© IPCRG 2007 Achieving asthma control in practice: understanding the reasons for poor control...

© IPCRG 2007© IPCRG 2007© IPCRG 2007

Achieving asthma control in practice: understanding the reasons for poor controlSeptember 2008

- © IPCRG 2007Page 2 - © IPCRG 2007Page 2 - © IPCRG 2007

International panel discussion, Aberdeen, Sept 2007

How to develop tools for use in primary care:

o To identify causes of poor asthma control

o To manage causes of poor asthma control

We're not treating asthma; we're treating patients. Many of our patients would not be eligible for inclusion in randomised controlled trials because of comorbidities and other factors. Thus, the asthma guidelines, which are based on results of these trials, often do not provide the answers we need for patient care, particularly in the primary care setting.

-Dr. John Haughney

Haughney J et al. Achieving asthma control in practice: understanding the reasons for poor control. Respir Med. 2008;102:1681–93.


What is asthma control?As defined by the Global Initiative for Asthma (GINA), 2007

• Minimal to no daytime asthma symptoms

• No limitations on activities

• No nocturnal symptoms or awakenings

• Minimal to no need for reliever or rescue

therapy

• Normal lung function (FEV1 or PEF)

• No exacerbations

www.ginasthma.org


Reasons for poor asthma control

• Wrong diagnosis or confounding illness

• Incorrect choice of inhaler or poor technique

• Concurrent smoking

• Concomitant rhinitis

• Unintentional or intentional nonadherence

• Individual variation in treatment response

• Undertreatment

Haughney J et al. Respir Med. 2008;102:1681–93.


Addressing poor asthma control

Step 1: Confirm the diagnosis of asthma

• If the patient is not responding as expected to asthma therapy: o Confirm the asthma diagnosis and rule out (or in)

confounding illness before changing or increasing medications

• Tools for diagnosing asthma must be stratified by age

• Objective measures of reversible airflow obstruction (spirometry, PEF) are important if available

IPCRG Guidelines: diagnosis of respiratory diseases in primary care. Prim Care Respir J. 2006;15:20–34.


Diagnosing asthma in primary care IPCRG guidelines. Prim Care Respir J. 2006;15:20–34.

• Compatible clinical historyo Episodic or persistent dyspnoea, wheeze, tightness, cough

o Triggers (allergic, irritant)

o Risk factors for asthma development

o Consider occupational asthma for adults with recent onset

• Objective evidenceo Spirometry or peak expiratory flow

o Bronchoprovocation test (methacholine challenge)

• Ancillary testso Chest x-ray

o Eosinophils, IgE level

o Allergy testing

o Exhaled nitric oxide

o Induced sputum


Diagnosing asthma in children

• Remember that young children commonly wheeze with colds

• Differentials for wheezing include respiratory (upper and lower) and non-respiratory causes:o Upper airway: allergic diseases

o Obstruction of large airway: foreign body, vocal cord dysfunction, vascular rings, laryngeal webs, tracheomalacia, or stenosis

o Obstruction of small airways: viral bronchiolitis, cystic fibrosis, bronchopulmonary dysplasia, heart disease

o Other: aspiration (gastro-oesophageal reflux disease)

• Spirometry is usually impractical for patients < 5 years old

Bush A. Diagnosis of asthma in children under five. Prim Care Respir J. 2007;16:7–15.


Modified Asthma Prediction Index (mAPI)A clinical index defining asthma risk in 2–3 year olds

• One of three major risk factors:1. Parental history of asthma

2. Physician-diagnosed atopic dermatitis

3. Allergic sensitization to ≥1 aeroallergen

• OR two of three minor risk factors:1. Allergic sensitization to milk, egg, or peanuts

2. Wheezing unrelated to colds

3. Blood eosinophils ≥4%

For a child ≥2 years old with a history of ≥4 wheezing episodes (≥1 confirmed by a physician), the likelihood of active asthma at age 6-13 yrs increases if the child has:

Guilbert TW et al. J Allergy Clin Immunol. 2004;114:1282–7.


