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Worcester, MA
Dr. Pbert is affiliated with the University of Massachusetts Medical School.
Correspondence to: Lori Pbert, PhD, University of Massachusetts Medical School, 55 Lake Ave North, Worcester, MA 01655; e-mail: lori.pbert{at}umassmed.edu
Cigarette smoking is the main cause of COPD, accounting for > 75% of all COPD cases.1234 Smoking cessation is the only treatment that has been found to unequivocally reduce the rate of FEV1 decline in patients with COPD,5 with the rate of FEV1 loss slowing and potentially returning to the rate of decline of similarly aged individuals who have never smoked soon after cessation.67 As such, smoking cessation is the single most important and effective intervention to improve outcomes in individuals with COPD.148
Clear evidence-based clinical practice guidelines are available for smoking cessation treatment in the general population of smokers, recommending both behavioral counseling and pharmacotherapy, including nicotine replacement therapy and bupropion therapy.9 But, despite the fact that smoking cessation is the only evidence-based intervention for treating COPD,8 surprisingly little is known about the effectiveness of these evidence-based interventions in COPD patients. Reviews1011 from the past few years identified only five randomized controlled trials and concluded that a combination of pharmacotherapy with intensive individual counseling over an extended period of time appears to be effective for treating patients with COPD. However, many gaps exist in our understanding of how best to help COPD patients stop smoking. First, although guidelines for COPD (eg, American Thoracic Society12) recommend the use of existing behavioral and pharmacologic smoking cessation therapies, the preliminary data suggest that smokers with COPD may have a different pattern of smoking than those without COPD (eg, greater nicotine dependence, heavier smoking, and higher CO concentrations in expired air).13 Therefore, it remains unclear whether smokers with COPD are comparable to healthy smokers in their response to existing interventions. Second, we do not know how quit rates compare in patients with varying degrees of COPD severity. In one study,14 prolonged abstinence rates were lower in patients with more severe COPD (stage II) compared to patients with stage I COPD, but this difference was not statistically significant. Third, no conclusions could be drawn regarding the effectiveness of behavioral intervention alone due to the lack of high-quality studies comparing such interventions with placebo or no treatment control conditions.
In this issue of CHEST (see page 334), Tonnesen and colleagues15 address some of these gaps by evaluating the efficacy of both pharmacologic and behavioral interventions in COPD smokers with a wide range of severity levels. The investigators utilized a 2 x 2 design to evaluate the independent and combined effects of nicotine sublingual tablets and what they describe as two levels of behavioral support. Three hundred seventy COPD patients from seven pulmonary outpatient clinics were enrolled in the study, and patients with a range of COPD severity were included. The results of the pharmacologic component of the intervention were encouraging. Point prevalence cessation rates were significantly greater with sublingual nicotine therapy compared to placebo at both the 6-month and the 12-month follow-up, which is consistent with the results of prior studies16 of the sublingual nicotine tablet in a general population of smokers (12-month abstinence rate, approximately 17%; range, 15 to 20%). Enthusiasm over this finding is somewhat tempered by the more modest odds ratio (OR) achieved in the present study when comparing active medication and placebo at 12 months (17% vs 10%, respectively; OR, 1.46; 95% CI, 0.79 to 2.68) compared to the pooled OR found in studies conducted with a general population of smokers (OR, 2.05; 95% CI, 1.62 to 2.59),16 suggesting a somewhat weaker effect in COPD patients. The increased abstinence rates achieved with the sublingual nicotine tablet in the present study are nonetheless quite encouraging.
The investigators compared their findings to the 1-year point prevalence abstinence rate of 35% found in the Lung Health Study,8 which evaluated the use of nicotine gum and an intensive intervention in smokers with mild or asymptomatic airways obstruction (mean FEV1, 75% predicted). In contrast, the COPD patients in the study by Tonnesen et al15 represented a sicker population with more severe COPD (mean FEV1, 56% predicted). It may be that patients with more severe COPD quit smoking at lower rates than patients with more mild disease,14 although Tonnesen et al15 found that COPD severity (expressed as the FEV1 percent predicted) was not predictive of smoking outcome in their study. An alternate explanation may be the greater intensity of the Lung Health Study8 behavioral intervention. A more comparable study may be one that evaluated bupropion with a similar intensity of behavioral intervention and similar delivery method (individual counseling and telephone contact).14 In that study, the effect of treatment at 6 months was lost at the 1-year follow-up, in contrast to the maintained effect of the nicotine sublingual tablet in the Tonnesen et al study.15 This further supports the potential for therapy with sublingual nicotine tablets in COPD patients.
