CHRONIC OBSTRUCTIVE PULMONARY DISEASE

:
The New Malaysian 2nd Edition CPG – Its Importance From The Perspective of Emergency Medicine

K S CHEW School of Medical Sciences Universiti Sains Malaysia

FREE DOWNLOAD at: Malaysian Thoracic Society Website http://www.mts.org.my/resources.html

DEFINITION

DEFINITION OF COPD

•  COPD is defined as a preventable and

treatable respiratory disorder largely caused by smoking, is characterised by progressive, partially reversible airflow obstruction and lung hyperinflation with significant extrapulmonary (systemic) manifestations and co-morbid conditions all of which may contribute to the severity of the disease in individual patients.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

SYSTEMIC EFFECTS OF COPD

•  Several recent studies have clearly shown

that COPD is associated not only with an abnormal inflammatory response of the lung parenchyma but also with evidence of systemic inflammation, including systemic oxidative stress, activation of circulating inflammatory cells and increased levels of pro-inflammatory cytokines

Agusti AG. Systemic effects of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005; 2 (4):367-70; discussion 71-2.

Examples of Co-morbidities Associated With COPD

•  Ischaemic heart disease •  Osteopenia, osteoporosis and bone

fractures •  Cachexia and malnutrition •  Normochromic normocytic anaemia •  Skeletal muscle wasting and peripheral muscle dysfunction

SYSTEMIC EFFECTS OF COPD

•  Various studies have shown that the lung

inflammatory response is characterised by

•  increased numbers of neutrophils, macrophages

and T-lymphocytes with a CD8+ predominance •  augmented concentrations of proinflammatory cytokines, such as leukotriene B4, interleukin (IL)-8 and tumour necrosis factor (TNF)-a •  evidence of oxidative stress caused by the inhalation of oxidants (tobacco smoke) and/or the activated inflammatory
Agusti AG. Systemic effects of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005; 2 (4):367-70; discussion 71-2.

WHY SYSTEMIC EFFECTS?
Hypothesis •  The tobacco smoke alone causes oxidative stress •  The pulmonary inflammatory process in the lung itself is the source of these systemic inflammation. •  The increased surface expression of several neutrophil adhesion molecules may be due to genetic predisposition
Agusti AG. Systemic effects of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005; 2 (4):367-70; discussion 71-2.

DISEASE BURDEN

COPD is projected to be the third biggest cause of mortality by 2020
1990
Ischaemic heart disease Cardiovascular disease Lower respiratory infection Diarrhoeal disease Perinatal disorders COPD Tuberculosis Measles Road traffic accident Lung cancer

2020 1st 2nd 3rd 4th 5th 6th 7th 8th 9th 10th
Ischaemic heart disease Cardiovascular disease COPD Lower respiratory infection Lung cancer Road traffic accident Tuberculosis Stomach cancer HIV Suicide

Murray CJ & Lopez AD. Lancet 1997;349:1498–1504.

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998
Proportion of 1965 Rate 3.0

2.5

Coronary Heart Disease

Stroke

Other CVD

COPD

All Other Causes

2.0

1.5

1.0

0.5

0

–59%

–64%

–35%

+163%

–7%

1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Source: NHLBI/NIH/DHHS

Model Projections of Moderate-Severe COPD in Population Aged ≥ 30 Years

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

PATHOPHYSIOLOGY

INFLAMMATION IN COPD

SMALL AIRWAY DISEASE Airway Inflammation Airway Remodeling

PARENCHYMAL DESTRUCTION Loss of alveolar attachment Decrease of elastic recoil

AIRFLOW LIMITATION

Pathogenesis of COPD
Host factors Amplifying mechanisms

Source: Peter J. Barnes, MD

Inflammatory Cells Involved in COPD

Source: Peter J. Barnes, MD

Oxidative Stress in COPD

Macrophage Neutrophil

Anti-proteases SLPI α1-AT Proteolysis

Plasma leak

Bronchoconstriction

↑ Mucus secretion
Source: Peter J. Barnes, MD

Inflammation plays a central role in the pathogenesis and pathology of COPD

Cigarette smoke Genetic susceptibility
(and other irritants)

