American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 329-332, (2002)
© 2002 American Thoracic Society
Can GOLD Stage 0 Provide Information of Prognostic Value in Chronic Obstructive Pulmonary Disease?
Jørgen Vestbo and
Peter Lange
Department of Respiratory Medicine, Hvidovre University Hospital, Hvidovre, Denmark
Correspondence and requests for reprints should be addressed to Dr. J. Vestbo, Department of Respiratory Medicine 223, Hvidovre University Hospital, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark. E-mail: joergen.vestbo{at}hh.hosp.dk
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ABSTRACT
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In the recently published guidelines of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) for chronic obstructive pulmonary disease (COPD), the staging system included a Stage 0 for subjects without airways obstruction but with respiratory symptoms, denoting these subjects "at risk" for COPD. Our aim was to validate this staging approach using data from three surveys in The Copenhagen City Heart Study, in which a sample of the general population was examined at baseline and in which, after 5 and 15 years, spirometry was performed at all surveys. Criteria for GOLD Stage 0 was fulfilled by 5.8% of the total adult population and 7.2% of smokers. After 5 and 15 years, 13.2 and 20.5%, respectively, of smokers with GOLD Stage 0 had developed COPD fulfilling criteria for GOLD Stage 1 or worse. This was the case for 11.6 and 18.5%, respectively, of smokers without respiratory symptoms. Further analyses using multivariate logistic regression analysis confirmed that GOLD Stage 0 was not identifying subsequent airways obstruction. When analyzing FEV1 decline, Stage 0 carried a risk of excess decline. GOLD Stage 0 was not a stable feature, which may explain the lack of predictive value. In the Western world, smoking is still in itself the most important indicator of risk of COPD, and alternative markers of susceptibility in the population must be investigated.
Key Words: COPD • epidemiology • guidelines • prognosis
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INTRODUCTION
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Global guidelines for chronic obstructive pulmonary disease (COPD), the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, were published in 2001 for the purpose of educating about COPD and setting global standards for the diagnosis, management, and prevention of COPD (1, 2). Much of the contents of the guidelines differ little from previously published guidelines (3–5). However, as a new approach GOLD introduced a Stage 0 in the staging system for COPD. Stage 0 represents absence of airflow limitation but presence of symptoms, e.g., cough and sputum. This stage is meant to include subjects "at risk" for developing COPD later in life.
The introduction of this new stage is based on symptoms to some degree being markers of susceptibility, a topic of debate in itself (6, 7). Symptoms are, however, easily assessed and standardized, and well-validated questionnaires are available. Inherent in all staging systems is the notion that patients move from one stage to the next, and for chronic diseases such as COPD this means from low stages upwards. For GOLD Stage 0 to be meaningful, this stage should be able to identify patients with a high risk of subsequently developing airways obstruction and GOLD Stage 1+, and it should be expected that most patients with COPD Stage 1+ have "passed through" Stage 0 during the development of their disease.
Because little evidence has been published supporting the use of a Stage 0, we wished to test the usefulness of Stage 0 using data from a large population-based panel study with information available over several years: The Copenhagen City Heart Study.
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METHODS
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All subjects included in this study participated in the Copenhagen City Heart Study, a prospective epidemiologic study initiated in 1976–1978 (8, 9). A sample of 19,698 individuals, aged 20 years or older, was selected at random after age stratification in 10-year age groups from residents of Copenhagen and invited to all three surveys if still alive. A total of 14,223 attended the first examination from 1976 through 1978 (response rate of 74%); 12,698 attended the second examination from 1981 through 1983 (response rate of 70%), and of these 11,135 had participated in the initial survey and this corresponds to 83.8% of those examined at first survey and alive at the time of the second survey. A total of 10,049 attended the third examination from 1991 through 1994 (response rate of 58%), 7,073 subjects had participated in the initial survey and this corresponds to 70.5% of those examined at first survey and alive at the time of the third survey. Subjects with self-reported asthma at any of the surveys were excluded.
