms, and
overall health.

Keep reading: 5 diet tips for people with COPD

Prevention

Can ACOS be prevented?

As far as researchers know, there is no way to prevent asthma, but you can lower your risk of
developing COPD. Its unclear if lowering your risk of COPD also lowers your risk of
developing ACOS.

If you have asthma, you may be more susceptible to developing COPD if your asthma is
severe and persistent. Managing your asthma is the best way to minimize the disease process.
See your doctor regularly, avoid smoke and other lung irritants, and take prescribed
medications as directed. Quitting smoking as soon as possible is key.

Smoking is the leading cause of COPD, and it makes asthma more difficult to manage. It can
also harm the health of those around you. If you cant quit smoking on your own, talk to your
doctor about smoking cessation programs. Or check out the American Lung Association
Freedom from Smoking program or call the Lung HelpLine at 1-800-LUNGUSA.

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