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dc.contributor.authorSævik, Åse Bjorvatn
dc.contributor.authorUeland, Grethe Åstrøm
dc.contributor.authorÅkerman, Anna-Karin
dc.contributor.authorMethlie, Paal
dc.contributor.authorQuinkler, Marcus
dc.contributor.authorJørgensen, Anders Palmstrøm
dc.contributor.authorHöybye, Charlotte
dc.contributor.authorDebowska, Aleksandra
dc.contributor.authorNedrebø, Bjørn Gunnar
dc.contributor.authorDahle, Anne Lise
dc.contributor.authorCarlsen, Siri
dc.contributor.authorTomkowicz, Aneta
dc.contributor.authorSollid, Stina Therese
dc.contributor.authorNermoen, Ingrid
dc.contributor.authorGrønning, Kaja
dc.contributor.authorDahlqvist, Per
dc.contributor.authorGrimnes, Guri
dc.contributor.authorSkov, Jakob
dc.contributor.authorFinnes, Trine Elisabeth
dc.contributor.authorValland, Susanna Fonneland
dc.contributor.authorWahlberg, Jeanette
dc.contributor.authorHolte, Synnøve Emblem
dc.contributor.authorKämpe, Olle
dc.contributor.authorBensing, Sophie
dc.contributor.authorHusebye, Eystein Sverre
dc.contributor.authorØksnes, Marianne
dc.date.accessioned2023-12-11T12:00:33Z
dc.date.available2023-12-11T12:00:33Z
dc.date.issued2023-10-09
dc.description.abstractObjective - Increased prevalence of cardiovascular disease has been reported in autoimmune Addison's disease (AAD), but pathomechanisms are poorly understood.<p> <p<Design - Cross-sectional study.<p> <p>Methods - We compared serum levels of 177 cardiovascular and inflammatory biomarkers in 43 patients with AAD at >18-h glucocorticoid withdrawal and 43 matched controls, overall and stratified for sex. Biomarker levels were correlated with the frequency of adrenal crises and quality of life (QoL) by AddiQoL-30. Finally, we investigated changes in biomarker levels following 250 µg tetracosactide injection in patients without residual adrenocortical function (RAF) to explore glucocorticoid-independent effects of high ACTH.<p> <p>Results - Nineteen biomarkers significantly differed between patients with AAD and controls; all but 1 (ST1A1) were higher in AAD. Eight biomarkers were significantly higher in female patients compared with controls (IL6, MCP1, GAL9, SPON2, DR4, RAGE, TNFRSF9, and PGF), but none differed between male patients and controls. Levels of RAGE correlated with the frequency of adrenal crises (r = 0.415, P = .006) and AddiQoL-30 scores (r = −0.347, P = .028) but not after correction for multiple testing. PDL2 and leptin significantly declined 60 min after injection of ACTH in AAD without RAF (−0.15 normalized protein expression [NPX], P = .0001, and −0.25 NPX, P = .0003, respectively).<p> <p>Conclusions - We show that cardiovascular and inflammatory biomarkers are altered in AAD compared with controls, particularly in women. RAGE might be a marker of disease severity in AAD, associated with more adrenal crises and reduced QoL. High ACTH reduced PDL2 and leptin levels in a glucocorticoid-independent manner but the overall effect on biomarker profiles was small.en_US
dc.identifier.citationSævik ÅBS, Ueland GÅ, Åkerman A, Methlie P, Quinkler M, Jørgensen AP, Höybye C, Debowska A, Nedrebø BG, Dahle AL, Carlsen S, Tomkowicz A, Sollid St, Nermoen I, Grønning K, Dahlqvist P, Grimnes G, Skov J, Finnes TE, Valland SF, Wahlberg J, Holte SE, Kämpe O, Bensing S, Husebye ES, Øksnes M. Altered biomarkers for cardiovascular disease and inflammation in autoimmune Addison's disease - a cross-sectional study. European Journal of Endocrinology (EJE). 2023
dc.identifier.cristinIDFRIDAID 2183552
dc.identifier.doi10.1093/ejendo/lvad136
dc.identifier.issn0804-4643
dc.identifier.issn1479-683X
dc.identifier.urihttps://hdl.handle.net/10037/31989
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.relation.journalEuropean Journal of Endocrinology (EJE)
dc.rights.holderCopyright 2023 The Author(s)en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0en_US
dc.rightsAttribution 4.0 International (CC BY 4.0)en_US
dc.titleAltered biomarkers for cardiovascular disease and inflammation in autoimmune Addison's disease - a cross-sectional studyen_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's license is described as Attribution 4.0 International (CC BY 4.0)