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Int J Chron Obstruct Pulmon Dis · Jan 2016
New evidence of increased risk of rhinitis in subjects with COPD: a longitudinal population study.
- Joel Bergqvist, Anders Andersson, Anna-Carin Olin, Nicola Murgia, Linus Schiöler, Mogens Bove, and Johan Hellgren.
- Department of Otorhinolaryngology, Head and Neck Surgery, Institute of Clinical Sciences.
- Int J Chron Obstruct Pulmon Dis. 2016 Jan 1; 11: 2617-2623.
BackgroundThe aim of this population-based study was to investigate the risk of developing noninfectious rhinitis (NIR) in subjects with chronic obstructive pulmonary disease (COPD).Materials And MethodsThis is a longitudinal population-based study comprising 3,612 randomly selected subjects from Gothenburg, Sweden, aged 25-75 years. Lung function was measured at baseline with spirometry and the included subjects answered a questionnaire on respiratory symptoms. At follow-up, the subjects answered a questionnaire with a response rate of 87%. NIR was defined as symptoms of nasal obstruction, nasal secretion, and/or sneezing attacks without having a cold, during the last 5 years. COPD was defined as a spirometry ratio of forced expiratory volume in 1 second divided by forced vital capacity (FEV1/FVC) <0.7. Subjects who reported asthma and NIR at baseline were excluded from the study. The odds ratios for developing NIR (ie, new-onset NIR) in relation to age, gender, body mass index, COPD, smoking, and atopy were calculated.ResultsIn subjects with COPD, the 5-year incidence of NIR was significantly increased (10.8% vs 7.4%, P=0.005) and was higher among subjects aged >40 years. Smoking, atopy, and occupational exposure to gas, fumes, or dust were also associated with new-onset NIR. COPD, smoking, and atopy remained individual risk factors for new-onset NIR in the logistic regression analysis.ConclusionsThis longitudinal population-based study of a large cohort showed that COPD is a risk factor for developing NIR. Smoking and atopy are also risk factors for NIR. The results indicate that there is a link present between upper and lower respiratory inflammation in NIR and COPD.
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