Diagnosing asthma in adults

• Differentiate between asthma and chronic

obstructive pulmonary disease (COPD)

• Identify triggers such as smoking, pet exposure,

occupational exposure

• Common differential diagnoses:

o COPD, cardiac disease, laryngeal, tracheal, or lung

tumour, bronchiectasis, foreign body, interstitial lung

disease, pulmonary emboli, aspiration, vocal cord

dysfunction, hyperventilation

IPCRG Guidelines: diagnosis of respiratory diseases in primary care. Prim Care Respir J. 2006;15:20–34.


Diagnosing asthma in adults

Comorbidities can worsen asthma symptoms— identify and treat them:

• allergic rhinitis

• COPD

• gastro-oesophageal reflux disease (GERD)

• respiratory infection

• cardiac disorders

• anaemia

• vocal cord dysfunction



Incorrect inhaler choice or poor technique

• There is no clinical difference between inhaler devices when used correctly, but each type requires a different pattern of inhalation for optimal drug delivery to the lungs

• Problems with inhaler technique are common in clinical practice & can lead to poor asthma control

• Asthma control worsens as the number of mistakes in inhaler technique increases

• All patients should be trained in technique, and trainers should be competent with the inhalation technique


Inhaler choice and techniqueKey recommendations:

• Take patient preference into account when choosing the inhaler device

• Simplify the regimen and do not mix inhaler device types

• The choice of steroid inhaler is most important because of the narrower therapeutic window

• Invest the time to train each patient in proper inhaler technique:

• Observe technique & let patient observe self (using video demonstrations)

• Devices to check technique & maintain trained technique are available (eg, 2Tone Trainer & Aerochamber Plus spacer for metered dose inhalers; In-Check Dial, Turbuhaler whistle, Novolizer for dry powder inhalers)

• Recheck inhaler technique on each revisit



Resources on inhaler use

• Inhaler & spacer diagrams on GINA website:o http://www.ginasthma.com/Userfiles/inhaler_charts.pdf

• American College of Chest Physicians/American College of Asthma, Allergy, and Immunology guidelines:o Dolovich et al. Chest. 2005;127:335-371.

• Educational CD-Roms by Ontario Thoracic Society Provider Education Program:o http://www.on.lung.ca/Health-Care-Professionals/Provider-

Education-Program/CD-ROMS.php

• Schematic cartoons on the Asthma UK website:o http://www.asthma.org.uk/using_your.html


Resources on inhaler use (cont.)

• Correct Inhaler Techniques and Common Mistakeso June 2008 newsletter, National Asthma Council, Australia:

http://www.nationalasthma.org.au/html/newsletter/2008/nl_08_006.asp#s2

o Woolcock Institute of Medical Research: http://www.woolcock.org.au/PDF/PR/WIMR_Press_Release_AsthmaMeds_June2008.pdf

• Asthma Management Handbook 2006, National Asthma Council, Australia: o Use & care of spacers: http://www.nationalasthma.org.au/cms/index.php?

option=com_content&task=view&id=200&Itemid=147

o Delivery devices: http://www.nationalasthma.org.au/cms/index.php?option=com_content&task=view&id=90&Itemid=112



Concurrent smoking

• Smoking adversely impacts asthma control

o Current smokers are almost 3 times more likely

than non-smokers to be hospitalised for their

asthma over a 12-month period

• Why does smoking adversely impact asthma?

o Asthma misdiagnosed as COPD or concomitant

COPD

o Relative steroid resistance

Price D et al. Clin Exp Allergy. 2005;35:282–7.


Inhaled steroids are less effective in smokers than nonsmokers with asthma

The pattern of airway inflammation differs

Smokers have a higher percentage of neutrophils in induced sputum, and

steroids are not very effective in reducing neutrophils.

Smoking produces oxidative stress

The oxidative stress produced by smoking impairs the activity of histone

deacetylase-2 (HDAC2), resulting in reduced anti-inflammatory activity of

steroids.

Smoking triggers leukotriene production

Leukotrienes are not reduced by steroid therapy.

Boulet LP et al. Chest. 2006;129:661–8. Barnes PJ et al. Lancet. 2004;363:731–3. Fauler J et al. Eur J Clin Invest. 1997;27:43–7.


