ABC of COPD 2017

Children’s Healthcare of Atlanta

Chronic Obstructive PulmonaryChronic Obstructive Pulmonary
DiseaseDisease
COPDCOPD

Smoking Is the Single Most Important
Risk Factor for COPD
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, Global Initiative for Chronic Obstructive
Lung Disease (GOLD) 2008. Available from: http://www.goldcopd.org.

8
But smoking is not the only risk factor!
Occupational exposure
Biomass smokeOutdoor pollution
Long-term exposure to ambient air pollutants
increased the risk of COPD by 2-fold
3 billion people exposed to biomass fuel
worldwide

Cumulative exposure to noxious
particles is the key risk factor for COPD

COPD is the only chronic disease that is rapidly
increasing in prevalence on a worldwide basis

COPD Mortality Worldwide

Children’s Healthcare of Atlanta 13
COPD: Global Burden
 An estimated 210 million people worldwide have
COPD
 More than 3 million people died of COPD in 2005 , this
represented 5% of all deaths worldwide
 COPD disproportionately affects the world's poorest ,
Almost 90% of COPD deaths occur in low- and middle-
income countries.
WHO , 2009

COPD: Reality
Under
diagnosed
perceived
treated

15
COPD Practice
Guidelines

Definition & Overview
GOLD 2017

17
COPD is used to describe emphysema, chronic
bronchitis or a combination of the two.

LUNG INFLAMMATIONLUNG INFLAMMATION
COPD PATHOLOGYCOPD PATHOLOGY
Oxidative
stress ProteinasesProteinases
RepairRepair
mechanismsmechanisms
Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants
Host factors
Amplifying mechanisms
Cigarette smoke
Biomass particles
Particulates
Pathogenesis
of COPD

EmphysemaObstructive Bronchiolitis

YYYY
YY
Mast cellMast cell
CD4+ cellCD4+ cell
(Th2)(Th2)
EosinophilEosinophil
AllergensAllergens
Ep cellsEp cells
ASTHMAASTHMA
BronchoconstrictionBronchoconstriction
AHRAHR
Alv macrophageAlv macrophageEp cellsEp cells
CD8+ cellCD8+ cell
(Tc1)(Tc1)
NeutrophilNeutrophil
Cigarette smokeCigarette smoke
Small airway narrowingSmall airway narrowing
Alveolar destructionAlveolar destruction
COPDCOPD
Reversible Not fully reversibleAirflow LimitationAirflow Limitation

Mechanical Origins of Airflow Limitation
Flow = Pressure
Resistance
In Respiratory Function
Chronic Airflow Limitation
(Flow)
Is Determined By
Loss of Elastic Recoil
(Pressure)
Airway Narrowing
(Resistance)

Chronic Bronchitis predominant
Airway obstruction is the main problem
Normal
Elastic Recoil
Chronic Bronchitis
Elastic Recoil
Increased airway resistance due
to thickened wall and secretionsAirway supported
by connective tissue

Emphysema Predominant
-This results in a loss of the elastic recoil of the lungs on expiration
-This also results in loss of tethering or support of the most distal portions
of the airway leading to collapse on expiration
Normal
Elastic Recoil
Airway supported
by connective tissue
Decreased
Elastic Recoil =
Lower Flow
Loss of support = Airway collapses=
Air gets trapped in lung

24

Pathophysiology

26
Is it Inevitably All Downhill ?

COPD: Progressive Diseaseอออออ/lungfunction
ออออออออ
Normal daily activity
Acute exacerbation

Natural History of COPDLungFunction
Time (Years)
Exacerbation
Exacerbation
Exacerbation
Never smoked
Smoker
Fletcher C. Br Med J. 1977

Frequent exacerbations are associated with
increased mortality
A = No exacerbations B = 1-2 exacerbations C = 3 or more exacerbations
Soler-Cataluna JJ, e t al. Tho rax 2005;60:925-931.
p < 0.0001
1.0
Probabilityofsurviving
0.8
0.6
0.4
0.2
0.0
0 10 20 30 40 50 60
Time (months)
A
B
C
p = 0.069
p< 0.0002

COPD is:
a multicomponent disease
with systemic involvement & inflammation
Respiratory system
Systemic
inflammation
Target organs
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
COPD is: More than just a lung disorder

