Respiratory atopic disease, Ascaris‐immunoglobulin E and tuberculin testing in urban South African children
Identifieur interne : 000650 ( Istex/Corpus ); précédent : 000649; suivant : 000651Respiratory atopic disease, Ascaris‐immunoglobulin E and tuberculin testing in urban South African children
Auteurs : C. C. Obihara ; N. Beyers ; R. P. Gie ; M. O. Hoekstra ; J. E. Fincham ; B. J. Marais ; C. J. Lombard ; L. A. Dini ; J. L. L. KimpenSource :
- Clinical & Experimental Allergy [ 0954-7894 ] ; 2006-05.
English descriptors
- KwdEn :
- Allergic, Allergic disease, Allergic rhinitis, Allergic symptom, Allergic symptoms, Allergy, Allergy clin immunol, Anthelminthic, Anthelminthic treatment, Ascaris, Ascaris eggs, Ascaris lumbricoides, Asthma, Atopic, Atopic asthma, Atopic disease, Atopic diseases, Atopic response, Atopic rhinitis, Atopic sensitization, Atopic symptoms, Atopy, Blackwell publishing, Cape town, Clin, Common aeroallergens, Environmental tobacco smoke, Experimental allergy, Helminth, Helminth infection, Histamine, Histamine bronchoprovocation, Histamine challenge, House dust mite, Immune response, Immunol, Infection, Intestinal, Intestinal helminth infection, Inverse association, Journal compilation, Mild intensity, Mite, Mycobacterium tuberculosis, Oradj, Parental, Positive skin prick test, Respir crit care, Respiratory atopic disease, Rhinitis, Risk factor, Sampling unit, Sensitization, Stellenbosch university, Study population, Symptom, Total serum, Tuberculin, Tuberculin testing, Wilhelmina hospital, World allergy organization nomenclature.
- Teeft :
- Allergic, Allergic disease, Allergic rhinitis, Allergic symptom, Allergic symptoms, Allergy, Allergy clin immunol, Anthelminthic, Anthelminthic treatment, Ascaris, Ascaris eggs, Ascaris lumbricoides, Asthma, Atopic, Atopic asthma, Atopic disease, Atopic diseases, Atopic response, Atopic rhinitis, Atopic sensitization, Atopic symptoms, Atopy, Blackwell publishing, Cape town, Clin, Common aeroallergens, Environmental tobacco smoke, Experimental allergy, Helminth, Helminth infection, Histamine, Histamine bronchoprovocation, Histamine challenge, House dust mite, Immune response, Immunol, Infection, Intestinal, Intestinal helminth infection, Inverse association, Journal compilation, Mild intensity, Mite, Mycobacterium tuberculosis, Oradj, Parental, Positive skin prick test, Respir crit care, Respiratory atopic disease, Rhinitis, Risk factor, Sampling unit, Sensitization, Stellenbosch university, Study population, Symptom, Total serum, Tuberculin, Tuberculin testing, Wilhelmina hospital, World allergy organization nomenclature.
Abstract
Background Epidemiological relation of intestinal helminth infection and atopic disease, both associated with a T‐helper (Th) 2 immune response, is controversial, as it has been reported that helminth infection may either suppress or pre‐dispose to atopic disease. This relation has not been tested in an area with a high burden of Mycobacterium tuberculosis (MTB) infection, a known Th1‐stimulating infection.
