By Dr.

sayeed Ahmed
 Asthma-COPD overlap syndrome (ACOS) or asthma-COPD
overlap captures the subset of patients with airways
disease who have features of both asthma and chronic
obstructive pulmonary disease (COPD).
It is generally thought to encompass persistent airflow
limitation in a patient older than 40 years of age with
either a history of asthma or large bronchodilator
reversibility.

ACOS affects about a quarter of patients with COPD and

almost a third of patients who previously had asthma.

Compared with their counterparts with asthma or COPD

alone, patients with ACOS have significantly worse
respiratory symptoms, poorer quality of life, and increased
risk of exacerbations and hospital admissions.
 ACOS affects about a quarter of patients with
COPD and almost a third of patients who
previously had asthma.

Compared with their counterparts with

asthma or COPD alone, patients with ACOS
have significantly worse respiratory
symptoms, poorer quality of life, and
increased risk of exacerbations and hospital
admissions.
 Given the nascence of ACOS, no single
accepted definition for ACOS exists.
More recently, the American Thoracic Society
and the National Heart, Lung, and Blood
Institute issued a workshop statement
concluding that ACOS should not be
considered a discrete disease entity, but
rather an airways disease phenotype of
mixed features
 GINA/GOLD identified diagnostic clues that
suggest ACOS, including persistent yet reversible
airflow limitation (post-bronchodilator forced
expiratory volume in 1 s (FEV1) to forced vital
capacity (FVC) ratio of <70% and FEV1
improvement of >12% and >400 mL from baseline
after bronchodilator therapy) ; a history of
asthma diagnosed by a doctor, atopy, allergies,
or exposure to noxious agents; either sputum
neutrophilia or eosinophilia; and age 40 years or
older. Other groups, working largely through
consensus opinion, have offered systems of
major and minor criteria by which to identify
patients who may have ACOS (fig 1).
 Curiously, many of these systems have not
featured environmental exposures (either
cigarette smoke or biomass fuel) as a key
component despite the clear links between such
exposures and the development of COPD.
Of lesser importance in the diagnostic algorithm
are biomarkers commonly used in the diagnosis
and management of asthma. Although helpful in
identifying COPD patients with possible asthma
overlap, immunoglobulin E (IgE), sputum or
peripheral blood eosinophil count, and fractional
exhaled nitric oxide (FeNO) are not sufficiently
sensitive or specific on their own for diagnosis of
ACOS.
 Estimates of ACOS in the general population,
using either self reported physician diagnoses or
a combination of airflow obstruction on
spirometry and symptom report, fall roughly
between 2% and 3%.
In comparison, estimates of asthma and COPD in
these same populations tend to be higher,
around 5-17% for asthma and 2-12% for COPD.
prevalence of ACOS may vary according to
geographic region, with estimates ranging
anywhere from 0.61% in China to 3.7% in the
United States.
 In cohorts of COPD patients specifically, the
prevalence of ACOS ranges from 6% to 55%,with
pooled estimates from a meta-analysis suggesting a
prevalence of just over 25%.
In cohorts of asthma patients, the prevalence ranges
from 10% to 31%. Many case-control studies
comparing ACOS with asthma and COPD suggest a
specific demographic type: patients with ACOS tend
to be younger,to be female, and to have higher body
mass index,lower socioeconomic status, and lower
education levels.
ACOS patients also carry a higher burden of
comorbidities, particularly for conditions such as gas
tro-oesophageal reflux disease, osteoarthritis,
osteoporosis, depression, and anxiety.
 By various disease control measures pulmonary function,
respiratory symptoms, exacerbation rates,use of
respiratory drugs,overall health status,quality of life,and
disability ACOS patients have greater decrements than
their counterparts with asthma or COPD alone.
Specifically, as high as a 20% decrement in per cent
predicted FEV1 has been shown in ACOS patients compared
with asthma patients,and up to a 10% difference has been
shown between ACOS and COPD patients.
Exacerbation rates are up to four to five times higher in
ACOS patients compared with asthma and COPD patients.
Emergency department visits,hospital admissions,and
healthcare use are also significantly higher in ACOS
patients, who incur twice the health related costs of
asthma and COPD patients,mainly through outpatient visits
and drugs.
 The clinical presentation of ACOS in a manner that exceeds the
expected disease burdens of either asthma or COPD alone raises
an important question as to its origin: is ACOS the manifestation
of a unique pathogenic mechanism, is it simply the additive (or
synergistic) result of two distinct pathologies combined together,
or is it the end result of various environmental stimuli and insults
applied to a patient already affected by asthma or COPD?
Dutch hypothesis posits that asthma and COPD are a single
disease of diffuse airway obstruction (termed by Orie and Sluiter
as chronic non-specific lung disease), but that both
endogenous and exogenous factors help to steer patients into
distinguishable phenotypes that we understand better today as
asthma or COPD.
These factors may include, but are certainly not limited to,
genetics, sex, age, allergens, smoking, air pollution, biomass
fuel, concomitant pulmonary diseases, and infections.
British hypothesis maintains separate origins for asthma and
COPD, underscored by the fact that each disease has its own
characteristic inflammatory profile, genetic polymorphisms,
response to treatment, and clinical course.
 Smoking :A quarter of patients with asthma
are current cigarette smokers,and in
comparison with non-smoking patients with
asthma, they carry a significantly greater risk
for developing fixed airflow obstruction and
ACOS.
Firstly,goblet cell hyperplasia and mucus
hypersecretion are well described
pathological findings in both asthma and
COPD, these features are aggravated in
current smokers with asthma compared with
ex-smokers or non-smokers with asthma.