Cutaneous glucocorticoid receptor sensitivity and proinflammatory cytokine levels in antidepressant-resistant depression

Show simple item record Fitzgerald, Peter O'Brien, Sinead M. Scully, Paul Rijkers, Kim Scott, Lucinda V. Dinan, Timothy G. 2013-02-14T13:33:29Z 2013-02-14T13:33:29Z 2005 2006-01
dc.identifier.citation PETER FITZGERALD, SINEAD M. O'BRIEN, PAUL SCULLY, KIM RIJKERS, LUCINDA V. SCOTT and TIMOTHY G. DINAN (2006). Cutaneous glucocorticoid receptor sensitivity and proinflammatory cytokine levels in antidepressantresistant depression. Psychological Medicine, 36,pp 3743 doi:10.1017/S003329170500632X en
dc.identifier.volume 36 en
dc.identifier.issued 1 en
dc.identifier.startpage 37 en
dc.identifier.endpage 43 en
dc.identifier.doi 10.1017/S003329170500632X
dc.description.abstract ABSTRACT Background. There is evidence to indicate that peripheral glucocorticoid receptor (GR) function is reduced in major depression, and a possible molecular explanation for this is the impact of raised pro-inflammatory cytokines. The topical steroid vasoconstriction assay provides a convenient probe of peripheral GR function. The present study sought to assess the sensitivity of peripheral GRs in antidepressant-resistant major depressives and investigate the association between GR sensitivity and circulating plasma cytokines. Method. Nineteen antidepressant-resistant depressives together with age- and sex-matched healthy controls underwent the steroid vasoconstriction assay using three commercial preparations of corticosteroids containing clobetasol propionate 0.05%, betamethasone valerate 0.1%, and clobetasone butyrate 0.05%, corresponding to very potent, potent, and moderately potent steroid creams respectively. The pro-inflammatory cytokines, tumour necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6) were measured using enzyme-linked immunosorbent assays. The severity of the depressive episode was assessed using the Hamilton Depression Scale (HAMD). Results. Depressed subjects had a significantly reduced vasoconstriction response across all three strengths of steroid. They also had significantly higher concentrations of TNF-a and IL-6. There was a significant inverse correlation between TNF-a concentration and vasoconstriction response and also between the HAMD score and vasoconstriction response. Conclusions. These findings suggest that cutaneous GR function is abnormal in antidepressantresistant depression, that circulating TNF-a may play a significant role in this abnormality and that the efficacy of topical steroids in antidepressant-resistant depressives is reduced. en
dc.description.sponsorship Science Foundation Ireland (SFI-CSET) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Cambridge University Press en
dc.rights ©2006, Cambridge University Press en
dc.subject Cutaneous glucocorticoid Receptor en
dc.subject Antidepressant-resistant en
dc.subject Pro-inflammatory cytokine levels en
dc.subject GR function en
dc.subject Hamilton depression scale en
dc.subject Depression en
dc.title Cutaneous glucocorticoid receptor sensitivity and proinflammatory cytokine levels in antidepressant-resistant depression en
dc.type Article (peer-reviewed) en
dc.internal.authorurl en
dc.internal.authorcontactother Prof. Timothy G. Dinan, Psychiatry, Unit GF, Cork University Hospital, Wilton, Cork. Email: en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.internal.rssid 43336857
dc.contributor.funder Science Foundation Ireland en
dc.contributor.funder Health Research Board en
dc.contributor.funder Wellcome Trust, United Kingdom en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Psychological Medicine en
dc.internal.copyrightchecked This is a Sherpa Romeo green journal. Policy: Institutional repositories - 2.4. The author may post the VoR version of the article (in PDF or HTML form) in the Institutional Repository of the institution in which the author worked at the time the article was first submitted, or (for appropriate journals) in PubMed Central or UK PubMed Central or arXiv, no sooner than one year after first publication of the article in the Journal, subject to file availability and provided the posting includes a prominent statement of the full bibliographical details, a copyright notice in the name of the copyright holder (Cambridge University Press or the sponsoring Society, as appropriate), and a link to the online edition of the Journal at Cambridge Journals Online. en
dc.internal.IRISemailaddress en

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