https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(07)61380-4.pdf

Global burden of COPD: risk factors, prevalence, and future trends.

The aim of this study was to quantify the global prevalence of chronic obstructive pulmonary disease (COPD) by means of a systematic review and random effects meta-analysis. PubMed was searched for population-based prevalence estimates published during the period 1990-2004. Articles were included if they: 1) provided total population or sex-specific estimates for COPD, chronic bronchitis and/or emphysema; and 2) gave method details sufficiently clearly to establish the sampling strategy, approach to diagnosis and diagnostic criteria. Of 67 accepted articles, 62 unique entries yielded 101 overall prevalence estimates from 28 different counties. The pooled prevalence of COPD was 7.6% from 37 studies, of chronic bronchitis alone (38 studies) was 6.4% and of emphysema alone (eight studies) was 1.8%. The pooled prevalence from 26 spirometric estimates was 8.9%. The most common spirometric definitions used were those of the Global Initiative for Chronic Obstructive Lung Disease (13 estimates). There was significant heterogeneity, which was incompletely explained by subgroup analysis (e.g. age and smoking status). The prevalence of physiologically defined chronic obstructive pulmonary disease in adults aged > or =40 yrs is approximately 9-10%. There are important regional gaps, and methodological differences hinder interpretation of the available data. The efforts of the Global Initiative for Chronic Obstructive Lung Disease and similar groups should help to standardise chronic obstructive pulmonary disease prevalence measurement.

https://erj.ersjournals.com/content/erj/28/3/523.full.pdf

Global burden of COPD: systematic review and meta-analysis

© 2014 The Cochrane Collaboration. Background: There are at least three reasons to believe antidepressants might help in smoking cessation. Firstly, nicotine withdrawal may produce depressive symptoms or precipitate a major depressive episode and antidepressants may relieve these. Secondly, nicotine may have antidepressant effects that maintain smoking, and antidepressants may substitute for this effect. Finally, some antidepressants may have a specific effect on neural pathways (e.g. inhibiting monoamine oxidase) or receptors (e.g. blockade of nicotinic-cholinergic receptors) underlying nicotine addiction. Objectives: The aim of this review is to assess the effect and safety of antidepressant medications to aid long-term smoking cessation. The medications include bupropion; doxepin; fluoxetine; imipramine; lazabemide; moclobemide; nortriptyline; paroxetine; S-Adenosyl-L-Methionine (SAMe); selegiline; sertraline; St. John's wort; tryptophan; venlafaxine; and zimeledine. Search methods: We searched the Cochrane Tobacco Addiction Group Specialised Register which includes reports of trials indexed in the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, and PsycINFO, and other reviews and meeting abstracts, in July 2013. Selection criteria: We considered randomized trials comparing antidepressant medications to placebo or an alternative pharmacotherapy for smoking cessation. We also included trials comparing different doses, using pharmacotherapy to prevent relapse or re-initiate smoking cessation or to help smokers reduce cigarette consumption. We excluded trials with less than six months follow-up. Data collection and analysis: We extracted data and assessed risk of bias using standard methodological procedures expected by the Cochrane Collaboration. The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline, expressed as a risk ratio (RR). We used the most rigorous definition of abstinence available in each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed-effect model. Main results: Twenty-four new trials were identified since the 2009 update, bringing the total number of included trials to 90. There were 65 trials of bupropion and ten trials of nortriptyline, with the majority at low or unclear risk of bias. There was high quality evidence that, when used as the sole pharmacotherapy, bupropion significantly increased long-term cessation (44 trials, N = 13,728, risk ratio [RR] 1.62, 95% confidence interval [CI] 1.49 to 1.76). There was moderate quality evidence, limited by a relatively small number of trials and participants, that nortriptyline also significantly increased long-term cessation when used as the sole pharmacotherapy (six trials, N = 975, RR 2.03, 95% CI 1.48 to 2.78). There is insufficient evidence that adding bupropion (12 trials, N = 3487, RR 1.9, 95% CI 0.94 to 1.51) or nortriptyline (4 trials, N = 1644, RR 1.21, 95% CI 0.94 to 1.55) to nicotine replacement therapy (NRT) provides an additional long-term benefit. Based on a limited amount of data from direct comparisons, bupropion and nortriptyline appear to be equally effective and of similar efficacy to NRT (bupropion versus nortriptyline 3 trials, N = 417, RR 1.30, 95% CI 0.93 to 1.82; bupropion versus NRT 8 trials, N = 4096, RR 0.96, 95% CI 0.85 to 1.09; no direct comparisons between nortriptyline and NRT). Pooled results from four trials comparing bupropion to varenicline showed significantly lower quitting with bupropion than with varenicline (N = 1810, RR 0.68, 95% CI 0.56 to 0.83). Meta-analyses did not detect a significant increase in the rate of serious adverse events amongst participants taking bupropion, though the confidence interval only narrowly missed statistical significance (33 trials, N = 9631, RR 1.30, 95% CI 1.00 to 1.69). There is a risk of about 1 in 1000 of seizures associated with bupropion use. Bupropion has been associated with suicide risk, but whether this is causal is unclear. Nortriptyline has the potential for serious side-effects, but none have been seen in the few small trials for smoking cessation. There was no evidence of a significant effect for selective serotonin reuptake inhibitors on their own (RR 0.93, 95% CI 0.71 to 1.22, N = 1594; 2 trials fluoxetine, 1 paroxetine, 1 sertraline) or as an adjunct to NRT (3 trials of fluoxetine, N = 466, RR 0.70, 95% CI 0.64 to 1.82). Significant effects were also not detected for monoamine oxidase inhibitors (RR 1.29, 95% CI 0.93 to 1.79, N = 827; 1 trial moclobemide, 5 selegiline), the atypical antidepressant venlafaxine (1 trial, N = 147, RR 1.22, 95% CI 0.64 to 2.32), the herbal therapy St John's wort (hypericum) (2 trials, N = 261, RR 0.81, 95% CI 0.26 to 2.53), or the dietary supplement SAMe (1 trial, N = 120, RR 0.70, 95% CI 0.24 to 2.07). Authors' conclusions: The antidepressants bupropion and nortriptyline aid long-term smoking cessation. Adverse events with either medication appear to rarely be serious or lead to stopping medication. Evidence suggests that the mode of action of bupropion and nortriptyline is independent of their antidepressant effect and that they are of similar efficacy to nicotine replacement. Evidence also suggests that bupropion is less effective than varenicline, but further research is needed to confirm this finding. Evidence suggests that neither selective serotonin reuptake inhibitors (e.g. fluoxetine) nor monoamine oxidase inhibitors aid cessation.