Lung Inflammation
• Inflammatory

cells • Inflammatory mediators • Oxidative stress • Proteases

COPD pathology
Obstructive bronchiolitis Mucus hypersecretion Alveolar wall destruction

Adapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2009. Available from http://www.goldcopd.com/

DIAGNOSIS AND CLASSIFICATION OF SEVERITY

DIAGNOSIS

•  Spirometry is essential for the diagnosis of
COPD.

•  The diagnosis should be confirmed by

spirometry showing a post-bronchodilator FEV1/FVC ratio of less than 70%.

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

DIAGNOSIS

•  A clinical diagnosis of COPD should be

considered in any individual with symptoms of chronic cough, sputum production or dyspnoea and a history of exposure to risk factors for the disease, especially cigarette smoking. •  But every effort should be made to refer the patient for spirometry to confirm the diagnosis.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

CLASSIFICATION OF COPD SEVERITY

Spirometry is essential for the diagnosis of COPD and is useful for assessment of the severity of airflow obstruction (Grade C)

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

The Modified Medical Research Council (MMRC) Dyspnoea Scale

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

Classification of COPD Severity Based on Spirometric Impairment and Symptoms

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

Reversible

Irreversible
Source: Peter J. Barnes, MD

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

RISK FACTORS

RISK FACTORS

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

RISK FACTORS

•  Cigarette smoking is the best known and

most studied risk factor for COPD. •  About 15% of smokers develop COPD. •  However, tobacco smoke is the risk factor for as much as 90% of the cases of COPD. •  Non-smokers may also develop the disease
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

TOBACCO SMOKE

•  Some studies have suggested that women
are more susceptible to the effects of tobacco smoke than men •  Quantification of tobacco consumption: total pack-years = (number of cigarettes smoked per day ÷ 20) x number of years of smoking

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

TOBACCO SMOKE

•  Smoking cessation is the single most

effective - and cost effective - intervention to reduce the risk of developing COPD and stop its progression.

•  Even a brief (three-minute) period of

counselling to urge a smoker to quit results in smoking cessation rates of 5-10%.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

PHARMACOTHERAPIES FOR SMOKING CESSATION

•  Nicotine replacement therapy (NRT) in the
form of transdermal patches, gums, lozenges and nasal sprays •  Varenicline
agonist

•  a nicotinic acetylcholine receptor partial

•  Bupropion •  Nortriptyline
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

5’A’s FOR SMOKING CESSATION

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

VICIOUS CIRCLE HYPOTHESIS: HOW INFECTION CONTRIBUTE TO THE PATHOGENESIS AND PROGRESSION OF COPD

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

MANAGEMENT OF STABLE COPD AND EXACERBATIONS

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

MANAGING STABLE COPD

•  COPD patients at any stage of disease

severity should be advised to quit smoking if they still smoke. [Grade A] •  In patients with mild COPD who are symptomatic, SABA or SAAC or a combination of both may be prescribed

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

MANAGING STABLE COPD

•  In patients with moderate to very severe

COPD with persistent symptoms, but without frequent COPD exacerbations, either a LAAC or LABA may be initiated. •  If symptoms persist despite this treatment, an ICS/LABA combination should be added; and vice versa. [Grade A]
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

INDICATIONS FOR HOSPITALISATION

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

Algorithm for Managing AECOPD: Home Management

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

Algorithm for Managing AECOPD: Hospital Management

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

INDICATIONS FOR NIV

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

CONTRAINDICATIONS FOR NIV

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

INDICATIONS FOR MECHANICAL VENTILATION

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

ANTIBIOTICS

•  Antibiotics should be given to patients with
AECOPD having at least 2 out of 3 cardinal symptoms (i.e., purulent sputum, increased sputum volume and/or increased dyspnoea). •  Antibiotics are beneficial during AECOPD but have no proven benefit to prevent exacerbations

