Smoking Cessation in Chronic Obstructive Pulmonary Disease.

Department of Medicine, David Geffen School of Medicine at UCLA, 37-131 Center for Health Sciences, 10833 Le Conte Avenue, Los Angeles, CA 90095-1690, USA.
Respiratory medicine (Impact Factor: 3.09). 04/2009; 103(7):963-74. DOI: 10.1016/j.rmed.2009.02.013
Source: PubMed


Smoking cessation is the most effective strategy for slowing down the progression of chronic obstructive pulmonary disease (COPD) and reducing mortality in the approximately 50% of patients with diagnosed COPD who continue to smoke. While behavioral interventions (including simple advice) have modest efficacy in improving smoking quit rates, the combination of counseling and pharmacotherapy is more effective than either alone. When combined with even brief counseling, nicotine replacement therapy (NRT), bupropion SR, and varenicline have all been shown to be effective in promoting smoking cessation and sustained abstinence in smokers with COPD to a degree comparable to that observed in the general smoking population. However, the recidivism rate is high after initial quitting so that at the end of 1 year, approximately 80% or more of patients are still smoking. Thus, new approaches to smoking cessation are needed. One approach is to combine different pharmacotherapies, for example, nicotine patch plus rapidly acting NRT (e.g., gum or nasal spray) and/or bupropion or even varenicline plus either NRT or bupropion, in a stepwise approach over a varying duration depending on the severity of nicotine dependence and nicotine withdrawal symptoms during the quit attempt, as proposed in the American College of Chest Physicians Tobacco Dependence Took Kit. Electronic (e)-cigarettes, which deliver vaporized nicotine without most of the noxious components in the smoke from burning tobacco cigarettes, also has potential efficacy as a smoking cessation aid, but their efficacy and safety as either substitutes for regular cigarettes or smoking cessation aids require additional study. This task is complicated because e-cigarettes are currently unregulated and hundreds of different brands are currently available.
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  • Source
    • "Although the incidence rate of COPD is likely to escalate in both developed and developing countries, COPD poses a heavier burden on the Asia-Pacific and African regions where smoking is still widespread and gradually increasing (Chan-Yeung, Ait-Khaled, White, Ip, & Tan, 2004; Adeloye et al., 2015). Cigarette smoke is inarguably the biggest risk factor for COPD, with 90% of deaths from COPD directly attributable to smoking (Tashkin & Murray, 2009). Other risk factors include exposure to air pollutants and biomass fuels (Song, Christiani, XiaorongWang, & Ren, 2014). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is an incurable global health burden and is characterised by progressive airflow limitation and loss of lung function. In addition to the pulmonary impact of the disease, COPD patients often develop comorbid diseases such as cardiovascular disease, skeletal muscle wasting, lung cancer and osteoporosis. One key feature of COPD, yet often underappreciated, is the contribution of oxidative stress in the onset and development of the disease. Patients experience an increased burden of oxidative stress due to the combined effects of excess reactive oxygen (ROS) and nitrogen species (RNS) generation, antioxidant depletion and reduced antioxidant enzyme activity. Currently, there is a lack of effective treatments for COPD, and an even greater lack of research regarding interventions that treat both COPD and its comorbidities. Due to the involvement of oxidative stress in the pathogenesis of COPD and many of its comorbidities, a unique therapeutic opportunity arises where the treatment of a multitude of diseases may be possible with only one therapeutic target. In this review, oxidative stress and the roles of ROS/RNS in the context of COPD and comorbid cardiovascular disease, skeletal muscle wasting, lung cancer, and osteoporosis is discussed and the potential for therapeutic benefit of anti-oxidative treatment in these conditions is outlined. Because of the unique interplay between oxidative stress and these diseases, oxidative stress represents a novel target for the treatment of COPD and its comorbidities. Copyright © 2015. Published by Elsevier Inc.
    Full-text · Article · Aug 2015 · Pharmacology [?] Therapeutics
  • Source
    • "None of these instruments seems to fully explore the difficulties patients with COPD deal with when they try to quit smoking. Patients with COPD and especially women seem to find it harder to quit smoking than patients without this diagnosis (Tashkin & Murray 2009, Vozoris & Stanbrook 2011), although the reasons of this difference are not clear. "
    [Show abstract] [Hide abstract]
    ABSTRACT: AimsTo test internal consistency and factor structure of a brief instrument called Trying to Quit smoking.Background The most effective treatment for patients with chronic obstructive pulmonary disease is to quit smoking. Constant thoughts about quitting and repeated quit attempts can generate destructive feelings and make it more difficult to quit.DesignDevelopment and psychometric testing of the Trying to Quit smoking scale.Methods The Trying to Quit smoking, an instrument designed to assess pressure-filled states of mind and corresponding pressure-relief strategies, was tested among 63 Swedish patients with chronic obstructive pulmonary disease. Among these, the psychometric properties of the instrument were analysed by Exploratory Factor Analyses.ResultsFourteen items were included in the factor analyses, loading on three factors labelled: (1) development of pressure-filled mental states; (2) use of destructive pressure-relief strategies; and (3) ambivalent thoughts when trying to quit smoking. These three factors accounted for more than 80% of the variance, performed well on the Kaiser-Meyer-Olkin (KMO) test and had high internal consistency.
    Full-text · Article · Dec 2014
  • Source
    • "This should elicit a response and open discussion regarding the dangers of continuing smoking. Referral to support groups, educational and counseling sessions, and the use of newer pharmaceuticals all offer avenues for success [34] [35]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background. Published reference equations predicting estimated-lung-age (ELA) didn’t reliably predict chronological-lung-age (CLA) data in North African population. Aims. To develop and to validate novel reference equations for ELA from varied anthropometric data and FEV1. Methods. Applying multiple regression analysis, equations predicting ELA were invented using data from 540 never-smokers with normal spirometry (group I). Validation was made based on data from 41 never-smokers with normal spirometry (group II). Equations were further applied for 91 subjects with confirmed COPD. Results. Novel regression equations allowing prediction of reference value of ELA and normal limits of difference between ELA and CLA were elaborated in both sexes. In males, ELA (yrs) = 42.85 - 20.74 x FEV1 (L) + 47.41 x Body Surface Area (m2) - 0.62 x Body-Mass-Index (BMI, kg/m2). In females, ELA (yrs) = 64.64 - 8.00 x FEV1 (L) - 0.17 x BMI (kg/m2) + 8.82 x Height (m). Normal limits of difference between ELA and CLA were ±16.9 yrs in males and ±14.8 yrs in females. Established equations predicted ELA of group II with no significant difference between CLA and ELA in either sex (respectively, 42.9±16.6 vs. 40.3±13.7 yrs in males, 42.0±13.5 vs. 45.6±7.7 yrs in females) ELA was significantly older than CLA age only in COPD with grades III and IV ((ELA minus CLA) (yrs) averaged, respectively, +21.7, +26.4). Conclusion. North African reference equations enrich the World Bank of reference equations from which the physician should choose according to the patient’s ethnic background.
    Full-text · Article · Apr 2014
Show more