Use of the CAPTURE case-finding tool to identify COPD patients who may need treatment
Jinping ZhengYun LiFuqiang WenQianli MaRongchang ChenYongchang SunTiantian LiuChenjuan GuShuling HuJie SongChris ComptonNanshan ZhongPaul Jones
0
Citation
0
Reference
10
Related Paper
Abstract:
Background: CAPTURE was developed to identify individuals who may have COPD (Martinez et al. Am J Respir Crit Care Med. 2017;195:748). This study aimed to test its ability to identify patients with significant dyspnoea, impaired health status or at risk of exacerbations or hospitalisation. Methods: Data are from COMPASS, a prospective study of COPD in China (Liang et al. ERJ Open Res. 2021;7:00201). Patients were categorised as CAPTURE positive if they met both criteria: questionnaire score ≥2 and peak expiratory flow <250L/min (females) or <350L/min (males). Sensitivity and specificity were tested for GOLD I-IV, and patients with CAT ≥10 vs <10, mMRC ≥2 vs <2, or ≥1 moderate exacerbation or hospitalisation in the previous year vs zero. Positive and negative predicted values (PPV and NPV) were calculated. Results: COPD patients, n=1696, mean age 65.4±7.5 (SD) years, 91% males, post-bronchodilator FEV1 66.6±20.1 % pred were compared with 307 controls (chronic bronchitis and never smokers), mean age 60.3±7.0 years, 65% males, FEV1/FVC 0.77±0.04. Data are tabulated; the difference between upper and lower bounds for 95% CIs was <15% in each case. Conclusion: CAPTURE has high sensitivity and specificity to detect COPD, but low sensitivity for GOLD I. Equally important for case finding, the high sensitivity and NPV estimates suggest that it may identify individuals who could benefit from treatment and those who may not. Funding GSK (208630)Keywords:
Chronic bronchitis
Gold standard (test)
Concepts relating to the natural history of chronic obstructive pulmonary disease (COPD) arise most importantly from the classic study of Fletcher and colleagues (The Natural History of Chronic Bronchitis and Emphysema, Oxford University Press, New York, 1976). This study, which evaluated working English men over 8 years, was used to construct a proposed life-long natural history. Although this is a classic study that has greatly advanced understanding of COPD, it has a number of limitations. Its duration is relatively short compared with the duration of COPD, so it is more cross-sectional than longitudinal. It was unable to distinguish among varied "natural histories." It assessed primarily the FEV(1), and the natural history of other features of COPD is largely undescribed. With advances in understanding the clinical features of COPD and with the development of evaluating new tools to assess patients with COPD, longitudinal studies evaluating COPD in novel ways and for longer durations are needed.
Chronic bronchitis
Cite
Citations (69)
To explore the risk factors of chronic obstructive pulmonary disease (COPD) in patients with chronic bronchitis in following-up 8 years.The baseline survey of the study was carried out on 1,999 patients with chronic bronchitis screened out from 67,251(15 years or more) rural people in 1992. In 2000, 1,114 patients were reexamined by simple random sampling method.869 (78.0% of 1,114) with complete data entered analysis of this study. Smoking, and family history of COPD were associated significantly positively with the decrement per capita yearly of FEV1(forced expiratory volume in the first second) and/or FEV1/FVC (forced vital capacity) ratio. Ex-smoking decreased the decrement of lung function in smokers. The accumulative incidence of COPD was associated positively with smoking and family history of COPD and negatively with baseline FEV1 and FEV1/FVC. The relative risk of COPD was not significantly different between non-smokers and ex-smokers.For Chinese rural patients with chronic bronchitis, aging, smoking, family history of COPD, lower pulmonary function are independent risk factors of COPD while sex is not one. Ex-smoking can almost decrease the relative risk of COPD to the approximative risk level of non-smoking.
Chronic bronchitis
Vital capacity
Cite
Citations (3)
COPD is common and is mostly caused by smoking. Patients with COPD represent a large proportion of inpatient and outpatient work for the chest physician. COPD encompasses a number of underlying pathologies, including chronic bronchitis and emphysema.