Declining lung functionDeclining lung function
SymptomsSymptoms
ExacerbationsExacerbations
Decreased exercise toleranceDecreased exercise tolerance
Deteriorating health statusDeteriorating health status
and increasing morbidityand increasing morbidity
MortalityMortality
AirflowAirflow
limitationlimitation
SystemicSystemic
componentcomponent
StructuralStructural
changeschanges
MucociliaryMucociliary
dysfunctiondysfunction
AirwayAirway
inflammationinflammation
Agusti. RespirMed 2005
Agusti et al. Eur RespirJ2003
Bernard et al. Am JRespirCrit Care Med 1998
COPD is a multicomponent disease with
inflammation at its core leading to mortality

LungVolumes
IRV
TV
ERV
o 4Volumes
o 4 Capacities
– Sum of 2 or
more lung
volumes
RV
IC
FRC
VC
TLC
RV

Lung Volumes in Obstructive DiseaseLung Volumes in Obstructive Disease
VT
VT
NormalNormal COPDCOPD
RVRV
RVRV
TLCTLC
FRCFRC
ICIC
ICIC
TLCTLC
FRCFRC
VolumeVolume

36
Progressive Hyperinflation Reduces Inspiratory
Capacity
FRC/
EELV

37

39
Dynamic hyperinflation in patients with emphysema during exercise.
Note that V T increases with exercise. Note also that the expiratory
phase decreases progressively with continued exercise indicating
progressive air trapping .

Effects of Exercise on Hyperinflation
VVTT
IRVIRVERVERV
ICIC
FRCFRC
RVRV
TLCTLC
NormalNormal
Years - Decades
Progression
Rest
Static
Hyperinflation
Air Trapping
at Rest
Seconds - Minutes
Exercise
Dynamic
Hyperinflation
Air Trapping
During Exercise

 Despite its heterogeneity, the pathophysiological
hallmark of COPD is expiratory flow limitation and
Lung hyperinflation .
 Dyspnea (breathlessness) and exercise intolerance
are the most common symptoms in COPD and
progress relentlessly as the disease advances.
41

Expiratory airflow obstruction
Reduced recoil
Reduced tethering
Increased airways resistance
PL = translung pressure; V = ventilation

Alveolar Emptying in COPD
In COPD, airflow is limited because alveoli lose their elasticity, supportive
structures are lost, and small airways are narrowed
In COPD, airflow is limited because
alveoli lose their elasticity, supportive
structures are lost, and small airways
are narrowed

Airflow limitation includes irreversible and partially
reversible components
Irreversible components include :
Alveolar destruction
- loss of elastic recoil
Destruction of alveolar attachments
- maintain patency of small airways
Small airway fibrosis
Partially reversible components include :
- Accumulation of mucus
- Smooth muscle bronchoconstriction2
- Inflammatory infiltrate in airway mucosa
1. GOLD 2009; 2. Brusasco Eur Respir Rev 2006

Patients avoid dyspnoea by becoming less active,
leading to a dyspnea/inactivity downward spiral
Becomes more
sedentary to avoid
dyspnoea-producing
activity
(decreases activity)
Dyspnoea with
activities
Deconditioning
aggravates dyspnoea;
patients adjust by
reducing activity
further
The dyspnea inactivity downward spiral
Adapted from Reardon et al. Am J Med 2006
ZuWallack R. COPD 2007

To the COPD
patient, this is a
breathtaking view

49

V
BD
 Air flowDeflation
 Improvement in flow – FEV1
 Improvement in volumes – FVC and IC
Bronchodilator therapy deflates the lung
BD = bronchodilator; V = ventilation; FEV1= forced expiratory volume in 1 second;
FVC= forced vital capacity; IC = inspiratory capacity

Bronchodilators work by:
Eur Respir Rev 2006; 15: 99, 37–41
Relieve dyspnea by
deflating the lungs
Allowing improved lung
emptying with each breath
Improvement in
exercise tolerance
Reduces the
elastic load
on
inspiratory
muscles.

Bronchodilators are the cornerstone
of COPD treatment
 Target airflow limitation bronchodilating by altering airway→
smooth muscle tone
 Improve emptying of the lung
 Ideally : reduce hyperinflation at rest and during exercise
GOLD 2011. Available from: www.goldcopd.org
Spencer et al. Cochrane Database Syst Rev 11;10:CD007033

53

• The use of bronchodilators is now recommended as
the cornerstone of maintenance treatment of
COPD , since this disease is no longer regarded as
one characterised by irreversible airflow limitation
but rather as a disease with at least partial
reversibility of airflow limitation.
54