(Malaysian COPD CPG, 2nd Edition, Nov 2009)

Understanding Potential Long Term Impacts on Function with Tiotropium (UPLIFT) TRIAL

•  Tiotropium confers symptomatic and

spirometric improvement in patients with COPD but does not influence the underlying gradual decline in lung function as measured by FEV1 – Tashkin DP et al. A 4-year trial of tiotropium in
chronic obstructive pulmonary disease. N Engl J Med 2008 Oct 9; 359:1543.

RECENT TRIALS

Towards a Revolution in COPD Health (TORCH) study

•  In this study of COPD patients, inhaled

therapy with fluticasone plus salmeterol was associated with a 2.6 percentagepoint reduction in mortality that just failed to reach statistical significance (p=0.052). – Calverley PMA et al. Salmeterol and fluticasone
propionate and survival in chronic obstructive pulmonary disease. N Engl J Med 2007 Feb 22; 356:775-89.

Towards a Revolution in COPD Health (TORCH) study

•  In several respects, salmeterol

monotherapy appeared superior to fluticasone monotherapy — an interesting outcome given the current controversy about potential harms with long-acting ßagonists in asthma. – Calverley PMA et al. Salmeterol and fluticasone
propionate and survival in chronic obstructive pulmonary disease. N Engl J Med 2007 Feb 22; 356:775-89.

Towards a Revolution in COPD Health (TORCH) study

•  At the current moment, the conclusion
from TORCH study is:

•  combination therapy offers several

advantages (but not clear-cut mortality reduction) •  that steroid monotherapy should not be advocated •  that salmeterol monotherapy appears to be safe •  the increased incidence of pneumonia with fluticasone requires further investigation.

OPTIMAL TRIAL

•  Addition of fluticasone–salmeterol to

tiotropium therapy did not statistically influence rates of COPD exacerbation but did improve lung function, quality of life, and hospitalization rates in patients with moderate to severe COPD
•  Aaron SD et al. Tiotropium in combination with
placebo, salmeterol, or fluticasone–salmeterol for treatment of chronic obstructive pulmonary disease. A randomized trial. Ann Intern Med 2007 Feb 19;

Can we give COPD patients a brighter start to their day and reduce their future risk ?

The impact of COPD Exacerbations
Increased symptoms Reduced lung function
“I get less air… I panic and think now I’m going to die” 1

Increased mortality2,3
Lower QoL is a powerful indicator of hospitalisation & mortality4

Reduced quality of life
91% of patients reported an impact on activities of daily living 50% of patients stop all activities1

1 Vogelmeier 2 Donaldson

et al, ATS abstract 2004. et al, Thorax 2002. 3 Fabbri et al, Thorax 1998 4 Fan et al; Chest; August, 2002

Increased frequency of exacerbations increases the risk of mortality in COPD
1.0
0 exacerbations 1–2 exacerbations ≥ 3 exacerbations

0.8
Survival probability
P < 0.0002

0.6

P < 0.0001

0.4

P = 0.069

0.2

0

0

10

20

30

40

50

60

Time (months)
Soler-Cataluna JJ, et al. Thorax 2005;60:925–931.

COPD symptoms are the worst in the morning
Patients (%)

50
46%

All COPD patients (N=803) Severe COPD patients (N=289)

45 40
37%

35 30 25
21%

34%

27% 25%

28%

20
16%

17%

15
11%

10 5 0
Morning
Mid-day

9% 4%

9% 7%

Afternoon

Evening

Night

No particular time of day

Difficult to say

Results from 803 interviews in seven EU countries and the USA
Partridge MR et al. Current Medical Research and Opinion 2009; 25(8): 2043-2048

A slow and difficult morning can impact the rest of the day

•  Getting out of bed •  Washing •  Dressing •  Walking up and down stairs •  Making breakfast

Partridge MR et al. Current Medical Research and Opinion 2009; 25(8): 2043-2048

COPD patients want faster symptom relief

Faster symptom relief Longer intervals between flare-ups Fewer side effects Better ability to cope with daily chores Lower costs of treatment Better doses 0

55% 40% 36% 27% 27% 23% 10 20 30 40 50 60

Patients (%)

Results from 1100 interviews in five EU countries and the USA
Miravitlles M, et al. Respir Med 2007;101:453–460.

