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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<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>
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<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>
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<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>
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<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>
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<mods version="3.6"><titleInfo lang="en"><title>A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma</title>
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<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>
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<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>
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