• Besides bronchodilatation , inhaled bronchodilators,
probably by reducing hyperinflation both at rest and
during exercise (a so-called pharmacological volume
reduction effect), offer beneficial effects on real world
outcomes important for the patient, such as dyspnoea
and exercise tolerance.
55

 Short-acting and long-acting bronchodilators form
the cornerstone of pharmacologic management.
 Unlike asthmatic patients who experience dyspnea
when acute bronchospasm occurs, patients with
COPD most commonly experience dyspnea due to
increased respiratory demands, such as occurs with
exertion.
56

What can we do ???What can we do ???COPD

Disease Management should now be focusing on
2 key areas
1.
Goal of COPD Management

Road Map

• Smoking cessation is the single most effective
and cost-effective intervention to reduce the
risk of developing COPD and stop its
progression (Evidence A) .

COPD progression
Age (year)
FEV1%ofvalueatage25yr
100
75
50
25
5025 75
Death
Disability
Adapted from:Fletcher C,et al.Br Med J.1977;1:1645-1648
Nonsmokers
20-30 ml/year
COPD
60 mL/year
Symptoms

67
LABA
DPI Diskus Serevent®
(Salmeterol)
DPI Aerolizer Foradil®
(Formoterol)
DPI Breezhaler Onbrez®
(Indacaterol)
SMI Respimat Striverdi®
(Olodaterol)
LABA inhalers for COPD

68
LAMA
DPI HandiHaler/
SMI Respimat
Spiriva®
(Tiotropium)
DPI Breezhaler Seebri®
(Glycopyrronium)
DPI Genuair Eklira®
(Aclidinium)
DPI Ellipta Incruse®
(Umeclidinium)
LAMA inhalers for COPD

69
Fixed-dose
combination
LABA/LAMA
DPI Ellipta Anoro®
(vilanterol/umeclidinium)
DPI Breezhaler Ultibro®
(indacaterol/glycopyrronium)
SMI Respimat Inspiolto®
(olodaterol/tiotropium)
DPI Genuair Duaklir®
(formoterol/aclidinium)
Combination LABA/LAMA inhalers for COPD

Proskocil BJ et al. Proc Am Thorac Soc. 2005;2(4):305-310.
SMC relaxationSMC contraction
M3- muscarinic
receptors
Beta Agonists
(LABA)Antocholinergics
(LAMA)
β2-adrenergic
receptors
Mechanisms of action of bronchodilators
on airway smooth muscle

73
ICS/LABA
DPI Diskus Advair®
(Fluticasone/salmeterol)
DPI Turbuhaler Symbicort®
(Budesonide/formoterol)
DPI Ellipta Relvar®
(Fluticasone/vilanterol)

 Instructions and demonstration of a proper inhalation
technique are essential & needs to be assessed regularly
AND re-check at each visit to ensure a correct use of the
inhaler to improve therapeutic outcomes
 Choice of inhaler device has to be individualised and will
depend most importantly on patient’s ability and
preference
 Inhaler technique (and adherence) should be evaluated
before a treatment is assessed as insufficient .

78
GOLD2001GOLD2001
GOLD2011GOLD2011
GOLD2017GOLD2017

COPD: Management
Clinical diagnosis
Spirometry
Gold Severity stage
Drugs a/t stages

SYMPTOMS
Cough
Sputum
Shortness of breath
EXPOSURE TO RISK
FACTORS
Tobacco
Occupation
Indoor/outdoor pollution
SPIROMETRY
Diagnosis of COPD

Pharmacological treatment of stable COPD based on GOLD
guidelines 2001.

88
ABCD assessment (GOLD 2011)

89

GOLD report 2017:
Current pathways to the diagnosis of COPD
Symptoms to
consider
COPD
•Dyspnoea
•Chronic cough
or
•Sputum
production
Symptoms to
consider
COPD
•Dyspnoea
•Chronic cough
or
•Sputum
production
Spirometry (post-bronchodilator)
FEV1/FVC <0.7 confirms the presence of airway limitation
and/or
history of
exposure to
risk factors
and/or
history of
exposure to
risk factors
Spirometry: Required to establish diagnosis
Symptoms
•Shortness of
breath
•Chronic cough
•Sputum
Risk factors
•Host factors
•Tobacco
•Occupation
•Indoor/outdoor
pollution

