Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome
Identifieur interne : 000B80 ( Istex/Corpus ); précédent : 000B79; suivant : 000B81Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome
Auteurs : Jens Gaab ; Nicolas Rohleder ; Vera Heitz ; Tanja Schad ; Veronika Engert ; Thomas H. Schürmeyer ; Ulrike EhlertSource :
- Acta Neuropsychiatrica [ 0924-2708 ] ; 2003-08.
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Abstract
Objective: Alterations of the immune–neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticoids (GCs) when under stress.
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DOI: 10.1034/j.1601-5215.2003.00033.x
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Schürmeyer</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Ehlert, Ulrike" sort="Ehlert, Ulrike" uniqKey="Ehlert U" first="Ulrike" last="Ehlert">Ulrike Ehlert</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C</idno><date when="2003" year="2003">2003</date><idno type="doi">10.1034/j.1601-5215.2003.00033.x</idno><idno type="url">https://api.istex.fr/document/6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000B80</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000B80</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome</title><author><name sortKey="Gaab, Jens" sort="Gaab, Jens" uniqKey="Gaab J" first="Jens" last="Gaab">Jens Gaab</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jgaab@klipsy.unizh.ch</mods:affiliation></affiliation></author><author><name sortKey="Rohleder, Nicolas" sort="Rohleder, Nicolas" uniqKey="Rohleder N" first="Nicolas" last="Rohleder">Nicolas Rohleder</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Heitz, Vera" sort="Heitz, Vera" uniqKey="Heitz V" first="Vera" last="Heitz">Vera Heitz</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schad, Tanja" sort="Schad, Tanja" uniqKey="Schad T" first="Tanja" last="Schad">Tanja Schad</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Engert, Veronika" sort="Engert, Veronika" uniqKey="Engert V" first="Veronika" last="Engert">Veronika Engert</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schurmeyer, Thomas H" sort="Schurmeyer, Thomas H" uniqKey="Schurmeyer T" first="Thomas H" last="Schürmeyer">Thomas H. Schürmeyer</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Ehlert, Ulrike" sort="Ehlert, Ulrike" uniqKey="Ehlert U" first="Ulrike" last="Ehlert">Ulrike Ehlert</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neuropsychiatrica</title><idno type="ISSN">0924-2708</idno><idno type="eISSN">1601-5215</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-08">2003-08</date><biblScope unit="volume">15</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="184">184</biblScope><biblScope unit="page" to="191">191</biblScope></imprint><idno type="ISSN">0924-2708</idno></series><idno type="istex">6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C</idno><idno type="DOI">10.1034/j.1601-5215.2003.00033.x</idno><idno type="ArticleID">ACN033</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0924-2708</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ACTH</term><term>HPA axis</term><term>chronic fatigue syndrome</term><term>cortisol</term><term>dexamethasone</term><term>glucocorticoid sensitivity</term><term>interleukin‐6</term><term>psychosocial stress</term><term>tumor necrosis factor‐alpha</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Objective: Alterations of the immune–neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticoids (GCs) when under stress.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jens Gaab</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string><json:string>E-mail: jgaab@klipsy.unizh.ch</json:string></affiliations></json:item><json:item><name>Nicolas Rohleder</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string></affiliations></json:item><json:item><name>Vera Heitz</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string></affiliations></json:item><json:item><name>Tanja Schad</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string></affiliations></json:item><json:item><name>Veronika Engert</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string></affiliations></json:item><json:item><name>Thomas H Schürmeyer</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string></affiliations></json:item><json:item><name>Ulrike Ehlert</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>ACTH</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chronic fatigue syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cortisol</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dexamethasone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glucocorticoid sensitivity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HPA axis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>interleukin‐6</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>psychosocial stress</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tumor necrosis factor‐alpha</value></json:item></subject><articleId><json:string>ACN033</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><qualityIndicators><score>4.703</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 782 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Rief</name></json:item><json:item><name>F Pilger</name></json:item><json:item><name>D Ihle</name></json:item><json:item><name>E Bosmans</name></json:item><json:item><name>B Egyed</name></json:item><json:item><name>M Maes</name></json:item></author><host><volume>105</volume><pages><last>174</last><first>165</first></pages><author></author><title>Psychiatry Res</title></host><title>Immunological differences between patients with major depression and somatization syndrome</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>15</volume><publisherId><json:string>ACN</json:string></publisherId><pages><total>8</total><last>191</last><first>184</first></pages><issn><json:string>0924-2708</json:string></issn><issue>4</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1601-5215</json:string></eissn><title>Acta Neuropsychiatrica</title><doi><json:string>10.1111/(ISSN)1601-5215</json:string></doi></host><categories><wos></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>psychiatry</json:string></scienceMetrix></categories><publicationDate>2003</publicationDate><copyrightDate>2003</copyrightDate><doi><json:string>10.1034/j.1601-5215.2003.00033.x</json:string></doi><id>6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C</id><score>1.3382981</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2003</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome</title><author xml:id="author-1"><persName><forename type="first">Jens</forename><surname>Gaab</surname></persName><email>jgaab@klipsy.unizh.ch</email><note type="biography">Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</note><affiliation>Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</affiliation><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">Nicolas</forename><surname>Rohleder</surname></persName><note type="biography">Current address: Institute of Experimental Psychology II, University of Düsseldorf, Germany.