A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma
Identifieur interne : 000223 ( Istex/Corpus ); précédent : 000222; suivant : 000224A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma
Auteurs : Y. Y. Koh ; Y. W. Kim ; J. D. Park ; J. W. OhSource :
- Clinical & Experimental Allergy [ 0954-7894 ] ; 1996-10.
English descriptors
Abstract
Background Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy. Objective To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy. Methods We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE. Results The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects (n= 19) who responded poorly (post‐bronchodi‐lator FEV1 < 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those (n= 31) who responded well (post‐bronchodilator FEV1± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy (r=−0.36, P < 0.05), whereas it had no relationship with the severity of exacerbation (r= 0.04. P= 0.79). Conclusion Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.
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DOI: 10.1111/j.1365-2222.1996.tb00509.x
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ISTEX:3926BEBB62DB396C26B095004C4E731EC6A45E81Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title><author><name sortKey="Koh, Y Y" sort="Koh, Y Y" uniqKey="Koh Y" first="Y. Y." last="Koh">Y. Y. Koh</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Y W" sort="Kim, Y W" uniqKey="Kim Y" first="Y. W." last="Kim">Y. W. Kim</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Park, J D" sort="Park, J D" uniqKey="Park J" first="J. D." last="Park">J. D. Park</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Oh, J W" sort="Oh, J W" uniqKey="Oh J" first="J. W." last="Oh">J. W. Oh</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:3926BEBB62DB396C26B095004C4E731EC6A45E81</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1111/j.1365-2222.1996.tb00509.x</idno><idno type="url">https://api.istex.fr/document/3926BEBB62DB396C26B095004C4E731EC6A45E81/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000223</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title><author><name sortKey="Koh, Y Y" sort="Koh, Y Y" uniqKey="Koh Y" first="Y. Y." last="Koh">Y. Y. Koh</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Y W" sort="Kim, Y W" uniqKey="Kim Y" first="Y. W." last="Kim">Y. W. Kim</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Park, J D" sort="Park, J D" uniqKey="Park J" first="J. D." last="Park">J. D. Park</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Oh, J W" sort="Oh, J W" uniqKey="Oh J" first="J. W." last="Oh">J. W. Oh</name><affiliation><mods:affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical & Experimental Allergy</title><idno type="ISSN">0954-7894</idno><idno type="eISSN">1365-2222</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1996-10">1996-10</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1202">1202</biblScope><biblScope unit="page" to="1209">1209</biblScope></imprint><idno type="ISSN">0954-7894</idno></series><idno type="istex">3926BEBB62DB396C26B095004C4E731EC6A45E81</idno><idno type="DOI">10.1111/j.1365-2222.1996.tb00509.x</idno><idno type="ArticleID">CEA1202</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0954-7894</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>acute exacerbation</term><term>airway inflammation</term><term>bronchial asthma</term><term>clinical remission</term><term>haptogtobin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy. Objective To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy. Methods We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE. Results The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects (n= 19) who responded poorly (post‐bronchodi‐lator FEV1 < 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those (n= 31) who responded well (post‐bronchodilator FEV1± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy (r=−0.36, P < 0.05), whereas it had no relationship with the severity of exacerbation (r= 0.04. P= 0.79). Conclusion Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Y. Y. KOH</name><affiliations><json:string>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</json:string></affiliations></json:item><json:item><name>Y. W. KIM</name><affiliations><json:string>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</json:string></affiliations></json:item><json:item><name>J. D. PARK</name><affiliations><json:string>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</json:string></affiliations></json:item><json:item><name>J. W. OH</name><affiliations><json:string>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>haptogtobin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>bronchial asthma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>acute exacerbation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>clinical remission</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>airway inflammation</value></json:item></subject><articleId><json:string>CEA1202</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy. Objective To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy. Methods We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE. Results The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly (P > 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects (n= 19) who responded poorly (post‐bronchodi‐lator FEV1 > 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those (n= 31) who responded well (post‐bronchodilator FEV1± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy (r=−0.36, P > 0.05), whereas it had no relationship with the severity of exacerbation (r= 0.04. P= 0.79). Conclusion Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.</abstract><qualityIndicators><score>8.411</score><pdfVersion>1.6</pdfVersion><pdfPageSize>569 x 764 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1969</abstractCharCount><pdfWordCount>3911</pdfWordCount><pdfCharCount>23810</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>313</abstractWordCount></qualityIndicators><title>A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>CEA</json:string></publisherId><pages><total>8</total><last>1209</last><first>1202</first></pages><issn><json:string>0954-7894</json:string></issn><issue>10</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1365-2222</json:string></eissn><title>Clinical & Experimental Allergy</title><doi><json:string>10.1111/(ISSN)1365-2222</json:string></doi></host><publicationDate>1996</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1111/j.1365-2222.1996.tb00509.x</json:string></doi><id>3926BEBB62DB396C26B095004C4E731EC6A45E81</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/3926BEBB62DB396C26B095004C4E731EC6A45E81/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/3926BEBB62DB396C26B095004C4E731EC6A45E81/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3926BEBB62DB396C26B095004C4E731EC6A45E81/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1996</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title><author><persName><forename type="first">Y. Y.</forename><surname>KOH</surname></persName><note type="correspondence"><p>Correspondence: Dr Young Yull Koh, Department of Pediatrics. Seoul National University Children's Hospital, 28 Yongon‐dong, Chongno‐gu, Seoul 110‐744, Korea.</p></note><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation></author><author><persName><forename type="first">Y. W.</forename><surname>KIM</surname></persName><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation></author><author><persName><forename type="first">J. D.