Chronic bronchitis
Pulmonary emphysema
Cite
Citations (23)
Chronic bronchitis
Copd exacerbation
Cite
Citations (26)
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease. Historically, two COPD phenotypes have been described: chronic bronchitis and emphysema. Although these phenotypes may provide additional characterization of the pathophysiology of the disease, they are not extensive enough to reflect the heterogeneity of COPD and do not provide granular categorization that indicates specific treatment, perhaps with the exception of adding inhaled glucocorticoids (ICS) in patients with chronic bronchitis. In this review, we describe COPD phenotypes that provide prognostication and/or indicate specific treatment. We also describe COPD-like phenotypes that do not necessarily meet the current diagnostic criteria for COPD but provide additional prognostication and may be the targets for future clinical trials.
Chronic bronchitis
Cite
Citations (4)
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines over the last few years have stopped emphasizing the categorization of chronic obstructive pulmonary disease (COPD) into emphysema or chronic bronchitis.[1] This happened as a result of the fact that we do not find isolated pure emphysema or a pure chronic bronchitis, clinical COPD is always a mixture of these two entities. That is an example of the evolution of COPD based on available evidence. On the other hand, we are going to have new phenotype nonsmoker COPD. Nonsmoker COPD still remains inadequately covered in GOLD COPD guidelines. The etiology, pathophysiology, clinical presentation, and prognosis may significantly differ in nonsmoker COPD. Therefore, there is need to address this group of COPD more clearly. The traditional COPD research includes GOLD-defined COPD and exclusion of parameters that do not fit in this frame. Over the years, there has been the growth of more and scientific evidence on approach and management of COPD.[2] COPD is mainly attributed to a smoking-related accelerated decline in lung function mainly the forced expiratory volume in 1 s (FEV1). However, recent reports have clearly shown that usual decline in lung function in people having low initial FEV1 may also lead to COPD.[3] It may also mean that people having lung damage due to underlying lung disease of varying etiologies may also develop lung function defects definable as COPD. Recent research has also focused on different phenotypes of COPD. A COPD phenotype is defined as “a single or combination of disease attributes that describe differences between individuals with COPD as they relate to clinically meaningful outcomes (symptoms, exacerbations, response to therapy, rate of disease progression, or death).”[4] COPD may be considered to exist in a variety of phenotypic subgroups and the basis of characterization ranging from demographic factors such as age, gender, obesity to clinical characteristics, and comorbidities of COPD.[567] Although certain distinct COPD phenotypes have been identified over the years such as asthma-COPD overlap syndrome, frequent exacerbators, classic emphysema, and chronic bronchitis, the research so far in this field has been unconvincing. There is no clear consensus on what would be the best approach to diagnose and manage these individual phenotypes. This is mainly due to great heterogeneity of COPD, and for the sake of clarity, we will not emphasize the term “phenotypes” further here. According to Augusti, as far as disease characterization of COPD is concerned, we are moving from characterization by FEV1 towards personalized medicine of COPD. It is likely that the concept of COPD phenotypes is likely to be abandoned in future.[8] In our opinion, to have a comprehensive approach aimed at performing current research and management, COPD should be grouped into two broad groups. One is classic COPD caused by smoking as the main etiological factor. Other is nonsmoker COPD which may be related to biomass fuel, diesel smoke, tuberculosis, silicosis, and others etiologies of COPD where small airways, alveoli are affected as a consequence of significant damage to lung due to a variety of disease processes. This group is more likely to be seen outside the western world. Studies suggest that these patients may behave differently than classic COPD.[9] Some of these diseases may present as restriction in combination with obstruction on lung function tests. Although there may be some overlap, this distinction will help in planning specific research and formulating specific management strategies for this group of patients. Nonsmoker COPD simply means that there is no exposure to tobacco smoke. This does not mean that a person is not exposed to any other form of environmental pollutants or an endogenous ailment. The biomass fuel exposure is one of the main indoor air pollutant studied in this group of patients. In an interesting study conducted by Mohan et al. serum matrix, metalloproteinase-9 and tissue inhibitor of metalloproteinases-1 in COPD due to tobacco smoking were compared with COPD in nonsmokers having exposure to biomass-related indoor air pollution.