Url:
DOI: 10.1111/j.1365-2222.2006.02479.x
Links to Exploration step
ISTEX:15093C051A532710A1702C47A95CD37BCDDD8052Le document en format XML
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This relation has not been tested in an area with a high burden of Mycobacterium tuberculosis (MTB) infection, a known Th1‐stimulating infection.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>atopic</json:string><json:string>allergy</json:string><json:string>helminth</json:string><json:string>ascaris</json:string><json:string>atopic disease</json:string><json:string>rhinitis</json:string><json:string>tuberculin</json:string><json:string>asthma</json:string><json:string>atopy</json:string><json:string>histamine</json:string><json:string>atopic diseases</json:string><json:string>sensitization</json:string><json:string>helminth infection</json:string><json:string>atopic rhinitis</json:string><json:string>ascaris eggs</json:string><json:string>intestinal</json:string><json:string>anthelminthic</json:string><json:string>experimental allergy</json:string><json:string>allergic symptoms</json:string><json:string>journal compilation</json:string><json:string>atopic asthma</json:string><json:string>clin</json:string><json:string>immunol</json:string><json:string>blackwell publishing</json:string><json:string>atopic sensitization</json:string><json:string>oradj</json:string><json:string>allergic</json:string><json:string>house dust mite</json:string><json:string>cape town</json:string><json:string>anthelminthic treatment</json:string><json:string>respiratory atopic disease</json:string><json:string>atopic symptoms</json:string><json:string>respir crit care</json:string><json:string>allergy clin immunol</json:string><json:string>sampling unit</json:string><json:string>intestinal helminth infection</json:string><json:string>immune response</json:string><json:string>common aeroallergens</json:string><json:string>positive skin prick test</json:string><json:string>mild intensity</json:string><json:string>inverse association</json:string><json:string>environmental tobacco smoke</json:string><json:string>tuberculin testing</json:string><json:string>infection</json:string><json:string>mite</json:string><json:string>wilhelmina hospital</json:string><json:string>total serum</json:string><json:string>histamine challenge</json:string><json:string>stellenbosch university</json:string><json:string>study population</json:string><json:string>allergic symptom</json:string><json:string>atopic response</json:string><json:string>world allergy organization nomenclature</json:string><json:string>allergic disease</json:string><json:string>mycobacterium tuberculosis</json:string><json:string>risk factor</json:string><json:string>histamine bronchoprovocation</json:string><json:string>allergic rhinitis</json:string><json:string>ascaris lumbricoides</json:string><json:string>symptom</json:string><json:string>parental</json:string></teeft></keywords><author><json:item><name>C. C. Obihara</name><affiliations><json:string>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</json:string><json:string>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</json:string></affiliations></json:item><json:item><name>N. Beyers</name><affiliations><json:string>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</json:string></affiliations></json:item><json:item><name>R. P. Gie</name><affiliations><json:string>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</json:string></affiliations></json:item><json:item><name>M. O. Hoekstra</name><affiliations><json:string>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</json:string></affiliations></json:item><json:item><name>J. E. Fincham</name><affiliations><json:string>Nutritional Intervention Research Unit,</json:string></affiliations></json:item><json:item><name>B. J. Marais</name><affiliations><json:string>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</json:string></affiliations></json:item><json:item><name>C. J. Lombard</name><affiliations><json:string>Biostatistics Unit, Medical Research Council of South Africa, Cape Town, South Africa</json:string></affiliations></json:item><json:item><name>L. A. Dini</name><affiliations><json:string>Parasitology Reference Unit, National Institute for Communicable Diseases, National Health Laboratory Services, Johannesburg, South Africa</json:string></affiliations></json:item><json:item><name>J. L. L. Kimpen</name><affiliations><json:string>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Ascaris specific IgE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>atopic disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>childhood</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tuberculin skin