(Diagnosis and initial assessment)
Refined A, B, C, D assessment tool: overview
(C) (D)
(A) (B)
FEV1 (%
predicted)
GOLD 1 ≥ 80%
GOLD 2 50-79
GOLD 3 30-49
GOLD 4 < 30
Post-
bronchodilator
FEV1/FVC < 0.7
Post-
bronchodilator
FEV1/FVC < 0.7
≥ 2 or ≥ 1
leading to
hospital
admission
≥ 2 or ≥ 1
leading to
hospital
admission
0 or 1
(not leading
to hospital
admission)
0 or 1
(not leading
to hospital
admission)
Spirometrically
confirmed
diagnosis
Spirometrically
confirmed
diagnosis
Assessment of
airflow
limitation
Assessment of
airflow
limitation
Assessment of
symptoms/risk
of exacerbations
Assessment of
symptoms/risk
of exacerbations
Exacerbation
history
Symptoms
CAT < 10 CAT > 10
mMRC 0–1 mMRC > 2

ABCD assessment 2017 has been refined: Spirometry
Spirometry is still relevant
for:
•Diagnosis
•Prognostication
•Treatment with non-
pharmacological therapies
Classification unchanged!
FEV1 (%
predicted)
GOLD 1 ≥ 80%
GOLD 2 50-79
GOLD 3 30-49
GOLD 4 < 30
Post-
bronchodilator
FEV1/FVC < 0.7
Post-
bronchodilator
FEV1/FVC < 0.7
Spirometrically
confirmed
diagnosis
Spirometrically
confirmed
diagnosis
Assessment of
airflow
limitation
Assessment of
airflow
limitation

ABCD assessment 2017 has been refined:
(C) (D)
(A) (B)
0 or 1
(not leading
to hospital
admission)
0 or 1
(not leading
to hospital
admission)
Assessment of
symptoms/risk
of exacerbations
Assessment of
symptoms/risk
of exacerbations
Exacerbation
history
Symptoms
CAT < 10 CAT > 10
mMRC 0–1 mMRC > 2
Assessment of A, B, C, D and
therapy recommendations
are based exclusively on:
Respiratory symptoms
Exacerbation history
≥ 2 or ≥ 1
leading to
hospital
admission
≥ 2 or ≥ 1
leading to
hospital
admission

99
0-1 = less breathlessness
>2 = more breathlessness

100
Cough
Sputum
Chest tightness
Walking up hill
ADLs
Leaving the house
Sleep
Energy levels

102
Bronchodilators
Continue , stop or
try alternative
class of
bronchodilators
Evaluate effect
Group A Group B
A long – acting bronchodilators
( LABA or LAMA )
LAMA + LABA
Persistent
Symptoms
Group C
LAMA
LAMA + LABA LABA + ICS
Further
exacerbation(s)
Group D
LAMA LAMA + LABA LABA + ICS
LAMA
+ LABA
+ ICS
Consider Roflumilast
if FEV1 50% pred.˂
And patient has
chronic bronchitis
Consider
macrolides in
former smokers
Further exacerbation(s)
Further
exacerbation(s)
Persistent
Symptoms / further
exacerbation(s)

Pharmacologic treatment in detail:
GOLD Group A patients
(A)
Continue, stop or try
alternative class of
bronchodilator
Continue, stop or try
alternative class of
bronchodilator
A bronchodilatorA bronchodilator
Evaluate effect
GOLDGroup A
As a preferred choice all group A
patients should be offered a
short- or a long-acting
bronchodilator (dependent on its
effect on breathlessness).
Continuation with treatment if
symptomatic benefit is
documented
GOLDGroup A
As a preferred choice all group A
patients should be offered a
short- or a long-acting
bronchodilator (dependent on its
effect on breathlessness).
Continuation with treatment if
symptomatic benefit is
documented
In patients with a majordiscrepancy between the perceived level of
symptoms
and severity of airflow limitation, furtherevaluation is warranted

Preferred
treatment
GOLD Group B patients
(B)
A long-acting
bronchodilator
(LABA or LAMA)
A long-acting
bronchodilator
(LABA or LAMA)
Persistent
symptoms
LAMA + LABALAMA + LABA
GOLD Group B
Although a long-acting
bronchodilator is yet
recommended as initial
therapy, LAMA/LABA are
recommended
- if symptoms persist
or
- from the start in patients with
severe breathlessness
GOLD Group B
Although a long-acting
bronchodilator is yet
recommended as initial
therapy, LAMA/LABA are
recommended
- if symptoms persist
or
- from the start in patients with
severe breathlessness
symptoms

105
 For Group B patients, therapy should begin with a long-
acting bronchodilator LABA or LAMA , (no evidence to
recommend one over another), and should be escalated
to two bronchodilators if breathlessness continues with
monotherapy.
 If breathlessness is severe, starting the patient on dual
long-acting bronchodilators can be considered, however
if the second therapy does not improve symptoms, the
guidelines suggest stepping down to one bronchodilator.

