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dc.contributor.authorHokstad, Ingrid
dc.contributor.authorDeyab, Gia
dc.contributor.authorFagerland, Morten
dc.contributor.authorLyberg, Torstein
dc.contributor.authorHjeltnes, Gunnbjørg
dc.contributor.authorFørre, Øystein Thorleiv
dc.contributor.authorAgewall, Stefan
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorHollan, Ivana
dc.identifier.citationPLOS ONE. 2019, 14 (7), 1-16.nb_NO
dc.description.abstractBackground The complement system is involved in pathogenesis of cardiovascular disease, and might play a role in accelerated atherogenesis in spondylarthropathies (SpA). Hence, we examined complement activation in SpA, and its relationship to antirheumatic treatment, inflammatory and cardiovascular markers. Methods From PSARA, a prospective observational study, we examined 51 SpA patients (31 psoriatic arthritis (PsA), and 20 ankylosing spondylitis (AS)), starting tumor necrosis factor (TNF) inhibitor alone (n = 25), combined with methotrexate (MTX) (n = 10), or MTX monotherapy (n = 16). Complement activation was determined by the soluble terminal complement complex (sC5b-9), inflammation by erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and endothelial function by finger plethysmography (Endopat) at baseline, after 6 weeks and 6 months of treatment. Results SpA patients had sC5b-9 levels at (PsA) or above (AS) the upper limit of the estimated reference range. Median sC5b-9 levels decreased significantly from baseline to 6 weeks, with no significant difference between the AS and PsA group. Notably, a significant reduction in sC5b-9 was observed after administration of TNF inhibitor ± MTX, whereas no significant changes were observed in patients treated with MTX alone. Between 6 weeks and 6 months, sC5b-9 remained stable across all subgroups. Reduction in sC5b-9 was independently related to decreased ESR and CRP, and to increased high density cholesterol and total cholesterol. Reduction in sC5b-9 from baseline to 6 weeks was associated with improved EF in age and gender adjusted analyses. Conclusion TNF-inhibition, but not MTX monotherapy, led to rapid and sustained reduction of complement activation in SpA. