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A comparison of exhaled nitric oxide and induced sputum as markers of airway inflammation
Background: Exhaled nitric oxide (ENO) has been proposed as a noninvasive marker of airway inflammation in asthma. Objective: We investigated the relationships among ENO, eosinophilic airway inflammation as measured by induced sputum, and physiologic parameters of disease severity (spirometry and me...
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Published in: | Journal of allergy and clinical immunology 2000-10, Vol.106 (4), p.638-644 |
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description | Background: Exhaled nitric oxide (ENO) has been proposed as a noninvasive marker of airway inflammation in asthma. Objective: We investigated the relationships among ENO, eosinophilic airway inflammation as measured by induced sputum, and physiologic parameters of disease severity (spirometry and methacholine PC20). We also examined the effect of corticosteroid treatment and atopy on ENO levels and eosinophil counts in induced sputum. Methods: Measurements were taken on one day in 22 healthy nonatopic subjects, 28 healthy atopic subjects, 38 asthmatic subjects not taking inhaled steroids, 35 asthmatic subjects taking inhaled steroids, and 8 subjects with eosinophilic bronchitis without asthma. Results: ENO levels showed significant but weak correlations with eosinophil differential counts in the steroid-naive asthmatic and healthy atopic groups (rs < 0.05). ENO levels were significantly lower in the asthmatic subjects taking steroids compared with the asthmatic subjects not taking steroids, despite there being no difference in the sputum cell counts, and a tendency to increased airflow limitation. ENO levels and sputum eosinophil counts were equally good at differentiating from steroid-naive asthmatic subjects. ENO levels were consistently raised in subjects with eosinophilic bronchitis without asthma. Atopy had no effect on ENO levels in the healthy subjects. Conclusion: We conclude that ENO is likely to have limited utility as a surrogate clinical measurement for either the presence or severity of eosinophilic airway inflammation, except in steroid-naive subjects. (J Allergy Clin Immunol 2000;106:638-44.) |
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Objective: We investigated the relationships among ENO, eosinophilic airway inflammation as measured by induced sputum, and physiologic parameters of disease severity (spirometry and methacholine PC20). We also examined the effect of corticosteroid treatment and atopy on ENO levels and eosinophil counts in induced sputum. Methods: Measurements were taken on one day in 22 healthy nonatopic subjects, 28 healthy atopic subjects, 38 asthmatic subjects not taking inhaled steroids, 35 asthmatic subjects taking inhaled steroids, and 8 subjects with eosinophilic bronchitis without asthma. Results: ENO levels showed significant but weak correlations with eosinophil differential counts in the steroid-naive asthmatic and healthy atopic groups (rs < 0.05). ENO levels were significantly lower in the asthmatic subjects taking steroids compared with the asthmatic subjects not taking steroids, despite there being no difference in the sputum cell counts, and a tendency to increased airflow limitation. ENO levels and sputum eosinophil counts were equally good at differentiating from steroid-naive asthmatic subjects. ENO levels were consistently raised in subjects with eosinophilic bronchitis without asthma. Atopy had no effect on ENO levels in the healthy subjects. Conclusion: We conclude that ENO is likely to have limited utility as a surrogate clinical measurement for either the presence or severity of eosinophilic airway inflammation, except in steroid-naive subjects. (J Allergy Clin Immunol 2000;106:638-44.)</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1067/mai.2000.109622</identifier><identifier>PMID: 11031333</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Administration, Inhalation ; Adrenal Cortex Hormones - administration & dosage ; Adrenal Cortex Hormones - pharmacology ; Adult ; asthma ; Biological and medical sciences ; Biomarkers - analysis ; Bronchitis - diagnosis ; Chronic obstructive pulmonary disease, asthma ; eosinophilic bronchitis ; Eosinophils - cytology ; Exhaled nitric oxide ; Female ; Forced Expiratory Volume ; Humans ; Hypersensitivity, Immediate - diagnosis ; Leukocyte Count ; Male ; Medical sciences ; Middle Aged ; Nitric Oxide - physiology ; Pneumology ; Respiration ; Sensitivity and Specificity ; sputum ; Sputum - chemistry ; Sputum - cytology</subject><ispartof>Journal of allergy and clinical immunology, 2000-10, Vol.106 (4), p.638-644</ispartof><rights>2000 Mosby, Inc.