 For Group B patients, therapy should begin with a long-
acting bronchodilator LABA or LAMA , (no evidence to
recommend one over another), and should be escalated to
two bronchodilators if breathlessness continues with
monotherapy.
 If breathlessness is severe, starting the patient on dual long-
acting bronchodilators can be considered, however if the
second therapy does not improve symptoms, the guidelines
suggest stepping down to one bronchodilator.

(C)
LAMA + LABALAMA + LABA LABA + ICSLABA + ICS
LAMALAMA
Further
exacerbation(s)
GOLD Group C patients
Preferred
treatment
GOLD Group C
Starting therapy with a LAMA
In case of persistent
exacerbations addition of a
LABA  LAMA/LABA as
first choice
(LABA/ICS could be an
alternative but patients are on
higher risk for developing
pneumonia)
GOLD Group C
Starting therapy with a LAMA
In case of persistent
exacerbations addition of a
LABA  LAMA/LABA as
first choice
(LABA/ICS could be an
alternative but patients are on
higher risk for developing
pneumonia)
symptoms

108
 For Group C patients, it is recommended that treatment be
started with a single long-acting bronchodilator,
preferably a LAMA (LAMA was superior to the LABA
regarding exacerbation prevention).
 A second long-acting bronchodilator or the combination of
LABA/ICS may be used for persistent exacerbations;
 The guidelines recommend LABA/LAMA as the addition of
ICS has been shown to increase pneumonia risk in some
patients.

The use of ICS-containing therapies in COPD
• Compared to non-ICS-containing therapies in COPD,
therapies containing ICS, eg, LABA/ICS FDC are
associated with greater risk of:
– Pneumonia1-6
– Bone density decline and fractures7-10
– Candidiasis and skin lesions6,11,12
– Cataracts13
• Evidence linking ICS-containing therapies with
increased risk of diabetes mellitus14,15
1. Calverley PM, et al. N Engl J Med. 2007;356:775-789. 2. Crim C, et al. Eur Respir J. 2009;34:641-647;
3. Drummond MB, et al. JAMA. 2008;300:2407-2416;
4. Rodrigo GJ, et al. Chest. 2009;136:1029-1038. 5. Singh S, Loke YK. Curr Opin Pulm Med. 2010;16:118-122;
6. Yang IA, et al. Cochrane Database Syst Rev. 2012;7:CD002991. 7. Lung Health Study Research Group. N Engl J Med. 2000;343:1902-1909;
8. Scanlon PD, et al. Am J Respir Crit Care Med. 2004;170:1302-1309. 9. Hubbard R, et al. Chest. 2006;130:1082-1088;
10. Loke YK, et al. Thorax. 2011;66:699-708. 11. Alsaeedi A, et al. Am J Med. 2002;113:59-65;
12. Mahler DA, et al. Am J Respir Crit Care Med. 2002;166:1084-1091;
13. Weatherall M, et al. Respirology. 2009;14:983-990;
14. O’Byrne PM, et al. Respir Med. 2012;106:1487-1493;
15. Suissa S, et al. Am J Med. 2010;123:1001-1006.
COPD, chronic obstructive pulmonary disease; FDC, fixed-dose combination;
ICS, inhaled corticosteroid; LABA, long-acting β2-agonist

Patients at a higher risk of developing
pneumonia
 Current smokers
 ≥ 55 years of age
 History of prior exacerbations or pneumonia
 Body mass index (BMI) < 25 kg/m2
 Poor MRC dyspnoe grade
 And/or severe airflow limitation
Reference:
Crim C et al Ann ATS 2015; 12:27-34