Fast relief in the morning is a window of opportunity for better symptom control

PHARMACOLOGY OF SYMBICORT

Budesonide
•  Anti-inflammatory agent •  Fast onset within 3-5 hours •  Demonstrated dose response •  Greater efficacy in combination with formoterol vs. higher doses of budesonide alone

+

Formoterol
•  Long-acting bronchodilator •  Onset as fast as salbutamol (1-3 minutes) •  Demonstrated dose response 6 µg to 54 µg/day

Only Symbicort Turbuhaler can be prescribed in this manner
Symbicort® Turbuhaler® Product Monograph

®

 

 

 

Formoterol has a rapid onset with long duration of action Whereas salmeterol, though has an equivalent bronchodilator effect, has a slower onset of action This probably reflects the fact that formoterol is a full agonist, whereas salmeterol is a partial agonist

1. Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar;29 (3):587-95. 2. Bousquet J, Boulet LP, Peters MJ, Magnussen H, Quiralte J, Martinez-Aguilar NE, Carlsheimer A. Budesonide/formoterol for maintenance and relief in uncontrolled asthma vs. high-dose salmeterol/ fluticasone. Respir Med. 2007 Dec;101(12):2437-46. 3. Kuna P, Peters MJ, Manjra AI, Jorup C, Naya IP, Martinez-Jimenez NE, Buhl R. Effect of budesonide/ formoterol maintenance and reliever therapy on asthma exacerbations. Int J Clin Pract. 2007 May;61(5): 725-36.

 

 

 

Formoterol is a full β2-agonist, whereas salmeterol is a partial β2-agonist. Therefore, increasing the dose of formoterol in the presence of ICS is associated with increased protection from exacerbations. But higher doses are not recommended with salmeterol because it has a plateau in its efficacy at around 100µg/day.

1. Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar;29 (3):587-95. 2. Bousquet J, Boulet LP, Peters MJ, Magnussen H, Quiralte J, Martinez-Aguilar NE, Carlsheimer A. Budesonide/formoterol for maintenance and relief in uncontrolled asthma vs. high-dose salmeterol/ fluticasone. Respir Med. 2007 Dec;101(12):2437-46. 3. Kuna P, Peters MJ, Manjra AI, Jorup C, Naya IP, Martinez-Jimenez NE, Buhl R. Effect of budesonide/ formoterol maintenance and reliever therapy on asthma exacerbations. Int J Clin Pract. 2007 May;61(5): 725-36.

ICS upregulates the β2-receptors LABA increases the nuclear translocation of glucocorticoid receptors
Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar; 29(3):587-95.

 

Direct bronchodilator effect Non-bronchodilator effects
◦  Reduced plasma exudation ◦  Mast cell stabilization ◦  Reduced neutrophils
  by relaxes the endothelial cells, thus closes the gap

 

  Thus reduce the releases of reactive oxygen species via the activated neutrophils
Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar; 29(3):587-95.

Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar; 29(3):587-95.

How to help COPD patients achieve their goals in everyday life ?