At the first and second examinations, FEV1 and FVC were measured with an electronic spirometer (model N 403; Monaghan, Littleton, CO), which was calibrated daily with a 1-L syringe and weekly against a water-sealed Godard spirometer. At the third examination, a dry wedge spirometer (Vitalograph, Maidenhead, UK) calibrated daily with a 1-L syringe was used. At each examination three sets of values were obtained, and as a criterion for correct performance of the procedure at least two measurements differing by less than 5% had to be produced. The highest measurements of FEV1 and FVC were used in the analyses as absolute values and as percentage of predicted values, using internally derived reference values based on a subsample of healthy never-smokers (9). Women: FEV1 (ml) = 410 - 27.6 x age (yr) + 21.2 x height (cm). Men: FEV1 (ml) = -469 - 35.2 x age (yr) + 32.0 x height (cm). Productive cough was considered present at baseline when subjects answered affirmatively to the question, "Do you cough up phlegm (in the morning or during the day) for as much as 3 months every year?" At each examination, all subjects reported whether they were current smokers, ex-smokers, or never-smokers; their present amount and type of tobacco smoked; smoking history; and if they inhaled at present.
Staging was done according to GOLD, although we did not have information on respiratory failure available. For this reason Stage 2 is not divided into 2A and 2B. Stages are defined as follows: Stage 0, presence of productive cough, FEV1/FVC > 0.7; Stage 1, FEV1/FVC < 0.7, FEV1  80%pred; Stage 2, FEV1/FVC < 0.7, FEV1 < 80%pred, and FEV1 30%pred; Stage 3, FEV1/FVC < 0.7, FEV1 < 30%pred. For comparing prevalence of COPD Stage 1+ at subsequent surveys depending on absence/presence of Stage 0 at baseline, chi-square tests were used in simple cross-tabulations. For taking into account variables that may act as confounders, a multivariate logistic regression model was used. The following variables were considered as potential confounders: age (-50, 51–60, 61–70, 71+), sex, smoking (y/n), inhalation (y/n), and changes in smoking habits (smoking cessation y/n).
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RESULTS
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Information necessary for staging subjects participating in the first survey in 1976–1977 was available for 13,108 of the 13,393 participants without self-reported asthma at any survey. Baseline demographics for all participants are shown in Table 1
for each stage. Of the 11,903 subjects without asthma participating in the second survey in 1981–1983, 10,438 had participated in the first survey, and of these 10,108 provided sufficient information for grading according to GOLD. Of the 9,454 subjects without asthma participating in the third survey in 1992–94, 6,553 had participated in the first survey, and of these 6,217 provided sufficient information for grading according to GOLD. Thus, in the following analyses, numbers may vary slightly depending on the survey used for follow-up.
At baseline 7.1% of men and 4.8% of women had GOLD Stage 0; among these, mean age for women and men was 52.4 and 52.1 years, respectively, and 72.9% of women and 82.8% of men were smokers. GOLD Stage 1, 2, and 3 was found in 6.7%, 11.0%, and 0.4% of men and 3.7%, 7.6%, and 0.1% of women, respectively.
Development of COPD after 5 and 15 years is shown in Table 2
. Numbers and percentages are shown for subjects without COPD and with Stage 0 at baseline. Results are shown for the total population and for smokers at baseline. As shown in the upper part of the table, little difference was seen after 5-year follow-up. The difference between the progression in subjects without COPD and COPD Stage 0 in 5 years was not statistically significant. As shown in the lower part of the table, COPD Stage 1–3 after 15-year follow-up was more frequent in Stage 0. The difference between the progression in subjects without COPD and COPD Stage 0 in 15 years was statistically significant (chi-square, p = 0.01 for the total population and p = 0.02 for smokers). These findings did not differ according to sex.
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TABLE 2. Prevalence of different stages of copd after 5 and 15 years in subjects without copd and with copd stage 0 at baseline
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Table 3
shows the results of multivariate logistic regression models where the outcome was presence of COPD GOLD Stage 1+ at follow-up after 5 and 15 years. Again, the effect of GOLD Stage 0 at baseline was small. Restricting analyses to smokers only did not significantly change any of the odds ratios (ORs); for GOLD Stage 0, OR was 1.1 (95% confidence interval [CI] 0.9–1.5) and 1.1 (95% CI 0.8–1.5) after 5 and 15 years, respectively. Restricting analyses to subjects more than 50 years of age at baseline did not change the predictive value of GOLD Stage 0. In models similar to that shown in Table 3, OR for COPD Stage 1+ after 5 years was 1.07 (95% CI 0.66–1.74) and after 15 years 1.14 (95% CI 0.77–1.72) among those over 50 years of age.
