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      International Journal of COPD (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

      39,063 Monthly downloads/views I 2.893 Impact Factor I 5.2 CiteScore I 1.16 Source Normalized Impact per Paper (SNIP) I 0.804 Scimago Journal & Country Rank (SJR)

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      Exhaled nitric oxide in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis

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          Abstract

          Background

          Fractional exhaled nitric oxide (FENO) is a useful and noninvasive biomarker for eosinophilic airway inflammation, particularly in asthma. However, its utility in chronic obstructive pulmonary disease (COPD) remains controversial. In this study, we performed a systematic review and meta-analysis to evaluate FENO levels in COPD.

          Methods

          A search of PubMed, Embase, Cochrane Library, and clinical trial registry was conducted from inception to January 2018. Studies were included if they reported FENO levels in patients with COPD and healthy controls. We then extracted relevant information and analyzed data. Standard mean difference (SMD) with 95% confidence interval (CI) was applied in this meta-analysis.

          Results

          A total of 2,073 studies were reviewed for eligibility, with 24 studies pooled for analysis. The FENO levels in patients with COPD were elevated mildly compared with healthy controls (SMD 1.28, 95% CI 0.60–1.96). A similar result was also observed in stable COPD, with an SMD of 1.21 (95% CI 0.47–1.96). On the other hand, we found no association between FENO levels and exacerbated COPD. Additionally, for patients with COPD, ex-smokers had higher levels of FENO than current smokers (SMD 2.05, 95% CI 1.13–2.97).

          Conclusion

          Our studies demonstrated a mild elevation of FENO in COPD, and the association between exacerbated COPD and FENO levels needs to be further explored. The potential mechanism is still unknown and conflicting.

          Most cited references38

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          Prevalence of comorbidities in patients with chronic obstructive pulmonary disease.

          Mario Cazzola, Gianluca Biscione, Emiliano Sessa … (2009)
          Chronic obstructive pulmonary disease (COPD) is associated with many comorbidities, but the percentage of COPD patients who develop comorbidities has not been clearly defined. We aimed to examine the relationship between COPD and comorbidities using information obtained from the Health Search Database (HSD) owned by the Italian College of General Practitioners (SIMG), which stores information on about 1.5% of the total Italian population served by general practitioners. We conducted a population-based retrospective study using information obtained from the HSD. The software system used codes all the diagnostic records using the 9th Revision of the International Classification of Diseases. Compared to the non-COPD people, COPD patients were at increased risk for cardiovascular events [ischemic heart disease (6.9% in the general population vs. 13.6% in COPD patients), cardiac arrhythmia (6.6% in the general population vs. 15.9% in COPD patients), heart failure (2.0% in the general population vs. 7.9% in COPD patients), and other forms of heart disease (10.7% in the general population vs. 23.1% in COPD patients); with a higher impact of COPD in the elderly]; non-psychotic mental disorders, including depressive disorders (29.1% in the general population vs. 41.6% in COPD patients; with a higher impact of COPD on women aged <75 years); diabetes mellitus (10.5% in the general population vs. 18.7% in COPD patients); osteoporosis (10.8% in the general population vs. 14.8% in COPD patients), with a higher impact of COPD on women aged <75 years, and malignant pulmonary neoplasms (0.4% in the general population vs. 1.9% in COPD patients). Our results indicate that COPD is a risk factor for these comorbid conditions. Copyright 2010 S. Karger AG, Basel.
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            Inflammatory cells and mediators in bronchial lavage of patients with chronic obstructive pulmonary disease.

            B Balbi, M Majori, Claudio Donner … (1998)
            Cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD). Although the precise sequence of events that leads a smoker to experience airway obstruction is not completely clear, airway inflammation is a relevant factor. To investigate airway inflammation, 12 nonatopic smoking COPD patients with a forced expiratory volume in one second (FEV1) < or = 75% predicted and 10 normal nonsmoking subjects (NS) were studied with bronchoscopy and bronchial lavage (BL). Serum immunoglobulin (Ig)E levels of COPD patients correlated with the smoking history (r=0.7, p=0.008). In BL of COPD patients there was an increase of neutrophils (median, range) (COPD 62.6x10(3), 1.2-323, NS 1.35, 0-19.2, p=0.001), eosinophils (COPD 1.6, 0-6.9, NS 0.15, 0-3.7, p=0.035), the levels of interleukin (IL)-8 (COPD 1079 pg x mL(-1), 121-2,500, NS 20.4, 7.2-59, p=0.001), myeloperoxidase (MPO) (COPD 752 microg x L(-1), 11-5,500, NS 22.1, 8-70, p=0.001) and eosinophil cationic protein (ECP) (COPD 21.5 microg x L(-1), 1.8-161, NS 2, 1.8-4.9, p=0.001). Significant correlations were found in BL of COPD patients between IL-8 and neutrophils (p=0.02), MPO and neutrophils (p=0.02), IL-8 and MPO (p=0.0001) and ECP and eosinophils (p=0.02). In addition, the ratios between the BL levels of MPO and the number of neutrophils and between ECP levels and eosinophils were higher in COPD patients than in NS (p=0.03 and 0.01, respectively). These data suggest that cigarette smoke is associated with increased amounts of airway interleukin-8, a chemotactic factor for neutrophils and eosinophils. Recruited neutrophils and eosinophils are activated and they release increased amounts of inflammatory mediators capable of damaging the bronchial tissue.
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              Exhaled nitric oxide correlates with airway eosinophils in childhood asthma.