</note><affiliation>Current address: Institute of Experimental Psychology II, University of Düsseldorf, Germany.</affiliation><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author><author xml:id="author-3"><persName><forename type="first">Vera</forename><surname>Heitz</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author><author xml:id="author-4"><persName><forename type="first">Tanja</forename><surname>Schad</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author><author xml:id="author-5"><persName><forename type="first">Veronika</forename><surname>Engert</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">Thomas H</forename><surname>Schürmeyer</surname></persName><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author><author xml:id="author-7"><persName><forename type="first">Ulrike</forename><surname>Ehlert</surname></persName><note type="biography">Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</note><affiliation>Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</affiliation><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation></author></analytic><monogr><title level="j">Acta Neuropsychiatrica</title><idno type="pISSN">0924-2708</idno><idno type="eISSN">1601-5215</idno><idno type="DOI">10.1111/(ISSN)1601-5215</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-08"></date><biblScope unit="volume">15</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="184">184</biblScope><biblScope unit="page" to="191">191</biblScope></imprint></monogr><idno type="istex">6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C</idno><idno type="DOI">10.1034/j.1601-5215.2003.00033.x</idno><idno type="ArticleID">ACN033</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Objective: Alterations of the immune–neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticoids (GCs) when under stress.</p></abstract><abstract><p>Methods: A total of 21 CFS patients and 20 healthy age‐ and gender‐matched controls underwent a standardized psychosocial stress test (Trier Social Stress Test, TSST). Salivary and plasma cortisol levels were measured repeatedly following exposure to the stressor. GC sensitivity was assessed in vitro by dexamethasone inhibition of lipopolysaccharide‐stimulated production of interleukin‐6 (IL‐6) and tumor necrosis factor‐alpha (TNC‐α).</p></abstract><abstract><p>Results: Cortisol responses following the TSST did not differ significantly between CFS patients and healthy controls. GC sensitivity differed significantly between CFS patients and healthy controls, with CFS patients showing a greater sensitivity towards GCs (TNF‐α: F1/39 = 7.32, P = 0.01; IL‐6: F1/39 = 9.73, P = 0.004).</p></abstract><abstract><p>Conclusion: Consistent with recent evidence, CFS patients are characterized by an enhanced sensitivity to glucocorticoids. The implications for secondary processes, such as the regulatory influence of glucocorticoids on immune processes, are discussed.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>ACTH</term></item><item><term>chronic fatigue syndrome</term></item><item><term>cortisol</term></item><item><term>dexamethasone</term></item><item><term>glucocorticoid sensitivity</term></item><item><term>HPA axis</term></item><item><term>interleukin‐6</term></item><item><term>psychosocial stress</term></item><item><term>tumor necrosis factor‐alpha</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C/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>Munksgaard International Publishers</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1601-5215</doi><issn type="print">0924-2708</issn><issn type="electronic">1601-5215</issn><idGroup><id type="product" value="ACN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ACTA NEUROPSYCHIATRICA">Acta Neuropsychiatrica</title></titleGroup></publicationMeta><publicationMeta level="part" position="08004"><doi origin="wiley">10.1111/acn.2003.15.issue-4</doi><numberingGroup><numbering type="journalVolume" number="15">15</numbering><numbering type="journalIssue" number="4">4</numbering></numberingGroup><coverDate startDate="2003-08">August 2003</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0018400" status="forIssue"><doi origin="wiley">10.1034/j.1601-5215.2003.00033.x</doi><idGroup><id type="unit" value="ACN033"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2003-07-28"></event><event type="publishedOnlineFinalForm" date="2003-07-28"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-11"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2013-12-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="184">184</numbering><numbering type="pageLast" number="191">191</numbering></numberingGroup><correspondenceTo> ‡Dr phil. Jens Gaab, Institute for Psychology, Clinical Psychology II, University of Zürich, Zürichbergstr. 43, CH‐8044 Zürich, Switzerland. Tel. + 41 16343096; Fax: + 41 16343696. E‐mail: <email>jgaab@klipsy.unizh.ch</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ACN.ACN033.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="1"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="43"></count><count type="wordTotal" number="4971"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome</title><title type="shortAuthors"><b>Gaab et al.