[10] It was found that protease-antiprotease balance in COPD was similar in tobacco exposure and biomass exposure but was different than the controls. Large population-based studies are available documenting incidence and prevalence of nonsmoker COPD. In Copenhagen city heart study, 8045 individuals with normal lung function at baseline were followed for 25 years. The incidence of COPD among nonsmokers was very low (1% COPD GLOD Stage II or more). In comparison, it was 27% of similar GOLD stage COPD in continuous smokers.[11] The multicenter international burden of obstructive lung disease study showed that the prevalence of nonsmoker ≥II GLOD stage COPD was 5.6%. The prevalence of severe (GOLD Stage III) and very severe (GOLD Stage IV) airway obstruction was significantly lower in nonsmokers (5.9% vs. 14.1%, P = 0.001). Increased age, a prior diagnosis of asthma and among women, lower education levels were associated with an increased risk for COPD among nonsmokers.[12] Obstructive lung disease in Northern Sweden study, a population-based survey of 10,040 adults aged 20–77 in Norrbotten county in Sweden showed that the prevalence of nonsmoker ≥ GLOD Stage II COPD was 3.5% with an overall prevalence of 7% among nonsmokers. Increasing age, a previous diagnosis of asthma and family history of obstructive airway disease were significant risk factors for nonsmoker COPD.[13] Prevalence, risk factors, and other features of nonsmoker COPD in western hemisphere may be different than other parts of the world. This issue of Lung India contains an article on nonsmoker COPD. This observational institution-based cross-sectional study from Allahabad city of India included 200 COPD patients.[14] The proportion of nonsmoker patients was 56.5%. The most important and statistically significant risk factor for nonsmoker COPD was exposure to biomass smoke in 53.9% of patients. Other significant risk factors were treated pulmonary tuberculosis (PTB) in 32.7%, and long-standing asthma in14.2%. Other risk factors present in about 10% of patients were occupational exposure, exposure to outdoor air pollution, and lower respiratory tract infection during childhood. It was also found that as the number of risk factors in nonsmoker COPD patients increased, mean age for detection of COPD decreased. Biomass smoke exposure and treated PTB are important contributors to nonsmoker COPD outside western world especially in countries with high burden of tuberculosis and use of biomass fuel for cooking. We have seen above that pathogenetically biomass-related COPD may be same as smoker COPD. Moreover, smoking may coexist with biomass fuel exposure. A study on coke oven workers and in Southern China showed that the risk of COPD in those with the highest cumulative exposure to coke oven exposure and cigarette smoking was 58-fold as compared to nonsmokers not exposed to coke oven. While the risk of COPD was only 5.8-fold in coke oven exposed versus not exposed to coke oven.[15] Tuberculosis may affect the development of COPD in a variety of ways due to the occurrence of permanent scarring, bronchiectasis, and fibrosis. A systematic review and meta-analysis showed a three-time increased risk for COPD in patients with a history of tuberculosis. The association was strongest in people who never smoked, were <40 years of age and those living in countries with high incidence of tuberculosis.[16] A recent prospective, nested case–control study was conducted on new cases of PTB with initial restrictive respiratory function impairment and treated according to the directly observed treatment short course strategy in Nis city of Serbia.[17] The initial radiological extent of PTB and sputum conversion rate on culture were the most significant predictors for the risk of PTB-associated airflow obstruction. PTB-associated airflow obstruction occurs later, during the reparative processes in active PTB and initial spirometry may be normal or show restriction during treatment phase. Therefore, there is a continuous need for research into group of nonsmoker COPD and due emphasis should be given in current guidelines on diagnosis and management of this group of COPD. Regional researchers should specifically address their most prevalent obstructive airway disease groups rather than recruiting only smoker COPD. Tuberculosis and biomass exposure are very important risk factors for nonsmoker COPD in India. Therefore, nonsmoker COPD requires more attention in country like India where a lot of smoke is present inside and outside a home.
