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BMC Pulm Med. 2019 May 9;19(1):90. doi: 10.1186/s12890-018-0765-7.

Annual decline in forced expiratory volume and airway inflammatory cells and mediators in a general population-based sample.

Author information

1
Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. natalia.kononova@medisin.uio.no.
2
Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
3
Department of Respiratory Medicine, Oslo University Hospital, Oslo, Norway.
4
Unit of Medical Biochemistry, Division of Diagnostics and Technology, Akershus University Hospital, Lørenskog, Norway.
5
Department of Internal Medicine, Diakonhjemmet Hospital, Oslo, Norway.
6
Institute for Experimental Medical Research, Oslo University Hospital, Ullevål, Oslo, Norway.
7
Department of Pulmonology, Division of Medicine, Akershus University Hospital, Lørenskog, Norway.

Abstract

BACKGROUND:

Few studies have examined the relationships between sputum inflammatory markers and subsequent annual decline in forced expiratory volume in 1 s (dFEV1). This study investigated whether indices of airway inflammation are predictors of dFEV1 in a general population-based sample.

METHODS:

The study, conducted from 2003 to 2005, included 120 healthy Norwegian subjects aged 40 to 70 years old. At baseline, the participants completed a self-administered respiratory questionnaire and underwent a clinical examination that included spirometry, venous blood sampling, and induced sputum examination. From 2015 to 2016, 62 (52%) participants agreed to a follow-up examination that did not include induced sputum examination. Those with a FEV1/forced vital capacity (FVC) ratio <  0.70 underwent a bronchial reversibility test. The levels of cytokines, pro-inflammatory M1 macrophage phenotypes were measured in induced sputum using bead-based multiplex analysis. The associations between cytokine levels and dFEV1 were then analysed.

RESULTS:

The mean dFEV1 was 32.9 ml/year (standard deviation 26.3). We found no associations between dFEV1 and the baseline indices of sputum inflammation. Seven participants had irreversible airflow limitation at follow-up. They had lower FEV1 and gas diffusion at baseline compared with the remaining subjects. Moreover, two of these individuals had a positive reversibility test and sputum eosinophilia at baseline.

CONCLUSIONS:

In this cohort of presumably healthy subjects, we found no associations between sputum inflammatory cells or mediators and dFEV1 during 10 years of follow-up.

KEYWORDS:

Airway inflammation; Annual decline in forced expiratory volume; Healthy individuals; Induced sputum; Sputum cells; Sputum cytokines and chemokines

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