Asthma and lower airway disease
Fixed airflow obstruction due to asthma or chronic obstructive pulmonary disease: 5-year follow-up

https://doi.org/10.1016/j.jaci.2010.01.003Get rights and content

Background

Both smokers and patients with asthma can experience fixed airflow obstruction, which is associated with distinctive patterns of airway pathology. The influence of fixed airflow obstruction on the prognosis of these patients is unknown.

Objective

We sought to investigate lung function decline and exacerbations in a 5-year prospective study of subjects with fixed airflow obstruction due to asthma or chronic obstructive pulmonary disease (COPD). We also sought to explore correlations between functional, pathological, and clinical features.

Methods

Patients with fixed airflow obstruction due to asthma (n = 16) or COPD (n = 21) and a control group of asthmatic patients with fully reversible airflow obstruction (n = 15) were followed for 5 years.

Results

The rates of decline in FEV1 were similar in patients with fixed airflow obstruction caused by asthma (−49.7 ± 10.6 mL/y) or COPD (−51.4 ± 9.8 mL/y) and were higher than in asthmatic patients with reversible airflow obstruction (−18.1 ± 10.1 mL/y, P < .01). Exacerbation rates were also higher in patients with fixed airflow obstruction caused by asthma (1.41 ± 0.26 per patient-year) or COPD (1.98 ± 0.3 per patient-year) compared with those seen in asthmatic patients with reversible airflow obstruction (0.53 ± 0.11 per patient-year, P < .01). Baseline exhaled nitric oxide levels and sputum eosinophil counts correlated with the FEV1 decline in asthmatic patients with fixed airflow obstruction. By contrast, baseline sputum neutrophil counts, emphysema scores, comorbidities, and exacerbation frequency correlated directly and pulmonary diffusion capacity correlated inversely with the FEV1 decline in patients with COPD.

Conclusion

In both patients with asthma and those with COPD, fixed airflow obstruction is associated with increased lung function decline and frequency of exacerbations. Nevertheless, the decline in lung function entails the specific pathological and clinical features of the underlying diseases.

Section snippets

Study population

The study population consisted of the previously described11 cohort of patients with fixed airflow obstruction due to asthma (n = 19) or COPD (n = 27). For consistency, in the present follow-up study we maintained the same terminology: fixed airflow obstruction due to asthma or COPD. The presence of fixed airflow obstruction, both in patients with asthma and those with COPD, was defined as a postbronchodilator FEV1/forced vital capacity ratio of less than 70% in baseline stable conditions

Results

Of the 46 patients with fixed airflow obstruction constituting the population of the original cross-sectional study,11 80% completed the 5-year follow-up (21 with a history of COPD and 16 with a history of asthma). Nine patients did not complete the study for the following reasons: 4 died (3 patients with a history of COPD and 1 with a history of asthma, P > .5), and 5 patients (3 patients with a history of COPD and 2 with a history of asthma, P > .5) refused consent.

Demographic and baseline

Discussion

This is a 5-year follow-up study conducted in a cohort of patients previously described cross-sectionally as having fixed airflow obstruction with either a history of asthma or COPD. We found that patients with fixed airflow obstruction due to either COPD or asthma had a greater postbronchodilator FEV1 decline compared with that seen in asthmatic patients with reversible airflow obstruction. The rate of lung function decline was similar in patients with fixed airflow obstruction due to asthma

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    Supported by the Italian Ministry of Health and the Italian Ministry of Education (MURST).

    Disclosure of potential conflict of interest: M. Contoli has received consulting fees from Chiesi Farmaceutici and has received lecture fees from Boehringer Ingelheim and AstraZeneca. S. Baraldo has received lecture fees from Boehringer Ingelheim. M. Romagnoli has received lecture fees from AstraZeneca. G. Caramori has received lecture fees from Sigma Tau, has received research support from Novartis, and has served as an expert witness for GlaxoSmithKline. M. Saetta has received lecture fees from AstraZeneca, Farmindustria, GlaxoSmithKline, Abbott Laboratories, and Boehringer Ingelheim and has received research support from GlaxoSmithKline and AstraZeneca. L. M. Fabbri has received fees for lecturing, consultancies, and advisory boards from Nycomed, AstraZeneca, Boehringer Ingelheim, Chiesi Farmaceutici, GlaxoSmithKline, Merck Sharp & Dohme, Novartis, Roche, and Pfizer and has received research support from Chiesi Farmaceutici, Nycomed, Boehringer Ingelheim, Pfizer, Roche, and Novartis. A. Papi has received fees for lecturing, consultancies, and the advisory board from Chiesi Farmaceutici; fees for lecturing and consultancies from GlaxoSmithKline; fees for lecturing from AstraZeneca, Boehringer Ingelheim, and Merck Sharp & Dohme; and research support from AstraZeneca, Chiesi Farmaceutici, Boehringer Ingelheim, and Merck Sharp & Dohme. The rest of the authors have declared that they have no conflict of interest.

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