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PRACTICE:
Andrew McIvor and Paul Little
Chronic obstructive pulmonary disease
BMJ 2007; 334: 798 [Full text]
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Rapid Responses published:

[Read Rapid Response] Nicotine Addiction causes Smoking
Andrew J Ashworth   (15 April 2007)
[Read Rapid Response] spirometric criteria for chronic obstructive pulmonary disease are themselves controversial
oscar,m jolobe   (16 April 2007)
[Read Rapid Response] Drug management of COPD
Peter D Burrill   (16 April 2007)

Nicotine Addiction causes Smoking 15 April 2007
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Andrew J Ashworth,
GP Principal
Davidsons Mains Medical Centre, 5 Quality Street, EDINBURGH, EH4 5BP

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Re: Nicotine Addiction causes Smoking

In COPD it is probably the delivery method (smoke) of the addictive substance (Nicotine) that is harmful. In opiate addiction substitute substances are given by safer methods to prevent harm by, for example, preventing injecting behaviour: these substitutes are aften taken for long periods. There are many methods of addressing nicotine addiction including alternative delivery methods for Nicotine but these are all time limited by licence or/and guidelines and so, in addictions terminology constitute detoxification. Until we stop consididering nicotine use and smoking cigarettes as interchangeable concepts, safer delevery of nicotine to those with COPD (whose only real prospect of a better prognosis is to stop smoking) will be witheld on what constitute unethical moral grounds (since nicotine substitutes are available and so harm reduction to prevent smoking would be possible). A trial of unlimited nicotine substitution in COPD using pulmonary function as an outcome is required.

Competing interests: None declared

spirometric criteria for chronic obstructive pulmonary disease are themselves controversial 16 April 2007
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oscar,m jolobe,
retired geriatrician
manchester medical society, c/o John Rylands University Library, Oxford Road , Manchester M13 9PP

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Re: spirometric criteria for chronic obstructive pulmonary disease are themselves controversial

The allusion to the spirometric validation of chronic obstructive pulmonary disease(1), should be accompanied by the caveat that the spirometric criteria for airflow obstruction are, themselves, a matter of some controversy. On the one hand, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) defined airways obstruction as percentage 1 second forced expiratory volume/forced vital capacity(FEV1/FVC%) < 70%(2), whilst the most recent guideline from the American Thoracic Society (ATS) and European Respiratory Society defined an obstructive ventilatory defect as FEV1/FVC% ratio below the fifth percentile of the predicted value(3). In a study comprising 5906 never smokers and 3497 current smokers the comparison between GOLD criteria and ATS criteria revealed significant discrepancies between the two in terms of sensitivity and specificity for identifying subjects with airflow obstruction(4). The correct identification of airflow obstruction, and, hence, chronic obstructive pulmonary disease (COPD) is especially relevant to the use of beta adrenergic receptor blocking drugs (beta-blockers) in post myocardial infarct patients with co-existing COPD. Despite their proven survival benefit in post myocardial infarct patients with and without co-existing COPD, many doctors are reluctent to prescribe these drugs in the former category of patients(5) notwithstanding evidence from meta-analysis that cardioselective beta-blockers are well tolerated in the majority of patients with COPD, the latter being defined, in the meta-analysis, as a "baseline FEV1 of < 80% normal predicted value, or as defined by the guidelines of the American Thoracic Society"(6)

References

(1) McIvor A and Little p 10-minute consultation; Chronic Obstructive Pulmonary Disease British Medical Journal 2007:334:798

(2)Pauwels RA., Buist AS., Cakverley PM et al Global strategies for the diagnosis, management, and prevention of chronic obstructive pulmonary disease American Journal of Respiratory and Critical Care Medicine 2001:163:1256- 76

(3) Pelligrino R., Viegi G., Brusasco V et al ATS/ERS task force:standardisation of lung functiontesting: interpretative strategies for lung function tests European Respiratory Journal 2005:26:948-68

(4) Hansen JE., Sun X-G., Wasserman K Spirometric criteria for airway obstruction Use percentage of FEV1/FVC ratio below the fifth percentile, not < 70% Chest 2007:131:349-55

(5) Gottlieb SS and McCarter RJ., Vogel RA Effect of beta-blockade on mortality among high-risk and low-risk patients after myocardial infarction New England Journal of Medicine 1998:339:489-97

(6) Salpeter SR., Ormiston TM., Salpeter EE., Poole PJ., Cates CJ Cardioselective beta-blockers for chronic obstructive pulmonary disease: a meta-analysis Respiratory Medicine 2003:97:1094-1101

Competing interests: None declared

Drug management of COPD 16 April 2007
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Peter D Burrill,
Specialist Pharmaceutical Adviser for Public Health
Derbyshire County PCT, Chesterfield, S41 7PF

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Re: Drug management of COPD

I realise that covering the management of COPD in a single side is difficult and compromises on what goes in and what is left out are inevitable. I would like to bring some pertinent information to the attention of your readers.

In the box on the long term management, the authors recommend commencing prescribing with short-acting beta2-agonists as needed, supplemented by stepwise addition of regular short or long-acting anticholinergic inhalers. I agree with this and it is supported by evidence; tiotropium has advantages over a long-acting beta2-agonist (LABA). For the next step they recommend the addition of a LABA. NICE also recommends this in their COPD guideline (No.12, 2004). At that time there was no evidence to show whether this was a useful combination. There is now recently published evidence that shows the addition of LABA to tiotropium has no additional benefit over tiotropium alone (1), so this is not really a suitable option.

The authors' next step is to add an inhaled corticosteroid (ICS) or a combination of ICS and LABA as a single inhaler. If ICS is to be used in COPD then it should be inline with the NICE COPD guideline. Unfortunately, evidence that a combination inhaler such as Seretide produces clinically significant benefit over and above the separate components is lacking. For instance the recent TORCH study showed no benefit of Seretide over salmeterol or fluticasone alone at reducing severe exacerbations (2). This study worringly showed an increase in pneumonia in the fluticasone and Seretide arms, with a number-needed-to-harm of 17.

If a patient on regular tiotropium and as needed short-acting beta2- agonist requires additional drug treatment then I suggest that the two options are to add ICS (as per NICE guidance) or add an oral mucolytic. To assess the effectiveness of drug therapy I would suggest use of the 5 questions (similar to use of the 3 questions in asthma) as recommended by Jones (3).

1. Ann Intern Med 2007; 146: published early online 20/2/07

2. N Engl J Med 2007; 356: 775-89

3. Thorax 2001; 56: 880-87

Competing interests: None declared