GM-CSFGM-CSF IL-8IL-8 eotaxineotaxin

HistoneHistoneacetylationacetylation

Inflammatory stimuliInflammatory stimuli

Non-Smoking Asthma

NF-NF-B B

GRGR

HDAC2HDAC2

Histone acetylationHistone acetylation

CorticosteroidsCorticosteroids

SteroidSteroidresponseresponse

Steroid resistance in smokers with asthma

Cigarette smokeCigarette smoke

Oxidative stressOxidative stress

HistoneHistoneacetylationacetylation

PeroxynitritePeroxynitrite

Smoking AsthmaSmoking Asthma

HDAC2HDAC2

NF-NF-B B

GM-CSFGM-CSF IL-8IL-8 eotaxineotaxin

SteroidSteroidresistanceresistance

GM-CSFGM-CSFIL-8IL-8eotaxineotaxin

GR = glucocorticoid receptors; HDAC2 = histone deacetylase-2; NF- B = nuclear factor- B


Clinical approach to smoking

• Tools

o Take a smoking history

o Investigate the possibility of COPD

• IPCRG guidance includes tool to differentiate asthma from COPD*

• Solutions

o Encourage smokers to quit!

• IPCRG guidance on smoking cessation:

http://www.theipcrg.org/smoking/index.php

o Try alternative therapy:

• Leukotriene receptor antagonist

• Possibly theophylline*IPCRG Guidelines: diagnosis of respiratory diseases in primary care. Prim Care Respir J. 2006;15:20–34.



Concomitant rhinitis• Patients with asthma & concomitant rhinitis use more health

care resources than those without rhinitis

• In epidemiologic studies in the UK:

o Adults with asthma & concomitant rhinitis were 50% more likely to

be hospitalised for their asthma & significantly more likely to visit

their primary care physician than those without rhinitis

o Children with asthma & concomitant rhinitis had double the

likelihood of being hospitalised and significantly increased

likelihood of a physician visit for asthma than those without rhinitis

• >50% of patients with asthma have rhinitis

o Both allergic & nonallergic rhinitis are linked to asthma

Price D et al Clin Exp Allergy. 2005;35:282–7. Thomas M et al. Pediatrics. 2005;115:129–34.


Evidence linking asthma & rhinitis

• >50% of patients with asthma have rhinitis

• Similar epidemiology

• Common triggers

• Similar pattern of inflammation:

o T helper type 2 cells, mast cells, eosinophils

• Nasal challenge results in asthmatic inflammation

& vice versa

• Rhinitis predicts development of asthma

Thomas M. BMC Pulm Med. 2006;6:S4.


Does treatment of rhinitis improve asthma control?

Preliminary evidence suggests that it

does improve asthma control

In the COMPACT trial, patients with comorbid

rhinitis who received budesonide plus montelukast,

a leukotriene receptor antagonist effective in

treating rhinitis symptoms in patients with asthma,

showed significantly greater improvement in

morning PEF than the group receiving

monotherapy with doubled dose of budesonide.

This treatment difference was not seen among

patients without comorbid rhinitis, suggesting that

the effects of montelukast on rhinitis improved lung

function.

Price DB et al. Allergy. 2006;61:737–42.


Clinical approach to rhinitis

• Diagnosing rhinitis

o Use the International Study of Asthma and Allergies in

Childhood (ISAAC) question:• "Do you have an itchy, sneezy, runny, or blocked nose when you

don't have a cold?“

o Take a good history & examine the nose

o Assess severity – as relates to asthma control

• Treat the inflammation of both asthma & rhinitis

o Target upper & lower airways concomitantly or

o Combine upper plus lower airway therapies

IPCRG Guidelines: management of allergic rhinitis. Prim Care Respir J. 2006;15:58–70.


Treatment of comorbid rhinitis & asthma

Upper airway treatment options Lower airway treatment options

Nasal steroids Inhaled steroids

Antihistamines

Upper and lower airway treatment options

Leukotriene receptor antagonists

Anti-IgE

Immunotherapy



Unintentional & intentional nonadherence

• Nonadherence to asthma therapy, particularly to inhaled steroids, is a common problem contributing to poor asthma control

• Nonadherence is often a hidden problem as assessment of adherence is often not included in routine asthma review

• Barriers to assessing adherence:o Patient and physician may prefer to avoid the subject

o Lack of clear, easy methods for addressing barriers to adherence

o Perception that little can be done?

• Appreciating the factors involved is the first step toward improving adherence

Horne R. Chest. 2006;130:65S–72S.


Unintentional versus intentional nonadherence

Perceptual–Practical Model of Adherence(can’t take, won’t take)

UNINTENTIONAL

nonadherence

INTENTIONAL

nonadherence

Capacity & resources

Practical barriers

Motivational

Beliefs/preferences

Perceptual barriers

Horne R et al. 2005. National Co-ordinating Centre for NHS Service Delivery and Organisation R&D, London.

Intentional nonadherence derives from the balance between the patient’s beliefs about the personal necessity of taking a given medication relative to any concerns about taking it


Nonadherence: identifying the causes• Tools for identifying & assessing nonadherence:

o Beliefs about Medicines Questionnaire (BMQ) — developed to measure necessity beliefs and concerns

o Medication Adherence Report Scale (MARS) — developed to assess patient adherence

o Minimal Asthma Assessment Tool (MAAT) — undergoing pilot testing as a simple, self-administered patient questionnaire for use before a clinical consultation to evaluate asthma control, adherence to medication, and comorbidities such as allergic rhinitis and smoking

• Interventions to facilitate optimal adherence are likely to be more effective if they: o Facilitate honest discussion of adherence behaviouro Identify the mix of perceptual & practical barriers for the individual patiento Help clinicians to elicit and respond to patient beliefs and concerns

• We need to tailor the intervention & support according to specific barriers & patient preferences




Individual variation in treatment response

1. Fewer than 10% of people with asthma in a general practice population are eligible for the typical RCT

2. Patient adherence to therapy may be better in an RCT than in the real world

3. The definition of “response” to therapy in an RCT (eg, FEV1

improvement) may not correspond to results relevant for our patients (eg, improved asthma control, improved quality of life)

4. The inclusion/exclusion criteria can influence RCT results (eg, requirement for bronchodilator reversibility may favour β agonist)

5. Group mean data from RCTs may not predict individual patient response

Randomised controlled trials (RCTs) are the basis of recommendations made by clinical guidelines. However, several factors limit our ability to generalise RCT results to our patients.



Individual variation in treatment responseDistribution of FEV1 responses among adults with chronic asthma after 12 weeks of therapy

with inhaled beclometasone (white bars) or oral montelukast (striped bars). The mean FEV1

improvement from baseline was 13.1% for beclometasone & 7.4% for montelukast.

Malmstrom K et al. Ann Intern Med. 1999;130:487–95 .


Individual variation in treatment response

Individual patient versus

average patient

Intraindividual response profile to therapy

among children and adolescents with

persistent asthma. Individual patient

responses (change from baseline in

asthma control days) suggest that, while

some patients responded to both inhaled

steroid and montelukast, others showed a

better response to one or the other.

Zeiger RS et al. J Allergy Clin Immunol. 2006;117:45–52.


Difficulty in capturing & demonstrating subjective benefit in clinical trials

Factors driving clinical trials:

• Regulatory requirements

• The needs of industry

• Historyo what's been done in the past & is therefore still expected

• Ease of measuring certain endpoints

• Available technology to measure these endpoints

• The need to focus on short-term events of asthma

• The limited number of agents available for treating asthma

• The need to remove all possible confounding factors to allow assessment of the intervention studied



Real world measures are needed for clinical trials

Need measures of whatis important to ‘real’

people

Need to know:-What is effective?-In what patient?-In what circumstances?-How identify?-How deliver?

Do not need repeated studies for whatyou already know

Need people withasthma In real life

setting

What are realpeople looking for? What is of value to them?

Need measures of whatis important to ‘real’

people

Need to know:-What is effective?-In what patient?-In what circumstances?-How identify?-How deliver?

Do not need repeated studies for whatyou already know

Need people withasthma In real life

setting

What are realpeople looking for? What is of value to them?




Next steps—IPCRG GOALS

• Develop tools to aid asthma diagnosis and management

in primary care

• Translate tools into local languages and adapt them to

address cultural differences in perceptions about asthma

• Test all tools to address issue of low levels of health

literacy in many countries

• Coordinate efforts between the IPCRG, member

countries, and patients’ organisations to adapt tools for

individual countries

© IPCRG 2007 Achieving asthma control in practice: understanding the reasons for poor control...

Documents

Transcript of © IPCRG 2007 Achieving asthma control in practice: understanding the reasons for poor control...