Description of the condition
Chronic obstructive pulmonary disease (COPD), a common and largely preventable disease, is characterised by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response to noxious particles or gases in the airways and the lung (GOLD 2013). Exacerbations and co-morbidities contribute to overall severity in individual patients. The diagnosis must be confirmed by spirometry－the most widely available reproducible test of lung function (GOLD 2013).
COPD prevalence, morbidity and mortality vary across countries and across different groups within countries (GOLD 2013). A worldwide prevalence study showed that the prevalence, for example, of moderate COPD (i.e. Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II) in women 40 years of age or older ranged from 3.1% to 12.6%, and in men from 6.7% to 13.1% (Buist 2007). This variation in prevalence is due in part to differences in pack-years, which are shown by the odds ratios of COPD for 10-year intervals of pack-years: 1.28 (95% confidence interval (CI) 1.15 to 1.42) for women and 1.16 (95% CI 1.12 to 1.21) for men (Buist 2007). Except for exposure to risk factors, prevalence variation is due to differences in survey methods, diagnostic criteria and analytical approaches. Under-recognition and under-diagnosis of COPD also affect the accuracy of prevalence and mortality data. In a large-scale English study, the prevalence of COPD was highest among current smokers (19.3%), followed by ex-smokers (15.2%) and never smokers (8.2%) (Shahab 2006). Furthermore, the prevalence of undetected COPD was high among asymptomatic smokers. The prevalence of previously undiagnosed COPD in male smokers 40 years of age or older ranged from 12% in a Greek research population (Tzanakis 2004) to 30% in a Dutch research population (Geijer 2005). The Global Burden of Disease Study projected that COPD will become the third leading cause of death worldwide by 2020 (GOLD 2013). This increased mortality is driven mainly by the expanding epidemic of smoking, reduced mortality from other common causes of death and aging of the world population (GOLD 2013).
The risk for developing COPD results from an interaction between genetic factors and many different environmental exposures (Mannino 2007). Cigarette smoking is the most commonly encountered risk factor for COPD in high-income countries (Celli 2004; Kohansal 2009; GOLD 2013). Furthermore, a higher prevalence of respiratory symptoms and lung function abnormalities and a greater COPD mortality rate are seen among cigarette smokers with COPD than non-smokers with COPD (GOLD 2013). For example, an overview of the literature showed the effect of smoking on forced expiratory volume in one second (FEV1) in males with mild to moderate COPD (Willemse 2004). The FEV1 of these participants, who continued to smoke, declined within a range of 42 to 82 mL/y compared with 0 to 49 mL/y in COPD participants who quit smoking at the start of the study (Willemse 2004). This latter decline is comparable with the physiological lung function decline that naturally occurs with increasing age (Kerstjens 1997).
Smoking cessation is the only evidence-based intervention that reduces the risk of developing COPD and slows down the accelerated decline in lung function in patients with COPD (Anthonisen 2002). To date, none of the existing medications for COPD have been shown conclusively to modify the long-term decline in lung function (GOLD 2013). Furthermore, smoking cessation is the single most cost-effective way to reduce the risk of development of COPD and worsening of the disease (GOLD 2013).
Description of the intervention
For the current review, we will include randomised controlled trials if they assessed the effectiveness of any form of behavioural or pharmacological treatment, or combinations of both, as an aid to smoking cessation in patients with COPD. Behavioural treatment in this regard refers to any psychotherapeutic approach aimed at identifying and modifying the behaviours associated with smoking (Tobacco Use and Dependence Guideline Panel 2008). Pharmacological treatments include nicotine replacement therapy (NRT), nicotine replacement partial agonists (NRPAs), antidepressants for smoking cessation (ADs) and nicotine vaccines. Currently, the following NRT delivery systems are available: nicotine chewing gum, nicotine inhaler, nicotine lozenge, nicotine patch and nicotine nasal spray. Varenicline is the most commonly used NRPA, and bupropion and nortriptyline the most commonly used ADs. Currently, vaccines are not licensed for public use, but several vaccines are under development. A smoking cessation intervention is often a combination of a pharmacological and a behavioural treatment.
How the intervention might work
Smoking is an addictive behaviour; therefore, the chances of successful smoking cessation are minimal without the use of behavioural and/or pharmacological treatments. In the general smoking population, several behavioural and pharmacological treatments have demonstrated efficacy in helping to achieve abstinence. For example, the antidepressants nortriptyline and bupropion aid long-term smoking cessation, and evidence suggests that the mode of action is independent of their antidepressant effects (Hughes 2012). Their efficacy is similar to that of NRT (Hughes 2012). A review of NRPAs showed that varenicline increased the chances of successful long-term smoking cessation compared with bupropion (Cahill 2012). Comparison of NRT and varenicline suggested a minor benefit of varenicline tending towards equivalency (Cahill 2012). Furthermore, a recent review showed the NRPA cytisine to be an effective treatment for smoking cessation (Hajek 2013). Interventions that combine behavioural and pharmacological treatments are even more successful in achieving abstinence (Stead 2012). Providing behavioural treatment in person or via telephone for people using pharmacotherapy to stop smoking showed a small but important effect (Stead 2012). However, these studies did not make a distinction between different kinds of smokers. As smokers are not a homogeneous group, it is important to make the intervention fit best for each specific group, such as people with COPD (Borrelli 2010), for example, by giving valuable and clear information on how smoking is related to COPD and to respiratory symptoms. Furthermore, it might be useful to specifically address the increased co-morbidities and nicotine dependence levels reported in COPD patients.
Why it is important to do this review
Smoking cessation is the most important intervention to reduce the risk of developing COPD and to improve the prognosis of patients with the disease. COPD patients have a more urgent need to stop smoking than the average smoker; moreover, many often find it more difficult to do so (Tonnesen 2007). Therefore, it is important to provide an overview of the evidence base for different smoking cessation interventions directed at these patients.
Compared with smokers from the general population, smokers with COPD might have greater difficulty in quitting smoking, in part because of their higher pack-years of smoking history, stronger dependence on nicotine and particular inhalation pattern (Jimenez-Ruiz 2001; Shahab 2006). A Dutch study showed that smokers with mild to severe COPD were less likely to achieve abstinence than smokers without COPD but at risk of developing the disease; the prolonged abstinence rate after six months with nortriptyline therapy was 21% in smokers with COPD compared with 32% in smokers without COPD (Wagena 2005). That study, however, did not control for baseline differences. Therefore, interventions aimed at smokers with COPD might have to be more tailored to the needs of COPD patients to increase their desire to stop and to address their increased levels of nicotine dependence (Shahab 2006). However, evidence for the effectiveness of tailored versus general smoking cessation interventions in this patient group is scarce.
The scope of this review will be the same as this previous Cochrane review: to review the evidence 'whether and which treatments are effective in COPD smokers' (van der Meer 2001). However, results might have changed because new trials on this subject have been published since 2003.