test</value></json:item></subject><articleId><json:string>CEA2479</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><qualityIndicators><score>5.708</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>410</abstractCharCount><pdfWordCount>5179</pdfWordCount><pdfCharCount>34768</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>59</abstractWordCount></qualityIndicators><title>Respiratory atopic disease, Ascaris‐immunoglobulin E and tuberculin testing in urban South African children</title><genre><json:string>article</json:string></genre><host><title>Clinical & Experimental Allergy</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1365-2222</json:string></doi><issn><json:string>0954-7894</json:string></issn><eissn><json:string>1365-2222</json:string></eissn><publisherId><json:string>CEA</json:string></publisherId><volume>36</volume><issue>5</issue><pages><first>640</first><last>648</last><total>9</total></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>immunology</json:string><json:string>allergy</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>allergy</json:string></scienceMetrix></categories><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1111/j.1365-2222.2006.02479.x</json:string></doi><id>15093C051A532710A1702C47A95CD37BCDDD8052</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/15093C051A532710A1702C47A95CD37BCDDD8052/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/15093C051A532710A1702C47A95CD37BCDDD8052/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/15093C051A532710A1702C47A95CD37BCDDD8052/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Respiratory atopic disease, <hi rend="italic">Ascaris</hi>‐immunoglobulin E and tuberculin testing in urban South African children</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-05"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Respiratory atopic disease, <hi rend="italic">Ascaris</hi>‐immunoglobulin E and tuberculin testing in urban South African children</title><title level="a" type="short">Respiratory atopic disease, Ascaris‐IgE and tuberculin testing</title><author xml:id="author-0000"><persName><forename type="first">C. C.</forename><surname>Obihara</surname></persName><affiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,<address><country key="NL"></country></address></affiliation><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,<address><country key="ZA"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">N.</forename><surname>Beyers</surname></persName><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,<address><country key="ZA"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">R. P.</forename><surname>Gie</surname></persName><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,<address><country key="ZA"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">M. O.</forename><surname>Hoekstra</surname></persName><affiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,<address><country key="NL"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">J. E.</forename><surname>Fincham</surname></persName><affiliation>Nutritional Intervention Research Unit,</affiliation></author><author xml:id="author-0005"><persName><forename type="first">B. J.</forename><surname>Marais</surname></persName><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,<address><country key="ZA"></country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">C. J.</forename><surname>Lombard</surname></persName><affiliation>Biostatistics Unit, Medical Research Council of South Africa, Cape Town, South Africa<address><country key="ZA"></country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">L. A.</forename><surname>Dini</surname></persName><affiliation>Parasitology Reference Unit, National Institute for Communicable Diseases, National Health Laboratory Services, Johannesburg, South Africa<address><country key="ZA"></country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">J. L. L.</forename><surname>Kimpen</surname></persName><affiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,<address><country key="NL"></country></address></affiliation></author><idno type="istex">15093C051A532710A1702C47A95CD37BCDDD8052</idno><idno type="ark">ark:/67375/WNG-N7VP2VMH-9</idno><idno type="DOI">10.1111/j.1365-2222.2006.02479.x</idno><idno type="unit">CEA2479</idno><idno type="supplier">2479</idno><idno type="toTypesetVersion">file:CEA.CEA2479.pdf</idno></analytic><monogr><title level="j" type="main">Clinical & Experimental Allergy</title><title level="j" type="alt">CLINICAL EXPERIMENTAL ALLERGY</title><idno type="pISSN">0954-7894</idno><idno type="eISSN">1365-2222</idno><idno type="book-DOI">10.1111/(ISSN)1365-2222</idno><idno type="book-part-DOI">10.1111/cea.2006.36.issue-5</idno><idno type="product">CEA</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">36</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="640">640</biblScope><biblScope unit="page" to="648">648</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-05"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Summary</head><p><hi rend="bold">Background