Chronic bronchitis
Etiology
Obstructive lung disease
Cite
Citations (1)
Background/aim: Respiratory and peripheral muscle strength are reduced in chronic obstructive pulmonary disease (COPD). There is a well-known correlation between handgrip strength (HGS) and strenght extremity muscles. Our aim in this study was to measure HGS and investigate the related factors in COPD patients with exacerbation.Materials and methods: Subjects with COPD exacerbation (n = 101) and stable COPD (n = 22), and subjects without COPD (n = 201), were enrolled in this study. Age, sex, and body mass index were similar. HGS was measured using a Vigorimeter. Pulmonary function tests and 6-min walk tests were performed.Results: The mean HGS was significantly lower in subjects with COPD exacerbation than those with stable COPD and subjects without COPD. The mean HGS was similar between stable COPD and non-COPD subjects. The mean 6-min walk distance (6MWD) was significantly lower in subjects with COPD exacerbation than stable COPD. There was a significant correlation between HGS and 6MWD but no correlation between HGS and pulmonary function tests.Conclusion: In subjects with COPD exacerbation, the HGS was lower than that of stable COPD patients, and this difference was not explained by age, comorbidities, severity of obstruction, or smoking. Physical inactivity and steroid use during exacerbation might be possible factors affecting HGS. HGS was moderately correlated with 6MWD in cases of exacerbation. It may be used as a measure of muscle performance in COPD exacerbation, especially when the 6-min walk test cannot be performed
Copd exacerbation
Cite
Citations (17)
Chronic obstructive pulmonary disease (COPD), which encompasses both chronic bronchitis and emphysema, is one of the most common respiratory conditions of adults in the developed world. Despite the high prevalence and enormous cost to healthcare and society, COPD has received scant attention in comparison to other respiratory conditions such as asthma and lung cancer. It is often thought of as a self-inflicted disease. But not all people who smoke develop COPD and not all patients with COPD are smokers. The causes of COPD are different. Its pathogenesis is complex. There are very few effective treatments. Therefore, there is an urgent need to improve present therapy by drugs with new modes of actions. In contrast to many human diseases, chronic bronchitis and emphysema occur seldom in the animal world. Therefore, we have to mimic some characteristic features of these diseases in animals. For this reason, a wide variety of animal models have been developed and are employed in the search for new chemical entities for the treatment of COPD. In the present paper, the experimental models of COPD are critically reviewed.
Chronic bronchitis
Cite
Citations (4)
Chronic bronchitis
Genetic predisposition
Family aggregation
Cite
Citations (134)
Objective To explore the risk factors of chronic obstructive pulmonary disease (COPD) in patients with chronic bronchitis in following-up 8 years. Methods The baseline survey of the study was carried out on 1 999 patients with chronic bronchitis screened out from 67 251 (15 years or more) rural people in 1992. In 2000, 1 114 patients were reexamined by simple random sampling method. Results 869 (78.0% of 1 114 ) with complete data entered analysis of this study. Smoking, and family history of COPD were associated significantly positively with the decrement per capita yearly of FEV 1 (forced expiratory volume in the first second) and/or FEV 1/FVC (forced vital capacity) ratio. Ex-smoking decreased the decrement of lung function in smokers. The accumulative incidence of COPD was associated positively with smoking and family history of COPD and negatively with baseline FEV 1 and FEV 1/FVC. The relative risk of COPD was not significantly different between non-smokers and ex-smokers. Conclusion For Chinese rural patients with chronic bronchitis, aging, smoking, family history of COPD, lower pulmonary function are independent risk factors of COPD while sex is not one. Ex-smoking can almost decrease the relative risk of COPD to the approximative risk level of non-smoking.
Chronic bronchitis
Vital capacity
Cite
Citations (0)