Therapy at each stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe •  FEV1/FVC < 70% •  FEV1 < 30%

•  FEV1/FVC < 70% •  FEV1 ≥ 80% predicted

•  FEV1/FVC < 70% 70%   50% ≤ FEV1 <   30% ≤ FEV1 <
80% predicted

•  FEV1/FVC <

50% predicted

predicted •  or FEV1 < 50% predicted plus chronic respiratory failure

Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed)

Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations
Add long-term oxygen if chronic respiratory failure Consider surgical treatments
FVC = forced vital capacity
Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2008. Available from http://www.goldcopd.com/

Symbicort® rapidly improves FEV1 within 5 minutes
Symbicort® + TIO+ works faster than TIO+ alone
Morning FEV1 (I)

Symbicort works faster than Sal/Flu#
FEV1 change from pre-dose (ml)

1.32 1.28 1.24 1.20 1.16 1.12 1.08 1.04 1.00 -1 0 5
P < 0.001

Symbicort + tiotropium
P < 0.001

120 100
P < 0.001

Symbicort ® 320/9 µg bid
P < 0.001

80 60

Sal/Flu 50/500 µg bid
40

tiotropium

20 0

10

15

0
Minutes post-dose

5

10

15

Time (minutes) since drug intake

+TIO = tiotropium

Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

# Sal/Flu = salmeterol/fluticasone Partridge MR, et al. Ther Adv Respir Dis 2009

Greater control over morning activities with Symbicort®
Symbicort® 320/9µg bid salmeterol/fluticasone 50/500µg bid Change in CDLM questionnaire scores from run-in

0.30 0.25 ≠ 0.20 0.15 0.10 0.05 0.00 TOTAL SCORE
Wash yourself Dry yourself Get dressed Eat breakfast Walk early Walk late

+ +

Bid = twice daily; CDLM = Capacity of Daily Living During the Morning +p<0.02 vs salmeterol/fluticasone ≠p<0.05 vs salmeterol/fluticasone
Partridge MR et al. Ther Adv Respir Dis 2009

Greater control over morning activities with Symbicort® + tiotropium vs tiotropium alone
Change in CDLM total score from run-in*

0.35 0.30 0.25 0.20 0.15
p=0.027^

Symbicort + tiotropium
p=0.001†

0.10 0.05 0 1 2 3 4 5 6 7 Weeks 8 9 10

tiotropium

11

12

^Treatment comparison from randomisation to first week of treatment †Treatment comparison from randomisation to last week of treatment
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

Better symptom relief during the day and night with Symbicort® *
Mean difference in COPD symptom score from run-in to full treatment period

Breathlessness

Chest tightness

Night time awakenings

Cough
Better symptom relief with reduced COPD symptom score

-0.142* -0.142*

-0.142*

-0.157*

-0.161*

0.1

0.2
*

P<0.001

P<0.001

P<0.001

P<0.001

Symbicort + tiotropium vs tiotropium alone Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

Less reliever use with Symbicort® *
Reliever use at run-in and 12 week (last week)
Mean number of inhalations

Symbicort + tiotropium P<0.001 tiotropium

0.165 0.160 0.155 0.150 0.145 0.140 0.135 0.130
Run-in

P<0.001

Week 12

Run-in

Week 12

Daytime
* Symbicort + tiotropium vs tiotropium alone Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180:741-750

Night-time

Greater improvement in health status with Symbicort® *
Symbicort + tiotropium
Adjusted mean difference in SGRQ-C score

tiotropium

6 5 4 3 2 1 0 SGRQ-C total
Comparisons are from randomisation to last visit
P = 0.023

3.8

1.5

* Symbicort®+ tiotropium vs tiotropium alone Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180:741-750

62% lower rate of severe exacerbations with Symbicort®*
Exacerbations/patients/3 months

0.4

Ratio: 0.38 (95% CI: 0.25-0.57) P<0.001

0.3

tiotropium

0.2

Symbicort + tiotropium
0.1

0.0

15

30

45

60

75

90

Days since randomisation N=660 *Symbicort + tiotropium vs tiotropium alone Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

65% less Hospitalization/ER treatments with Symbicort®*
100 90 80 70 60 50 40 30 20 10
tiotropium N=331 *Symbicort + tiotropium vs. tiotropium alone

Events/1000 patients/3 months

80

Ratio: 0.35 (95% CI: 0.16-0.78) P=0.011

28

0

Symbicort + tiotropium N=329

Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

Budesonide and the risk of pneumonia: a meta-analysis of individual patient data

•  Budesonide, with or without formoterol, is not associated
with an increased risk of pneumonia adverse events (AE) or serious adverse events (SAEs)

•  The two most important risk factors for pneumonia AEs or
SAEs in patients with COPD are increasing age and reduced lung function

Sin DD et al. Lancet 2009; 374:712–719.