</hi> Epidemiological relation of intestinal helminth infection and atopic disease, both associated with a T‐helper (Th) 2 immune response, is controversial, as it has been reported that helminth infection may either suppress or pre‐dispose to atopic disease. This relation has not been tested in an area with a high burden of <hi rend="italic">Mycobacterium tuberculosis</hi> (MTB) infection, a known Th1‐stimulating infection.</p><p><hi rend="bold">Objective
</hi> To study the association of intestinal helminth infection and atopic disease in a community where helminth infection is endemic and MTB infection is high.</p><p><hi rend="bold">Methods
</hi> Three‐hundred and fifty‐nine randomly selected children aged 6–14 years from a poor urban suburb were tested with allergy questionnaire, skin prick test (SPT) to common aeroallergens, <hi rend="italic">Ascaris</hi>‐specific IgE (<hi rend="italic">Ascaris</hi>‐sIgE), fecal examination for pathogenic intestinal helminths and tuberculin skin testing (TST). Histamine bronchoprovocation was tested in the group of children aged 10 years and older. Results were corrected for demographic variables, socioeconomic status, parental allergy, environmental tobacco smoke (ETS) exposure in the household, recent anthelminthic treatment and for clustering in the sampling unit.</p><p><hi rend="bold">Results
</hi>
<hi rend="italic">Ascaris</hi>‐sIgE was elevated in 48% of children, <hi rend="italic">Ascaris</hi> eggs were found in 15% and TST was positive in 53%. Children with elevated <hi rend="italic">Ascaris</hi>‐sIgE had significantly increased risk of positive SPT to aeroallergens, particularly house dust mite, atopic asthma (<hi rend="italic">ever</hi> and <hi rend="italic">recent</hi>), atopic rhinitis (<hi rend="italic">ever</hi> and <hi rend="italic">recent</hi>) and increased atopy‐related bronchial hyper‐responsiveness. In children with negative TST (<10 mm), elevated <hi rend="italic">Ascaris</hi>‐sIgE was associated with significantly increased risk of atopic symptoms (adjusted odds ratio (OR<hi rend="subscript">adj</hi>) 6.5; 95% confidence interval (CI) 1.9–22.4), whereas in those with positive TST (<graphic url="ges.gif" rend="geqslant R: gt-or-equal, slanted"></graphic>10 mm) this association disappeared (OR<hi rend="subscript">adj</hi> 0.96; 95% CI 0.4–2.8).</p><p><hi rend="bold">Conclusions
</hi> These results suggest that immune response to <hi rend="italic">Ascaris</hi> (<hi rend="italic">Ascaris</hi>‐sIgE) may be a risk factor of atopic disease in populations exposed to mild <hi rend="italic">Ascaris</hi> infection and that MTB infection may be protective against this risk, probably by stimulation of anti‐inflammatory networks.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1"><hi rend="italic">Ascaris</hi> specific IgE</term><term xml:id="k2">atopic disease</term><term xml:id="k3">childhood</term><term xml:id="k4">tuberculin skin test</term></keywords><keywords rend="tocHeading1"><term>Original Papers</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/15093C051A532710A1702C47A95CD37BCDDD8052/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="05005"><doi origin="wiley">10.1111/cea.2006.36.issue-5</doi><numberingGroup><numbering type="journalVolume" number="36">36</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="2006-05">May 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="14" status="forIssue"><doi origin="wiley">10.1111/j.1365-2222.2006.02479.x</doi><idGroup><id type="unit" value="CEA2479"></id><id type="supplier" value="2479"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">Original Papers</title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-26"></event><event type="publishedOnlineFinalForm" date="2006-04-26"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" 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="640">640</numbering><numbering type="pageLast" number="648">648</numbering></numberingGroup><correspondenceTo><i>Correspondence:</i>
J.L.L. Kimpen, Department of Paediatrics, Wilhelmina Children's Hospital, University Medical Center, Lundlaan 6, PO Box 85090, 3508 AB Utrecht, The Netherlands. E‐mail: <email normalForm="ch.obihara@planet.nl">ch.obihara@planet.nl</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CEA.CEA2479.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Submitted 6 July 2005; revised 30 October 2005; accepted 17 January 2006</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="39"></count><count type="wordTotal" number="6437"></count><count type="linksCrossRef" number="56"></count></countGroup><titleGroup><title type="main">Respiratory atopic disease, <i>Ascaris</i>‐immunoglobulin E and tuberculin testing in urban South African children</title><title type="shortAuthors">C. C. Obihara <i>et al</i></title><title type="short">Respiratory atopic disease, <i>Ascaris</i>‐IgE and tuberculin testing</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>C. C.</givenNames><familyName>Obihara</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>N.</givenNames><familyName>Beyers</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>R. P.</givenNames><familyName>Gie</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>M. O.</givenNames><familyName>Hoekstra</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>J. E.</givenNames><familyName>Fincham</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2"><personName><givenNames>B. J.</givenNames><familyName>Marais</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a4"><personName><givenNames>C. J.</givenNames><familyName>Lombard</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a5"><personName><givenNames>L. A.</givenNames><familyName>Dini</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1"><personName><givenNames>J. L. L.</givenNames><familyName>Kimpen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="NL"><unparsedAffiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="ZA"><unparsedAffiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Nutritional Intervention Research Unit,</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="ZA"><unparsedAffiliation>Biostatistics Unit, Medical Research Council of South Africa, Cape Town, South Africa</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="ZA"><unparsedAffiliation>Parasitology Reference Unit, National Institute for Communicable Diseases, National Health Laboratory Services, Johannesburg, South Africa</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1"><i>Ascaris</i> specific IgE</keyword><keyword xml:id="k2">atopic disease</keyword><keyword xml:id="k3">childhood</keyword><keyword xml:id="k4">tuberculin skin test</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p><b>Background
</b> Epidemiological relation of intestinal helminth infection and atopic disease, both associated with a T‐helper (Th) 2 immune response, is controversial, as it has been reported that helminth infection may either suppress or pre‐dispose to atopic disease. This relation has not been tested in an area with a high burden of <i>Mycobacterium tuberculosis</i> (MTB) infection, a known Th1‐stimulating infection.</p><p><b>Objective
</b> To study the association of intestinal helminth infection and atopic disease in a community where helminth infection is endemic and MTB infection is high.</p><p><b>Methods
</b> Three‐hundred and fifty‐nine randomly selected children aged 6–14 years from a poor urban suburb were tested with allergy questionnaire, skin prick test (SPT) to common aeroallergens, <i>Ascaris</i>‐specific IgE (<i>Ascaris</i>‐sIgE), fecal examination for pathogenic intestinal helminths and tuberculin skin testing (TST). Histamine bronchoprovocation was tested in the group of children aged 10 years and older. Results were corrected for demographic variables, socioeconomic status, parental allergy, environmental tobacco smoke (ETS) exposure in the household, recent anthelminthic treatment and for clustering in the sampling unit.</p><p><b>Results
</b> <i>Ascaris</i>‐sIgE was elevated in 48% of children, <i>Ascaris</i> eggs were found in 15% and TST was positive in 53%. Children with elevated <i>Ascaris</i>‐sIgE had significantly increased risk of positive SPT to aeroallergens, particularly house dust mite, atopic asthma (<i>ever</i> and <i>recent</i>), atopic rhinitis (<i>ever</i> and <i>recent</i>) and increased atopy‐related bronchial hyper‐responsiveness. In children with negative TST (<10 mm), elevated <i>Ascaris</i>‐sIgE was associated with significantly increased risk of atopic symptoms (adjusted odds ratio (OR<sub>adj</sub>) 6.5; 95% confidence interval (CI) 1.9–22.4), whereas in those with positive TST (<inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" location="ges.gif" href=""></inlineGraphic>10 mm) this association disappeared (OR<sub>adj</sub> 0.96; 95% CI 0.4–2.8).</p><p><b>Conclusions
</b> These results suggest that immune response to <i>Ascaris</i> (<i>Ascaris</i>‐sIgE) may be a risk factor of atopic disease in populations exposed to mild <i>Ascaris</i> infection and that MTB infection may be protective against this risk, probably by stimulation of anti‐inflammatory networks.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Respiratory atopic disease, Ascaris‐immunoglobulin E and tuberculin testing in urban South African children</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Respiratory atopic disease, Ascaris‐IgE and tuberculin testing</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Respiratory atopic disease, Ascaris‐immunoglobulin E and tuberculin testing in urban South African children</title></titleInfo><name type="personal"><namePart type="given">C. C.</namePart><namePart type="family">Obihara</namePart><affiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</affiliation><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Beyers</namePart><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. P.</namePart><namePart type="family">Gie</namePart><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. O.</namePart><namePart type="family">Hoekstra</namePart><affiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. E.</namePart><namePart type="family">Fincham</namePart><affiliation>Nutritional Intervention Research Unit,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B. J.</namePart><namePart type="family">Marais</namePart><affiliation>Desmond Tutu TB Centre, Department of Paediatrics and Child Health, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. J.</namePart><namePart type="family">Lombard</namePart><affiliation>Biostatistics Unit, Medical Research Council of South Africa, Cape Town, South Africa</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L. A.</namePart><namePart type="family">Dini</namePart><affiliation>Parasitology Reference Unit, National Institute for Communicable Diseases, National Health Laboratory Services, Johannesburg, South Africa</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. L. L.</namePart><namePart type="family">Kimpen</namePart><affiliation>Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-05</dateIssued><edition>Submitted 6 July 2005; revised 30 October 2005; accepted 17 January 2006</edition><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">1</extent><extent unit="tables">3</extent><extent unit="formulas">0</extent><extent unit="references">39</extent><extent unit="linksCrossRef">56</extent><extent unit="words">6437</extent></physicalDescription><abstract>Background Epidemiological relation of intestinal helminth infection and atopic disease, both associated with a T‐helper (Th) 2 immune response, is controversial, as it has been reported that helminth infection may either suppress or pre‐dispose to atopic disease. This relation has not been tested in an area with a high burden of Mycobacterium tuberculosis (MTB) infection, a known Th1‐stimulating infection.</abstract><abstract>Objective To study the association of intestinal helminth infection and atopic disease in a community where helminth infection is endemic and MTB infection is high.</abstract><abstract>Methods Three‐hundred and fifty‐nine randomly selected children aged 6–14 years from a poor urban suburb were tested with allergy questionnaire, skin prick test (SPT) to common aeroallergens, Ascaris‐specific IgE (Ascaris‐sIgE), fecal examination for pathogenic intestinal helminths and tuberculin skin testing (TST). Histamine bronchoprovocation was tested in the group of children aged 10 years and older. Results were corrected for demographic variables, socioeconomic status, parental allergy, environmental tobacco smoke (ETS) exposure in the household, recent anthelminthic treatment and for clustering in the sampling unit.</abstract><abstract>Results Ascaris‐sIgE was elevated in 48% of children, Ascaris eggs were found in 15% and TST was positive in 53%. Children with elevated Ascaris‐sIgE had significantly increased risk of positive SPT to aeroallergens, particularly house dust mite, atopic asthma (ever and recent), atopic rhinitis (ever and recent) and increased atopy‐related bronchial hyper‐responsiveness. In children with negative TST (<10 mm), elevated Ascaris‐sIgE was associated with significantly increased risk of atopic symptoms (adjusted odds ratio (ORadj) 6.5; 95% confidence interval (CI) 1.9–22.4), whereas in those with positive TST (10 mm) this association disappeared (ORadj 0.96; 95% CI 0.4–2.8).</abstract><abstract>Conclusions These results suggest that immune response to Ascaris (Ascaris‐sIgE) may be a risk factor of atopic disease in populations exposed to mild Ascaris infection and that MTB infection may be protective against this risk, probably by stimulation of anti‐inflammatory networks.</abstract><subject lang="en"><genre>keywords</genre><topic>Ascaris specific IgE</topic><topic>atopic disease</topic><topic>childhood</topic><topic>tuberculin skin test</topic></subject><relatedItem type="host"><titleInfo><title>Clinical & Experimental Allergy</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">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>2006</date><detail type="volume"><caption>vol.</caption><number>36</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>640</start><end>648</end><total>9</total></extent></part></relatedItem><identifier type="istex">15093C051A532710A1702C47A95CD37BCDDD8052</identifier><identifier type="ark">ark:/67375/WNG-N7VP2VMH-9</identifier><identifier type="DOI">10.1111/j.1365-2222.2006.02479.x</identifier><identifier type="ArticleID">CEA2479</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/15093C051A532710A1702C47A95CD37BCDDD8052/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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