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TABLE 3. Results of multivariate logistic regression models where the outcome was presence of copd gold stage 1+ at follow-up after 5 and 15 years
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To look at predictive value of GOLD Stage 0 in more detail, we examined FEV1 decline between the first and the second survey. We did not look at decline between the first and the third survey as this decline to a higher extent is affected by selection bias such as survival and ill health effects. The crude declines in subjects without COPD and with Stage 0 were 36.8 ml/year and 59.6 ml/year, respectively. In smoking men more than 50 years of age at baseline presence of Stage 0 increased FEV1 decline by 19 ml/year (p = 0.08) after adjusting for inhalation habits; in nonsmokers the increase was 71 ml/year (p = 0.01) based on only 17 subjects with Stage 0. In women the corresponding excess declines attributable to Stage 0 were 19 ml/year (p = 0.04) and 13 ml/year (p = 0.51) for smokers and nonsmokers, respectively.
GOLD Stage 0 was not constant. After 5 years 303 subjects (39.6%) with Stage 0 at baseline reported no chronic phlegm. Young age, female sex, and smoking cessation were associated with disappearance of Stage 0. After 15 years only 49.4% of those in Stage 0 were still in Stage 0 or had Stage 1+. In a logistic regression model only smoking cessation could predict the subsequent absence of chronic symptoms with an OR of 5.7 (95% CI 3.5–9.2). Presence of GOLD Stage 0 did not increase quit rates among smokers at baseline, neither at 5-year follow-up nor after 15 years.
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DISCUSSION
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This study clearly indicates that Stage 0 is unsuitable for pointing out the population "at risk" for development of COPD in a random population in general and among smokers in the general population in particular. The study does not provide information as to whether the definition of an "at risk" group enables a better spread of information about the disease or facilitates promotion of smoking cessation, thus preventing the development of the disease.
At first it may seem contradictory that we find no prognostic value of productive cough in smokers, as we have previously found chronic mucus hypersecretion (CMH) to be strongly associated with both FEV1 decline and subsequent hospitalization because of COPD (7). Indeed, the analyses were done on the same dataset; also, in the present analyses, we did find an effect of chronic phlegm on FEV1 decline. The approaches, however, differ significantly. The excess decline in FEV1 found in this study does not lead to significantly more COPD after 5 and 15 years of follow-up. This could indicate that our follow-up period is too short; indeed, 5 years may be insufficient to look at development of COPD. A follow-up of 15 years is nevertheless a quite lengthy period of time. If our excess declines of 15–20 ml/year in Stage 0 compared with no symptoms are true findings, 15 years would lead to an excess loss of 225–300 ml, which would be expected to have an impact on COPD incidence. Our analyses have also shown that Stage 0 is an unstable feature and this may be the main explanation for the lack of predictive value of staging based on information from one time-point only. In our previous analyses we also found disappearance of mucus hypersecretion to be less strongly associated with FEV1 decline than persistent mucus hypersecretion (7). Also, in the present study only subjects with a normal FEV1/FVC ratio are included in GOLD Stage 0, and although we did adjust for level of FEV1 in our previous analyses (7) it seems that a productive cough in the absence of airways obstruction does not convey the same significant risk, whereas CMH in addition to airways obstruction does. In fact, these findings may explain why the seminal study by Fletcher and coworkers (6) found no effect at all of CMH on subsequent FEV1 decline whereas we did (7); in the British study a cohort of working men were included and in their text Fletcher and coworkers explicitly state that they are studying the early phases of COPD. In contrast, our study participants were recruited from the general population and included older subjects and obviously subjects with obvious COPD. In this setting CMH may have a larger impact, which is supported by the fact that in the Copenhagen study showing an association between CMH and mortality from COPD, the association between CMH and COPD mortality was most obvious in subjects with severe COPD (10).
