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      Determinants of airflow limitation in Danish adults – findings from the Health2006 cohort

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          Abstract

          Background and aim

          Airflow limitation may be found in patients with both asthma and COPD and is often associated with more symptoms and poorer outcome. We aimed to identify factors associated with airflow limitation in a well-characterized, population-based sample of adults.

          Methods

          From the Health2006 cohort, we selected participants aged ≥35 years at enrolment (n=2,959). Airflow limitation was defined as FEV 1/FVC < lower limit of normal. Participants with (cases) and without (controls) airflow limitation were compared with regard to self-reported symptoms, medical history, atopy, lung function and exhaled nitric oxide. Between-group differences were analyzed using Chi-square and Mann–Whitney U tests, and effect size was estimated by logistic regression (reported as OR and 95% CI).

          Results

          We identified 313 cases, majority of which were female, reported poor overall health, physically inactivity and experienced respiratory symptoms within the previous year. The presence of airflow limitation was associated with BMI (OR 3.1 for overweight, P<0.001, CI 1.97–4.78), age (OR 2.3, P<0.001 for age 55+, CI 1.7–3.2), tobacco exposure (OR 1.6, P=0.01, CI 1.1–2.32, and OR 1.76, P=0.019, CI 1.2–2.3 for former and current smokers, respectively), sex (OR 1.6 for being female, P=0.002, CI 1.2–2.2), presence of specific IgE to common aeroallergen(s) (OR 1.4, P=0.041, CI 1.2–2.0), and ever being diagnosed with asthma (OR 1.6, P=0.003, CI 1.3–2.0).

          Conclusion

          Apart from tobacco exposure and age, the presence of airflow limitation was associated with being overweight, female, sensitized to common aeroallergens or ever having a diagnosis of asthma.

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          Most cited references 31

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          Acute and chronic effects of cigarette smoking on exhaled nitric oxide.

          Cigarette smoking is associated with an increased risk of respiratory tract infections, chronic airway disease, and cardiovascular diseases, all of which may be modulated by endogenous nitric oxide (NO). We have investigated whether cigarette smoking reduces the production of endogenous NO. We compared exhalations of 41 current cigarette smokers with normal lung function and 73 age-matched non-smoking controls. Peak exhaled NO levels were measured by a modified chemiluminescence analyzer. The effects of inhaling a single cigarette in smokers were also measured. In control subjects we also measured the effects of inhalation of NO itself and carbon monoxide, both constituents of tobacco smoke. Peak exhaled NO concentrations were significantly reduced in smokers (42 +/- 3.9 compared with 88 +/- 2.7 parts per billion in nonsmokers, p < 0.01), with a significant relation between the exhaled NO and cigarette consumption (r = 0.77, p < 0.001). Smoking a single cigarette also significantly (p < 0.02), but transiently, reduced exhaled NO. Inhalation of carbon monoxide and NO had no effect on exhaled NO in normal subjects. Cigarette smoking decreased exhaled NO, suggesting that it may inhibit the enzyme NO synthase. Since endogenous NO is important in defending the respiratory tract against infection, in counteracting bronchoconstriction and vasoconstriction, and in inhibiting platelet aggregation, this effect may contribute to the increased risks of chronic respiratory and cardiovascular disease in cigarette smokers.
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            Obesity and asthma: an association modified by age of asthma onset.

            Studies of asthma phenotypes have identified obesity as a component of a group characterized by a high proportion of subjects with adult-onset asthma. However, whether age of asthma onset modifies the association between obesity and asthma is unknown. We sought to compare the associations between body mass index (BMI) categories with physiological, inflammatory, and clinical parameters across age of asthma onset phenotypes; and to compare the rate of BMI change in relation to asthma duration, by age of onset asthma phenotypes. From the Severe Asthma Research Program, we defined age of asthma onset as early (<12 years of age) and late (≥12 years of age). Comparisons of BMI categories were done within age-of-onset groups, and obesity was also compared across these groups. Multivariable logistic regression analysis was done to evaluate the association between BMI categories with health care use and respiratory symptoms and multivariable linear regression for the association between duration of asthma and weight gain (BMI change per year). An interaction between obesity and age of asthma onset was included in the multivariable analyses. The study population consisted of 1049 subjects, and the median age for asthma onset was 10 years (interquartile range, 4-25 years); 48% had late-onset asthma (≥12 years of age), and 52% had early-onset asthma (<12 years of age). Compared with obese subjects with late-onset asthma, obese subjects with early-onset asthma had more airway obstruction, bronchial hyperresponsiveness, and higher odds ratios of ever having 3 or more previous oral steroid tapers per year or intensive care unit admissions for asthma per preceding year (interactions between obesity and age of asthma onset were P = .055 and P = .02, respectively). In subjects with early-onset asthma but not in subjects with late-onset asthma, there was a significant association between increasing BMI and duration of asthma after adjusting for confounders. The interaction between asthma duration and age of asthma onset was a P value of less than .01. Asthmatic subjects are differentially affected by obesity based on whether they had asthma early (<12 years of age) or later in life. These results highlight the need to understand obesity as a comorbidity that affects specific clinical phenotypes and not all asthma subjects alike. Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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              Comparison of a beta 2-agonist, terbutaline, with an inhaled corticosteroid, budesonide, in newly detected asthma.

              The presence of airway inflammation even in mild asthma points to the potential value of antiinflammatory therapy. We compared the effect of an inhaled corticosteroid, budesonide, with that of an inhaled beta 2-agonist, terbutaline, in the long-term treatment of newly detected asthma. We studied 103 patients (29 male and 74 female patients 15 to 64 years old) in whom asthma had appeared within the previous year. The patients were randomly assigned in blinded fashion to two treatment groups: one to receive 600 micrograms of inhaled budesonide twice a day, and the other to receive 375 micrograms of inhaled terbutaline twice a day. The study period was two years. After six weeks of treatment, the patients treated with budesonide tolerated inhaled histamine better than the patients treated with terbutaline (a difference of one doubling dose step, P less than 0.001), and the difference was sustained. Patients' diaries kept during the first three months of the study and during the last month of the first and second years showed budesonide to be more effective than terbutaline in improving peak expiratory flow in the morning (average increase from the pretreatment value, 32.8 liters per minute for budesonide vs. 4.8 liters per minute for terbutaline; P less than 0.001) and in the evening (P less than 0.01). Budesonide was also more effective in reducing the symptoms of asthma (P less than 0.01) and the use of supplemental beta 2-agonist medication (P less than 0.01). Ten patients were withdrawn from the terbutaline group because treatment was insufficiently effective, whereas only one dropped out of the budesonide group. The adverse reactions to both treatments were few and mild. Antiinflammatory therapy with inhaled budesonide is an effective first-line treatment for patients with newly detected, mild asthma, and it is superior to the use of terbutaline in such patients.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2019
                26 March 2019
                : 14
                : 713-718
                Affiliations
                [1 ]Department of Respiratory Medicine, Hvidovre Hospital, Hvidovre, Denmark, csulrik@ 123456dadlnet.dk
                [2 ]Center for Clinical Research and Disease Prevention, Bispebjerg and Frederiksberg Hospital, The Capital Region, Copenhagen, Denmark
                [3 ]Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark, csulrik@ 123456dadlnet.dk
                Author notes
                Correspondence: Charlotte Suppli Ulrik, Department of Respiratory Medicine, Respiratory Research Unit Hvidovre, DK-2650 Hvidovre, Denmark, Email csulrik@ 123456dadlnet.dk
                Article
                copd-14-713
                10.2147/COPD.S173815
                6440446
                © 2019 Baarnes et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Respiratory medicine

                risk factors, copd, asthma, cohort study, epidemiology

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