GOLD Group D patients
(D)
LAMA + LABALAMA + LABALAMALAMA
LAMA +
LABA + ICS
LAMA +
LABA + ICS
Further
exacerbation(s)
Further
exacerbation(s)
Consider roflumilast
if FEV1 <50% pred.
and patient has
chronic bronchitis
Consider roflumilast
if FEV1 <50% pred.
and patient has
chronic bronchitis
Consider
macrolide
(in former
smokers)
Consider
macrolide
(in former
smokers)
Persistent
symptoms/further
exacerbation(s)
De-escalation from ICS containing to
LAMA/LABA treatments if ICS
shows lack of efficacy!
GOLD Group D
•LAMA/LABA is recommended from the
start
-Since a LAMA/LABA combination was superior to a
LABA/ICS combination in preventing exacerbations and
other patient reported outcomes in group D patients
-as the default treatment for patients who are de-
escalated from ICS-containing treatments
•For patients with a history and/or findings of
concurrent asthma, LABA/ICS may be the first
choice
•For patients who develop further exacerbations
on LAMA/LABA two alternatives are suggested
-escalation to triple therapy
-switch to LABA/ICS (but no evidence that switching from
LAMA/LABA results in better exacerbation prevention)
GOLD Group D
•LAMA/LABA is recommended from the
start
-Since a LAMA/LABA combination was superior to a
LABA/ICS combination in preventing exacerbations and
other patient reported outcomes in group D patients
-as the default treatment for patients who are de-
escalated from ICS-containing treatments
•For patients with a history and/or findings of
concurrent asthma, LABA/ICS may be the first
choice
•For patients who develop further exacerbations
on LAMA/LABA two alternatives are suggested
-escalation to triple therapy
-switch to LABA/ICS (but no evidence that switching from
LAMA/LABA results in better exacerbation prevention)
symptoms
and severity of airflow limitation, further evaluation is warranted
LABA + ICSLABA + ICS

112
 For Group D patients, a LABA/LAMA combination is
preferred as initial therapy over LABA/ICS as these patients
may be at higher risk of developing pneumonia with ICS
use.
 For patients with high blood eosinophil counts or those
with asthma-COPD overlap, LABA/ICS could be considered
first-line therapy.

The use of ICS-containing therapies in COPD
• Bronchodilators are central to symptom management in
COPD
– GOLD 2017 guidelines recommend bronchodilators in all
patients with COPD
• ICS-containing therapies currently over-used in management of COPD
– More than 70% of patients with COPD are currently receiving an
ICS-containing therapybut, based on GOLD guidelines, this should be
less than 20%
– ICS should be reserved for those patients in whom additional
bronchodilation is failing to control their exacerbations
• ICS in combination with LABA have limited role in COPD
1. Barnes PJ. Chest. 2000;117(2 Suppl):10S-14S;
2. Global Strategy for the

114
Is ICS Withdrawal or Step Down
Therapy Possible
in COPD?

116
WISDOM (Withdrawal of Inhaled Steroids During
Optimised bronchodilator Management) study

117
6-7 0
S
C
R
E
E
N
I
N
G
Treatment
52Week -6
ICS
(remained on triple therapy from run-in)
Stepwise ICS withdrawal
(remained on dual bronchodilator)
Run-in
Triple
therapy
12
R
A
N
D
O
M
I
S
A
T
I
O
N
ICS stepwise withdrawal Stable
treatment
Reduced to 250 µg BID
Reduced to 100 µg BID
Reduced to 0 µg (placebo)
Fluticasone propionate 12-week
withdrawal schedule
500 µg BID
18
• Tiotropium 18 µg QD
• Salmeterol 50 µg BID
• Fluticasone propionate 500 µg BID
Triple therapy
regimen
WISDOM: Study design

118
 With a controlled, stepwise withdrawal of ICS , the risk
of exacerbation would be similar to that with continued
use of ICS in patients with severe or very severe COPD
who were receiving a combination of a LAMA
(tiotropium) and a LABA (salmeterol).
WISDOM Study Results

119
Stepping Down ICS: A Proposed Algorithm
Kaplan AG. Int J COPD. 2015;10:2535-2548.

120

121
 The new GOLD Strategy provides clear guidance on when
and in which patients ICS can be added or withdrawn.
 Only those who have ≥2 exacerbations/year or ≥1 leading to
hospital admission may be considered for an ICS containing
therapy after LAMA/LABA.
 In addition, the new GOLD Strategy suggests that ICS therapy
may be withdrawn safely (de-escalation path ) in people with
COPD who are in GOLD group D and stable, by using a
LAMA/LABA regimen.

122
 ICS are not recommended as monotherapy in COPD .
 ICS-containing pharmaceutical regimens no longer
recommended as first-choice treatments for COPD of any
severity .

123
 The updated 2017 GOLD Strategy now positions a combination
of a LAMA (long-acting muscarinic receptor antagonists ) and
a LABA (long-acting beta2-agonist), as a mainstay treatment
for people with COPD in GOLD groups B-D.
 This represents a significant change versus previous GOLD
guidelines.

ABC of COPD 2017

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