</forename><surname>PARK</surname></persName><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation></author><author><persName><forename type="first">J. W.</forename><surname>OH</surname></persName><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation></author></analytic><monogr><title level="j">Clinical & Experimental Allergy</title><idno type="pISSN">0954-7894</idno><idno type="eISSN">1365-2222</idno><idno type="DOI">10.1111/(ISSN)1365-2222</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1996-10"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1202">1202</biblScope><biblScope unit="page" to="1209">1209</biblScope></imprint></monogr><idno type="istex">3926BEBB62DB396C26B095004C4E731EC6A45E81</idno><idno type="DOI">10.1111/j.1365-2222.1996.tb00509.x</idno><idno type="ArticleID">CEA1202</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy. Objective To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy. Methods We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE. Results The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects (n= 19) who responded poorly (post‐bronchodi‐lator FEV1 < 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those (n= 31) who responded well (post‐bronchodilator FEV1± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy (r=−0.36, P < 0.05), whereas it had no relationship with the severity of exacerbation (r= 0.04. P= 0.79). Conclusion Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>haptogtobin</term></item><item><term>bronchial asthma</term></item><item><term>acute exacerbation</term></item><item><term>clinical remission</term></item><item><term>airway inflammation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3926BEBB62DB396C26B095004C4E731EC6A45E81/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2222</doi><issn type="print">0954-7894</issn><issn type="electronic">1365-2222</issn><idGroup><id type="product" value="CEA"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="CLINICAL EXPERIMENTAL ALLERGY">Clinical & Experimental Allergy</title></titleGroup></publicationMeta><publicationMeta level="part" position="10010"><doi origin="wiley">10.1111/cea.1996.26.issue-10</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue" number="10">10</numbering></numberingGroup><coverDate startDate="1996-10">October 1996</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0120200" status="forIssue"><doi origin="wiley">10.1111/j.1365-2222.1996.tb00509.x</doi><idGroup><id type="unit" value="CEA1202"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Original article</title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-27"></event><event type="publishedOnlineFinalForm" date="2006-04-27"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-09"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1202">1202</numbering><numbering type="pageLast" number="1209">1209</numbering></numberingGroup><correspondenceTo>Dr Young Yull Koh, Department of Pediatrics. Seoul National University Children's Hospital, 28 Yongon‐dong, Chongno‐gu, Seoul 110‐744, Korea.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CEA.CEA1202.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 22 May 1995; revised 16 January 1996; accepted 28 March 1996.</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="39"></count><count type="linksCrossRef" number="5"></count></countGroup><titleGroup><title type="main">A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Y. Y.</givenNames><familyName>KOH</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Y. W.</givenNames><familyName>KIM</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>J. D.</givenNames><familyName>PARK</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>J. W.</givenNames><familyName>OH</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="KR"><unparsedAffiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">haptogtobin</keyword><keyword xml:id="k2">bronchial asthma</keyword><keyword xml:id="k3">acute exacerbation</keyword><keyword xml:id="k4">clinical remission</keyword><keyword xml:id="k5">airway inflammation</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p><b>Background </b> Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy.</p><p><b>Objective </b> To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy.</p><p><b>Methods </b> We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE.</p><p><b>Results </b> The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly (<i>P</i> < 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects (<i>n</i>= 19) who responded poorly (post‐bronchodi‐lator FEV<sub>1</sub> < 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those (<i>n</i>= 31) who responded well (post‐bronchodilator FEV<sub>1</sub>± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy (<i>r</i>=−0.36, <i>P</i> < 0.05), whereas it had no relationship with the severity of exacerbation (<i>r</i>= 0.04. <i>P</i>= 0.79).</p><p><b>Conclusion </b> Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title></titleInfo><name type="personal"><namePart type="given">Y. Y.</namePart><namePart type="family">KOH</namePart><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation><description>Correspondence: Dr Young Yull Koh, Department of Pediatrics. Seoul National University Children's Hospital, 28 Yongon‐dong, Chongno‐gu, Seoul 110‐744, Korea.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y. W.</namePart><namePart type="family">KIM</namePart><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. D.</namePart><namePart type="family">PARK</namePart><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. W.</namePart><namePart type="family">OH</namePart><affiliation>Department of Pediatrics. Seoul National University Children's Hospital, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1996-10</dateIssued><edition>Received 22 May 1995; revised 16 January 1996; accepted 28 March 1996.</edition><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">39</extent></physicalDescription><abstract lang="en">Background Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy. Objective To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy. Methods We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE. Results The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects (n= 19) who responded poorly (post‐bronchodi‐lator FEV1 < 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those (n= 31) who responded well (post‐bronchodilator FEV1± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy (r=−0.36, P < 0.05), whereas it had no relationship with the severity of exacerbation (r= 0.04. P= 0.79). Conclusion Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.</abstract><subject lang="en"><genre>Keywords</genre><topic>haptogtobin</topic><topic>bronchial asthma</topic><topic>acute exacerbation</topic><topic>clinical remission</topic><topic>airway inflammation</topic></subject><relatedItem type="host"><titleInfo><title>Clinical & Experimental Allergy</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0954-7894</identifier><identifier type="eISSN">1365-2222</identifier><identifier type="DOI">10.1111/(ISSN)1365-2222</identifier><identifier type="PublisherID">CEA</identifier><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1202</start><end>1209</end><total>8</total></extent></part></relatedItem><identifier type="istex">3926BEBB62DB396C26B095004C4E731EC6A45E81</identifier><identifier type="DOI">10.1111/j.1365-2222.1996.tb00509.x</identifier><identifier type="ArticleID">CEA1202</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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