/pdf/antidepressants-for-smoking-cessation-1eio4jus21.pdf

Antidepressants for smoking cessation

Aims Obstructive sleep apnoea (OSA) is associated with increased cardiovascular morbidity and mortality. Although it was previously assumed that this was due to its relation with obesity, recent data suggest that OSA is independently associated with the cardiovascular risk factors that comprise metabolic syndrome, including hypertension, insulin resistance, impaired glucose tolerance, and dyslipidaemia. However, as previous studies have only considered these variables individually, it has not been possible to determine the overall association of OSA with this syndrome. Methods and results We recruited 61 male subjects with OSA and 43 controls. Glucose, insulin, lipids, and blood pressure (BP) were measured following an overnight fast. Insulin resistance was estimated using homeostasis model assessment (HOMA). Metabolic syndrome was diagnosed according to National Cholesterol Education Program (NCEP) criteria. Subjects with OSA were more obese, had higher BP and fasting insulin, were more insulin resistant, had lower HDL cholesterol, and an increased incidence of metabolic syndrome (87% vs. 35%, \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} $p{<}0.0001$ \end{document}). In order to determine whether these associations were independent of obesity and other known covariates, a regression analysis adjusted for age, BMI, smoking, and alcohol consumption was performed. This demonstrated that OSA was independently associated with increased systolic and diastolic blood pressure, higher fasting insulin and triglyceride concentrations, decreased HDL cholesterol, increased cholesterol:HDL ratio, and a trend towards higher HOMA values. Metabolic syndrome was 9.1 (95% confidence interval 2.6, 31.2: \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} $p{<}0.0001$ \end{document}) times more likely to be present in subjects with OSA. Conclusions OSA is independently associated with an increase in the cardiovascular risk factors that comprise the metabolic syndrome and its overall prevalence. This may help explain the increased cardiovascular morbidity and mortality associated with this condition.

Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome

In a follow–up to the 2011 United Nations (UN) high level political declaration on non-communicable diseases (NCDs) [1], the World Health Assembly, in 2012, endorsed a new health goal (the “25 by 25 goal”), which focuses on reduction of premature deaths from COPD and other NCDs by 25% by the year 2025 [2]. Despite this initiative, experts have reported that COPD remains a growing [3], but neglected global epidemic [4]. The World Health Organization (WHO) estimated that there were about 62 million people with moderate to severe COPD in 2002, with the total number of COPD cases predicted to increase to about 200 million in 2010 [5,6]. According to the 2010 Global Burden of Disease (GBD) study, COPD was responsible for about 5% of global disability–adjusted life years – DALYs (76.7 million) – and 5% of total deaths (2.9 million) [7,8]. COPD is currently rated the fourth most common specific cause of death globally and predicted to be the third by 2030, in the absence of interventions that address the risks – especially tobacco smoking, exposures to combustion products of biomass fuels and environmental pollution [9,10].

The burden of COPD has been reported to be high in some high–income countries (HIC), particularly due to high prevalence of smoking in these settings [11]. For example, between years 2000 and 2010, about 4%–10% of adults were diagnosed with non–reversible and progressive airway obstruction (a basic feature of COPD) in population–based surveys across many European countries, with smoking indicated as a major risk [12]. The WHO has estimated that in many HIC up to 73% of COPD deaths are related to tobacco smoking [6]. The European Union (EU) reported that the direct cost from COPD was over 38.6 billion Euros in 2005, representing about 3% of total health care expenditure [13,14]. In the United States (US), over 2.7 million adults were estimated to have COPD in 2011, with about 135 000 deaths reported [15]. In 2010, the US government spent nearly US$ 49.9 billion on COPD, including 29.5 billion spent on direct health care, 8.0 billion on indirect morbidity and 12.4 billion on indirect mortality costs, respectively [15].

Meanwhile, it has been estimated that despite a high prevalence of COPD in some HIC, 90% of COPD deaths still occur in low– and middle–income countries (LMIC)in the future

[4] and 40% of these deaths are attributable to smoking [6]. The burden in LMIC has been comparatively high owing to relatively low COPD awareness, challenges with COPD diagnosis and increased exposures to additional risk factors, especially combustion products of biomass fuels [16]. Salvi and colleagues reported that about 3 billion people globally are exposed to smoke from biomass fuel, compared to 1 billion people who smoke tobacco globally [17]. In many developing countries COPD is neglected by governments, physicians, experts and the pharmaceutical industry, although it's been identified as an important public health problem [4].

In the last two decades, the Burden of Obstructive Lung Disease (BOLD) initiative has been collecting country–specific data on the prevalence, risk factors and socioeconomic burden of COPD, using standardized and tested methods for conducting COPD surveys in the general population [18]. This is expected to provide governments of many nations with country–specific evidence on which to develop policy on COPD prevention and management [18]. As noted above, this initiative is yet to take a full effect in many LMIC [19]. In addition, spirometry (the gold standard for COPD diagnosis) is not widely available in many LMIC [16]. Even when it is there, professionals in LMIC are often not being trained properly on how to use spirometers or interpret spirometry results. There is concern that COPD burden has been underestimated, owing to over–reliance on doctor’s diagnosis, with many diagnoses not being based on spirometry and international diagnostic guidelines [20]. The lack of routine COPD data collation and effective health information management system in many LMIC also implies that these settings could have been grossly under–represented in global burden of COPD estimates [11].

Some global and regional estimates of COPD burden have been published [1,21–23]. However, despite the fact that COPD is now prevalent in both HIC and LMIC, experts have raised concerns that reliable estimates of COPD prevalence are still few in many parts of the world. Moreover, many of the estimates are based on varying definitions and diagnostic criteria of COPD [9]. Also, some of the current estimates were reported before the BOLD surveys in several countries, thereby failing to account for the additional spirometry–based epidemiological data from the BOLD surveys. There is a need for a revised and updated estimate of COPD prevalence across world regions. We conducted a systematic review of COPD prevalence based on spirometry data across world regions. Our aim was to provide global and regional prevalence rates of COPD that could facilitate adequate policy response in these regions.