Risk of pneumonia as an AE No significant difference between treatment groups
N=7042 Szafranski et al.1 1.26 (0.64–2.49) Calverley et al.2 1.54 (0.67–3.53) Rennard et al.3 0.88 (0.57–1.36) Tashkin et al.4 1.14 (0.56–2.33) Bourbeau et al.5 0.79 (0.12–5.17) Pauwels et al.6 2.08 (0.85–5.10) Vestbo et al.7 0.56 (0.23–1.34)

Overall8 1.05 (0.81–1.37) 0.1 0.2 0.5 1 2 Hazard ratio (95% CI) 5 10

Control treatment

Inhaled budesonide treatment

Data were adjusted for age, sex, smoking status, body mass index and % of predicted FEV1. AE = adverse event; CI = confidence intervals

1. Szafranski W et al. Eur Respir J 2003; 21:74–81, 2. Calverley PM et al. Eur Respir J 2003; 22:912–919, 3. Rennard SI et al. Drugs 2009; 69:549–565, 4. Tashkin DP et al. Drugs 2008; 68:1975–2000, 5. Bourbeau J et al. Am J Respir Crit Care Med 1994; 149(4 Suppl 2):A183, 6. Pauwels RA et al. N Engl J Med 1999; 340:1948–1953, 7. Vestbo J et al. Lancet 1999; 353:1819–1823, 8. Sin DD et al. Lancet 2009; 374:712–719.

Risk of pneumonia as an SAE No significant difference between treatment groups
N=7042 Szafranski et al.1 0.82 (0.32–2.07) Calverley et al.2 1.21 (0.45–3.36) Rennard et al.3 0.72 (0.37–1.37) Tashkin et al.4 1.06 (0.40–2.83) Bourbeau et al.5 0.79 (0.12–5.17) Pauwels et al.6 5.48 (0.66–45.7) Overall7 0.92 (0.62–1.35) 0.1 1 Hazard ratio (95% CI) 10 100
1. Szafranski W et al. Eur Respir J 2003; 21:74–81, 2. Calverley PM et al. Eur Respir J 2003; 22:912–919, 3. Rennard SI et al. Drugs 2009; 69:549–565, 4. Tashkin DP et al. Drugs 2008; 68:1975–2000, 5. Bourbeau J et al. Am J Respir Crit Care Med 1994; 149(4 Suppl 2):A183, 6. Pauwels RA et al. N Engl J Med 1999; 340:1948–1953, 7. Sin DD et al. Lancet 2009; 374:712–719.

Control treatment

Inhaled budesonide treatment

Data were adjusted for age, sex, smoking status, body mass index and FEV1 (% predicted) CI = confidence intervals; SAE = serious adverse event

SUMMARY

•  COPD is no longer just considered a lung
parenchymal pathology, but one with significant systemic effects •  Spirometry is required for both diagnosis and assessment of severity. Every effort should be made to refer patient for spirometry.

SUMMARY

•  Smoking cessation is the single most cost

effective - intervention to reduce the risk of developing COPD and stop its progression. Even a brief 3-min of counselling may result in smoking cessation rates of 5-10%

SUMMARY

•  The combination of LABA/ICS has been

shown to improve lung function, quality of life and reduce exacerbations compared with placebo in COPD patients with FEV1 < 65% predicted. •  Consider NIV in patients with persistent hypercapnoeic respiratory failure despite optimal medical therapy

Sign up to vote on this title
UsefulNot useful