The idea of identifying subjects at risk for COPD is not new. Serial measurements of FEV1 can presumably identify COPD at a point in time where the impact of the disease is generally limited, and this concept of early detection of COPD has been promoted for several years (11). Because serial FEV1 measurements for detection of COPD require, e.g., annual measurements for at least 3–5 years, other measures of earlier and more subtle changes in airways function have been examined in some detail. The single-breath nitrogen test was regarded as a promising candidate in the 1970s and 1980s but turned out to be too unspecific for subsequent use in both epidemiology and clinical medicine (12–14). This test, as well as others (e.g., mid-expiratory flows), may well be able to demonstrate small changes in the airways; however, these changes are not indicative of more serious changes taking place and thus they lack predictive value.
We found no sex differences regarding the utility of GOLD Stage 0. This is not trivial, as different indices may have different prognostic value in men and women. We have previously hypothesized that there may be a sex bias in reporting phlegm because this symptom is significantly less frequent in men than in women (7). This difference could have meant that symptom reporting would reflect different perceptions and that this would lead to differences in prognosis; however, this was not seen. In the future where COPD is believed to become a much more prevalent disease among women (1, 15), who may even be more susceptible to developing COPD than men (15, 16), future markers of susceptibility need to be thoroughly evaluated in both men and women.
Our study has several limitations, the most significant of which is probably location. GOLD guidelines are for global use and our study only examines the value of GOLD Stage 0 in an urban population where smoking is responsible for the vast majority of COPD diagnosed. We cannot preclude that using GOLD Stage 0 in a different setting may have prognostic value: to our knowledge there are, nevertheless, no studies supporting this. We have only limited information on occupational exposures and it could be hypothesized that symptoms in occupationally exposed subjects would better identify subjects at risk than symptoms in smokers. To our knowledge, there are no data in the literature to support such a hypothesis. Also, we only have limited information available on symptoms at baseline. Whereas a more detailed description of symptoms at baseline would be preferable from the point of giving a more detailed description of the population studied, it seems unlikely that we have missed subjects with substantial symptoms, and inclusion of more subjects with minor symptoms would presumably only further dilute any relationship between symptoms at baseline and subsequent airways obstruction.
In conclusion, it seems that GOLD Stage 0 is of little help in identifying subjects at risk for COPD. The population at risk still mainly consists of smokers and at present we do not have clinical measures available that seem helpful in identifying subjects susceptible to smoking—smokers "at particular risk."
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Acknowledgments
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This study was supported by The Danish Lung Association and The Danish Heart Foundation.
Received in original form December 14, 2001;
accepted in final form April 30, 2002
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I. Cerveri, S. Accordini, A. Corsico, M.C. Zoia, L. Carrozzi, L. Cazzoletti, M. Beccaria, A. Marinoni, G. Viegi, and R. de Marco
Chronic cough and phlegm in young adults
Eur. Respir. J.,
September 1, 2003;
22(3):
413 - 417.
[Abstract]
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The pharmacoepidemiology of COPD: Recent advances and methodological discussion
Eur. Respir. J.,
September 1, 2003;
22(43_suppl):
1S - 44s.
[Full Text]
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D. Stanescu
Identifying Smokers at Risk of COPD and GOLD
Am. J. Respir. Crit. Care Med.,
August 15, 2003;
168(4):
500 - 500.
[Full Text]
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S.T. Weiss, D.L. DeMeo, and D.S. Postma
COPD: problems in diagnosis and measurement
Eur. Respir. J.,
June 1, 2003;
21(41_suppl):
4S - 12s.
[Abstract]
[Full Text]
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I. Cerveri, A. Corsico, M. C. Zoia, J. Vestbo, and P. Lange
Gold Stage 0
Am. J. Respir. Crit. Care Med.,
March 15, 2003;
167(6):
936 - 936.
[Full Text]
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M. J. Tobin
Chronic Obstructive Pulmonary Disease, Pollution, Pulmonary Vascular Disease, Transplantation, Pleural Disease, and Lung Cancer in AJRCCM 2002
Am. J. Respir. Crit. Care Med.,
February 1, 2003;
167(3):
356 - 370.
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Copyright © 2002 American Thoracic Society
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ABSTRACT
INTRODUCTION