/pdf/global-and-regional-estimates-of-copd-prevalence-systematic-hk9qdazoi3.pdf

Global and regional estimates of COPD prevalence: Systematic review and meta-analysis.

Background: Chronic obstructive pulmonary disease (COPD) is a common disease with a steadily increasing prevalence and mortality. However, recent epidemiological estimates differ depending on the population studied and methods used. Aim: To investigate the prevalence, severity and burden of COPD in a primary care setting. Methods: From 4730 patients registered in a single primary care practice, all 2250 patients aged 40 years or more were invited to participate. Participants completed a questionnaire on smoking, respiratory symptoms, education and social status. A physical examination was followed by pre- and post-bronchodilator (BD) spirometry. Results: Of the eligible patients, 1960 (87%) participated. 92% of spirometric tests met the ATS criteria. Airflow limitation was demonstrated in 299 (15%) of the participants pre-BD and in 211 (11%) post-BD. COPD was diagnosed in 183 patients (9.3%). Of these patients, the degree of post-BD airflow limitation was mild in 30.6%, moderate in 51.4%, severe in 15.3% and very severe in 2.7%. Only 18.6% of these patients had previously been diagnosed with COPD; almost all of these had severe or very severe airflow limitation. As a result of the study, a diagnosis of asthma was made in 122 patients. Conclusions: The prevalence and underdiagnosis of COPD in adult patients in this primary care setting made case finding worthwhile. Large numbers of newly detected patients were symptomatic and needed treatment. Limiting investigations to smokers would have reduced the number of COPD diagnoses by 26%.

https://thorax.bmj.com/content/thoraxjnl/63/5/402.full.pdf

Prevalence, severity and underdiagnosis of COPD in the primary care setting

Early detection of COPD in a high-risk population using spirometric screening.

Background: Chronic obstructive pulmonary disease (COPD), usually caused by tobacco smoking, is one of the leading causes of morbidity and mortality. Smoking cessation at an early stage of the disease usually stops further progression. A study was undertaken to determine if diagnosis of airway obstruction was associated with subsequent success in smoking cessation, as advised by a physician. Methods: 4494 current smokers (57.4% men) with a history of at least 10 pack-years of smoking were recruited from 100 000 subjects screened by spirometric testing for signs of airway obstruction. At the time of screening all received simple smoking cessation advice. 1177 (26.2%) subjects had airway obstruction and were told that they had COPD and that smoking cessation would halt rapid progression of their lung disease. No pharmacological treatment was proposed. After 1 year all subjects were invited for a follow up visit. Smoking status was assessed by history and validated by exhaled carbon monoxide level. Results: Nearly 70% attended a follow up visit (n = 3077): 61% were men, mean (SD) age was 52 (10) years, mean (SD) tobacco exposure 30 (17) pack-years, and 33.3% had airway obstruction during the baseline examination. The validated smoking cessation rate in those with airway obstruction was 16.3% compared with 12.0% in those with normal spirometric parameters (p = 0.0003). After correction for age, sex, nicotine dependence, number of cigarettes smoked daily, and lung function, success in smoking cessation was predicted by lower lung function, lower nicotine dependence, and lower tobacco exposure. Conclusions: Simple smoking cessation advice combined with spirometric testing resulted in good 1 year cessation rates, especially in subjects with airway obstruction.

https://thorax.bmj.com/content/thoraxjnl/61/10/869.full.pdf

Smokers with airway obstruction are more likely to quit smoking

Diagnosis of airflow limitation combined with smoking cessation advice increases stop-smoking rate.

Background: Both chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome (OSAS) are common diseases. Some recent studies suggest an increased prevalence of

Michał Bednarek

Papers

Prevalence, severity and underdiagnosis of COPD in the primary care setting

Early detection of COPD in a high-risk population using spirometric screening.

Smokers with airway obstruction are more likely to quit smoking

Diagnosis of airflow limitation combined with smoking cessation advice increases stop-smoking rate.

There Is No Relationship between Chronic Obstructive Pulmonary Disease and Obstructive Sleep Apnea Syndrome: A Population Study