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-51b9e9e6d1b7dc42d9cbc80dc9513c938877be6d1fa11bf8a1ed0714c3096e543</citedby><cites>FETCH-LOGICAL-c479t-51b9e9e6d1b7dc42d9cbc80dc9513c938877be6d1fa11bf8a1ed0714c3096e543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1536408$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11031333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Berlyne, Graham S.</creatorcontrib><creatorcontrib>Parameswaran, Krishnan</creatorcontrib><creatorcontrib>Kamada, Dennis</creatorcontrib><creatorcontrib>Efthimiadis, Ann</creatorcontrib><creatorcontrib>Hargreave, Frederick E.</creatorcontrib><title>A comparison of exhaled nitric oxide and induced sputum as markers of airway inflammation</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Background: Exhaled nitric oxide (ENO) has been proposed as a noninvasive marker of airway inflammation in asthma. Objective: We investigated the relationships among ENO, eosinophilic airway inflammation as measured by induced sputum, and physiologic parameters of disease severity (spirometry and methacholine PC20). We also examined the effect of corticosteroid treatment and atopy on ENO levels and eosinophil counts in induced sputum. Methods: Measurements were taken on one day in 22 healthy nonatopic subjects, 28 healthy atopic subjects, 38 asthmatic subjects not taking inhaled steroids, 35 asthmatic subjects taking inhaled steroids, and 8 subjects with eosinophilic bronchitis without asthma. Results: ENO levels showed significant but weak correlations with eosinophil differential counts in the steroid-naive asthmatic and healthy atopic groups (rs < 0.05). ENO levels were significantly lower in the asthmatic subjects taking steroids compared with the asthmatic subjects not taking steroids, despite there being no difference in the sputum cell counts, and a tendency to increased airflow limitation. ENO levels and sputum eosinophil counts were equally good at differentiating from steroid-naive asthmatic subjects. ENO levels were consistently raised in subjects with eosinophilic bronchitis without asthma. Atopy had no effect on ENO levels in the healthy subjects. Conclusion: We conclude that ENO is likely to have limited utility as a surrogate clinical measurement for either the presence or severity of eosinophilic airway inflammation, except in steroid-naive subjects. (J Allergy Clin Immunol 2000;106:638-44.)</description><subject>Administration, Inhalation</subject><subject>Adrenal Cortex Hormones - administration & dosage</subject><subject>Adrenal Cortex Hormones - pharmacology</subject><subject>Adult</subject><subject>asthma</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Bronchitis - diagnosis</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>eosinophilic bronchitis</subject><subject>Eosinophils - cytology</subject><subject>Exhaled nitric oxide</subject><subject>Female</subject><subject>Forced Expiratory Volume</subject><subject>Humans</subject><subject>Hypersensitivity, Immediate - diagnosis</subject><subject>Leukocyte Count</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nitric Oxide - physiology</subject><subject>Pneumology</subject><subject>Respiration</subject><subject>Sensitivity and Specificity</subject><subject>sputum</subject><subject>Sputum - chemistry</subject><subject>Sputum - cytology</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNp1kDtPxDAMgCME4o7HzIYyILZC0rRNMyLES0JigYEpchNXBNrmSFrg_j2p7iQmJtvyZ8v-CDnh7IKzSl724C5yxuZKVXm-Q5YpkVlV5-UuWTKmeFbJQi3IQYzviVOiVvtkwTkTXAixJK9X1Ph-BcFFP1DfUvx5gw4tHdwYnKH-x1mkMFjqBjuZ1IiraZx6CpH2ED4wxHkKXPiGdWLaDvoeRueHI7LXQhfxeBsPycvtzfP1ffb4dPdwffWYmUKqMSt5o1BhZXkjrSlyq0xjamaNKrkw6d5aymZut8B509bA0TLJCyPSx1gW4pCcb_augv-cMI66d9Fg18GAfopa5kLkhWQJvNyAJvgYA7Z6FVz6Ya0507NNnWzq2abe2EwTp9vVU9Oj_eO3-hJwtgUgGujaAINx8Y8rRVWwOmFqg2Hy8OUw6GgcDsmmC2hGbb3794ZfdX6Qsg</recordid><startdate>20001001</startdate><enddate>20001001</enddate><creator>Berlyne, Graham S.</creator><creator>Parameswaran, Krishnan</creator><creator>Kamada, Dennis</creator><creator>Efthimiadis, Ann</creator><creator>Hargreave, Frederick E.