A strength of the study by Tonnesen et al15 was the inclusion of lighter smokers in their sample, smokers who are often excluded from pharmacologic trials. The investigators found that the number of cigarettes smoked per day was not predictive of outcome, leading to their recommendation that nicotine replacement therapy be considered for COPD patients who were lighter smokers as well. Indeed, they reported that approximately one third of smokers with severe COPD who were seen in their clinic have reduced their level of smoking to < 10 cigarettes per day, making this finding and recommendation relevant for clinicians serving this population.
In contrast to the pharmacologic findings, implications of the behavioral support intervention results are less clear-cut. Tonnesen et al15 reported that there was no statistically significant difference in abstinence rates between what they describe as low vs high behavioral support. This is potentially a misrepresentation, as the authors themselves state in the "Discussion" section of their article that "both of our approaches could be classified as moderate support" and that the number of contacts participants in each group received during the initial treatment period was fairly similar, potentially accounting for the lack of a statistically significant effect for the behavioral intervention comparison. It may be more accurate to describe this component of the study as a comparison between two different models for delivering moderate intensity smoking cessation treatment. This is consistent with their interpretation of their findings, suggesting that clinics serving COPD smokers could choose between two different methods for delivering treatment depending on their resources and clinical setup, utilizing either fewer visits combined with more proactive telephone counseling or more clinic visits. This finding in and of itself has important implications for real-world practice, offering clinics flexibility in the delivery of smoking cessation treatment. Unfortunately, the design of the study does not allow it to address the question of the effect of behavioral interventions compared to "placebo" or to no intervention control conditions in COPD patients, which is a major gap in the literature. This is an area that is ripe for future investigation. In such studies, behavioral intervention protocols need to be clearly described and fidelity to intervention protocols explicitly evaluated. In the present study, it is unclear how fidelity was evaluated and ensured across the 20 nurses who were delivering the intervention and the level of fidelity to the protocol that was achieved. Such process data are increasingly being valued in trials investigating the effectiveness of behavioral treatments.
A limitation of the study by Tonnesen et al15 is the uncertainty regarding whether smoking status at the 1-year follow-up was based on self-report or expired CO levels. The investigators state that point prevalence abstinence and sustained abstinence were defined as self-reported abstinence verified by an expired CO level of < 10 ppm, but later in the article note that 1-year assessments for 174 of 288 patients, a full 60%, were conducted by telephone. If confirmation by the measurement of expired CO levels was not obtained for these participants, which one might assume, how was abstinence defined in this large subset of the sample, and how was this lack of expired CO confirmation handled in the analyses? Biochemical validation of self-reported smoking status is considered to be the "gold standard" in evaluations of smoking cessation interventions and can be considered even more imperative in smokers with COPD, who have an even greater perceived demand to report quitting due to the nature of their disease. The potential for COPD smokers to report abstinence when continuing to smoke, particularly in the groups receiving moderately intense behavioral support, is significant. For instance, Monninkhof and colleagues17 found that approximately half (52%) of COPD smokers who self-reported abstinence following a minimal-contact smoking cessation program misreported their smoking status. It would have been helpful for the investigators to report the distribution of the 60% of participants not completing biochemical validation across the four conditions and to address this limitation in their interpretation of the results.
The finding of significant improvement in FEV1 in maintained abstainers and a stabilizing of lung function in those who reduced their number of cigarettes smoked compared to decreases in lung function in continuous smokers is encouraging and is consistent with the findings of the Lung Health Study.8 This physiologic improvement parallels the statistically and clinically significant improvements in health-related quality of life found in both sustained abstainers and reducers, with the most pronounced improvements noted in symptoms. Given that COPD patients with symptoms such as dyspnea that impact on their quality of life are more likely to seek treatment for their disease, the positive effect of smoking cessation on FEV1 and symptoms provides clinicians with a potentially powerful and tangible motivation for smokers with COPD to stop smoking, which is a significant implication of the findings for clinical care. Sharing information on potential improvements in lung function and symptoms could potentially "prime" COPD smokers for receiving and benefiting from smoking cessation treatment by enhancing their motivation to quit prior to a quit attempt.
Footnotes
The author has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
References
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