              P. Fitch, M Ennis, Anne V. Brown … (2002)
              Exhaled nitric oxide has been proposed as a marker for airway inflammation in asthma. The aim of this study was to compare exhaled nitric oxide levels with inflammatory cells and mediators in bronchoalveolar lavage fluid from asthmatic and normal children. Children were recruited from elective surgical lists and a non-bronchoscopic bronchoalveolar lavage (BAL) was performed after induction of anaesthesia. Exhaled nitric oxide (parts per billion) was measured by two techniques: tidal breathing and restricted breath. Median (interquartile range) exhaled nitric oxide measured by restricted breath was increased in asthmatics compared with normal children (24.3 (10.5-66.5) v 9.7 (6.5-16.5), difference between medians 14.6 (95% CI 5.1 to 29.9), p=0.001). In asthmatic children exhaled nitric oxide correlated significantly with percentage eosinophils (r=0.78, p<0.001 (tidal breathing) and r=0.78, p<0.001 (restricted breath)) and with eosinophilic cationic protein (r=0.53, p<0.01 (restricted breath)), but not with other inflammatory cells in the BAL fluid. The area under the receiver operator characteristic curves for the prediction of the presence of eosinophilic airways inflammation by exhaled nitric oxide (tidal and restricted) was 0.80 and 0.87, respectively. Exhaled nitric oxide correlates closely with percentage eosinophils in BAL fluid in asthmatic children and is therefore likely to be a useful non-invasive marker of airway inflammation.
              Article 0 comments Cited 51 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Chron Obstruct Pulmon Dis
                Journal ID (iso-abbrev): Int J Chron Obstruct Pulmon Dis
                Journal ID (publisher-id): International Journal of COPD
                Title: International Journal of Chronic Obstructive Pulmonary Disease
                Publisher: Dove Medical Press
                ISSN (Print): 1176-9106
                ISSN (Electronic): 1178-2005
                Publication date Collection: 2018
                Publication date (Electronic): 30 August 2018
                Volume: 13
                Pages: 2695-2705
                Affiliations
                [1 ]Department of Respiratory Medicine, Ningbo First Hospital, Ningbo, People’s Republic of China, caocdoctor@ 123456163.com
                [2 ]Ningbo University School of Medicine, Ningbo, People’s Republic of China
                [3 ]Department of Respiratory Medicine, The Affiliated Hospital of Medical School of Ningbo University, Ningbo, People’s Republic of China, ccding2005@ 123456163.com
                Author notes
                Correspondence: Chao Cao, Department of Respiratory Medicine, Ningbo First Hospital, 59 Liuting Road, Ningbo, Zhejiang 315010, People’s Republic of China, Tel/fax +86 574 8708 9878, Email caocdoctor@ 123456163.com
                Qunli Ding, Department of Respiratory Medicine, The Affiliated Hospital of Medical School of Ningbo University, 247 Renmin Road, Ningbo, Zhejiang 315020, People’s Republic of China, Tel/fax +86 574 8703 5778, Email ccding2005@ 123456163.com
                Article
                Publisher ID: copd-13-2695
                DOI: 10.2147/COPD.S165780
                PMC ID: 6124452
                PubMed ID: 30214187
                SO-VID: ea215518-e2b1-4001-8601-5132e1bc032a
                Copyright © © 2018 Lu et al. This work is published and licensed by Dove Medical Press Limited
                License:

                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.

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                Subject: Review

                ScienceOpen disciplines: Respiratory medicine
                Keywords: biomarker,chronic obstructive pulmonary disease,fractional exhaled nitric oxide,meta-analysis
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: biomarker, chronic obstructive pulmonary disease, fractional exhaled nitric oxide, meta-analysis

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