</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20001001</creationdate><title>A comparison of exhaled nitric oxide and induced sputum as markers of airway inflammation</title><author>Berlyne, Graham S. ; Parameswaran, Krishnan ; Kamada, Dennis ; Efthimiadis, Ann ; Hargreave, Frederick E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-51b9e9e6d1b7dc42d9cbc80dc9513c938877be6d1fa11bf8a1ed0714c3096e543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Administration, Inhalation</topic><topic>Adrenal Cortex Hormones - administration & dosage</topic><topic>Adrenal Cortex Hormones - pharmacology</topic><topic>Adult</topic><topic>asthma</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Bronchitis - diagnosis</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>eosinophilic bronchitis</topic><topic>Eosinophils - cytology</topic><topic>Exhaled nitric oxide</topic><topic>Female</topic><topic>Forced Expiratory Volume</topic><topic>Humans</topic><topic>Hypersensitivity, Immediate - diagnosis</topic><topic>Leukocyte Count</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nitric Oxide - physiology</topic><topic>Pneumology</topic><topic>Respiration</topic><topic>Sensitivity and Specificity</topic><topic>sputum</topic><topic>Sputum - chemistry</topic><topic>Sputum - cytology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Berlyne, Graham S.</creatorcontrib><creatorcontrib>Parameswaran, Krishnan</creatorcontrib><creatorcontrib>Kamada, Dennis</creatorcontrib><creatorcontrib>Efthimiadis, Ann</creatorcontrib><creatorcontrib>Hargreave, Frederick E.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Berlyne, Graham S.</au><au>Parameswaran, Krishnan</au><au>Kamada, Dennis</au><au>Efthimiadis, Ann</au><au>Hargreave, Frederick E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A comparison of exhaled nitric oxide and induced sputum as markers of airway inflammation</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2000-10-01</date><risdate>2000</risdate><volume>106</volume><issue>4</issue><spage>638</spage><epage>644</epage><pages>638-644</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Background: Exhaled nitric oxide (ENO) has been proposed as a noninvasive marker of airway inflammation in asthma. Objective: We investigated the relationships among ENO, eosinophilic airway inflammation as measured by induced sputum, and physiologic parameters of disease severity (spirometry and methacholine PC20). We also examined the effect of corticosteroid treatment and atopy on ENO levels and eosinophil counts in induced sputum. Methods: Measurements were taken on one day in 22 healthy nonatopic subjects, 28 healthy atopic subjects, 38 asthmatic subjects not taking inhaled steroids, 35 asthmatic subjects taking inhaled steroids, and 8 subjects with eosinophilic bronchitis without asthma. Results: ENO levels showed significant but weak correlations with eosinophil differential counts in the steroid-naive asthmatic and healthy atopic groups (rs < 0.05). ENO levels were significantly lower in the asthmatic subjects taking steroids compared with the asthmatic subjects not taking steroids, despite there being no difference in the sputum cell counts, and a tendency to increased airflow limitation. ENO levels and sputum eosinophil counts were equally good at differentiating from steroid-naive asthmatic subjects. ENO levels were consistently raised in subjects with eosinophilic bronchitis without asthma. Atopy had no effect on ENO levels in the healthy subjects. Conclusion: We conclude that ENO is likely to have limited utility as a surrogate clinical measurement for either the presence or severity of eosinophilic airway inflammation, except in steroid-naive subjects. (J Allergy Clin Immunol 2000;106:638-44.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>11031333</pmid><doi>10.1067/mai.2000.109622</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Administration, Inhalation Adrenal Cortex Hormones - administration & dosage Adrenal Cortex Hormones - pharmacology Adult asthma Biological and medical sciences Biomarkers - analysis Bronchitis - diagnosis Chronic obstructive pulmonary disease, asthma eosinophilic bronchitis Eosinophils - cytology Exhaled nitric oxide Female Forced Expiratory Volume Humans Hypersensitivity, Immediate - diagnosis Leukocyte Count Male Medical sciences Middle Aged Nitric Oxide - physiology Pneumology Respiration Sensitivity and Specificity sputum Sputum - chemistry Sputum - cytology |
title | A comparison of exhaled nitric oxide and induced sputum as markers of airway inflammation |
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