</b></title><title type="short"><b>Enhanced glucocorticoid sensitivity in CFS</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" noteRef="#fn1" corresponding="yes"><personName><givenNames>Jens</givenNames><familyName>Gaab</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1" noteRef="#fn2"><personName><givenNames>Nicolas</givenNames><familyName>Rohleder</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Vera</givenNames><familyName>Heitz</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Tanja</givenNames><familyName>Schad</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Veronika</givenNames><familyName>Engert</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>Thomas H</givenNames><familyName>Schürmeyer</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1" noteRef="#fn1"><personName><givenNames>Ulrike</givenNames><familyName>Ehlert</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">ACTH</keyword><keyword xml:id="k2">chronic fatigue syndrome</keyword><keyword xml:id="k3">cortisol</keyword><keyword xml:id="k4">dexamethasone</keyword><keyword xml:id="k5">glucocorticoid sensitivity</keyword><keyword xml:id="k6">HPA axis</keyword><keyword xml:id="k7">interleukin‐6</keyword><keyword xml:id="k8">psychosocial stress</keyword><keyword xml:id="k9">tumor necrosis factor‐alpha</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!-- Gaab J, Rohleder N, Heitz V, Schad T, Engert V, Schürmeyer TH, Ehlert U. Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome --><p><b>Objective: </b> Alterations of the immune–neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticoids (GCs) when under stress.</p><p><b>Methods: </b> A total of 21 CFS patients and 20 healthy age‐ and gender‐matched controls underwent a standardized psychosocial stress test (Trier Social Stress Test, TSST). Salivary and plasma cortisol levels were measured repeatedly following exposure to the stressor. GC sensitivity was assessed <i>in vitro</i> by dexamethasone inhibition of lipopolysaccharide‐stimulated production of interleukin‐6 (IL‐6) and tumor necrosis factor‐alpha (TNC‐α).</p><p><b>Results: </b> Cortisol responses following the TSST did not differ significantly between CFS patients and healthy controls. GC sensitivity differed significantly between CFS patients and healthy controls, with CFS patients showing a greater sensitivity towards GCs (TNF‐α: <i>F</i><sub>1/39</sub> = 7.32, <i>P</i> = 0.01; IL‐6: <i>F</i><sub>1/39</sub> = 9.73, <i>P</i> = 0.004).</p><p><b>Conclusion: </b> Consistent with recent evidence, CFS patients are characterized by an enhanced sensitivity to glucocorticoids. The implications for secondary processes, such as the regulatory influence of glucocorticoids on immune processes, are discussed.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><label>* </label><p> Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</p></note><note xml:id="fn2"><label>† </label><p> Current address: Institute of Experimental Psychology II, University of Düsseldorf, Germany.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Enhanced glucocorticoid sensitivity in CFS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome</title></titleInfo><name type="personal"><namePart type="given">Jens</namePart><namePart type="family">Gaab</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><description>Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</description><affiliation>E-mail: jgaab@klipsy.unizh.ch</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicolas</namePart><namePart type="family">Rohleder</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><description>Current address: Institute of Experimental Psychology II, University of Düsseldorf, Germany.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vera</namePart><namePart type="family">Heitz</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tanja</namePart><namePart type="family">Schad</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Veronika</namePart><namePart type="family">Engert</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas H</namePart><namePart type="family">Schürmeyer</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ulrike</namePart><namePart type="family">Ehlert</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany</affiliation><description>Current address: Institute for Psychology, Clinical Psychology II, University of Zürich, Switzerland.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2003-08</dateIssued><copyrightDate encoding="w3cdtf">2003</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="figures">3</extent><extent unit="tables">1</extent><extent unit="references">43</extent><extent unit="words">4971</extent></physicalDescription><abstract>Objective: Alterations of the immune–neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticoids (GCs) when under stress.</abstract><abstract>Methods: A total of 21 CFS patients and 20 healthy age‐ and gender‐matched controls underwent a standardized psychosocial stress test (Trier Social Stress Test, TSST). Salivary and plasma cortisol levels were measured repeatedly following exposure to the stressor. GC sensitivity was assessed in vitro by dexamethasone inhibition of lipopolysaccharide‐stimulated production of interleukin‐6 (IL‐6) and tumor necrosis factor‐alpha (TNC‐α).</abstract><abstract>Results: Cortisol responses following the TSST did not differ significantly between CFS patients and healthy controls. GC sensitivity differed significantly between CFS patients and healthy controls, with CFS patients showing a greater sensitivity towards GCs (TNF‐α: F1/39 = 7.32, P = 0.01; IL‐6: F1/39 = 9.73, P = 0.004).</abstract><abstract>Conclusion: Consistent with recent evidence, CFS patients are characterized by an enhanced sensitivity to glucocorticoids. The implications for secondary processes, such as the regulatory influence of glucocorticoids on immune processes, are discussed.</abstract><subject lang="en"><genre>keywords</genre><topic>ACTH</topic><topic>chronic fatigue syndrome</topic><topic>cortisol</topic><topic>dexamethasone</topic><topic>glucocorticoid sensitivity</topic><topic>HPA axis</topic><topic>interleukin‐6</topic><topic>psychosocial stress</topic><topic>tumor necrosis factor‐alpha</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neuropsychiatrica</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0924-2708</identifier><identifier type="eISSN">1601-5215</identifier><identifier type="DOI">10.1111/(ISSN)1601-5215</identifier><identifier type="PublisherID">ACN</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>184</start><end>191</end><total>8</total></extent></part></relatedItem><identifier type="istex">6464DDD0B7095776A5AE934C1E6FE72CC9C0BB0C</identifier><identifier type="DOI">10.1034/j.1601-5215.2003.00033.x</identifier><identifier type="ArticleID">ACN033</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Munksgaard International Publishers</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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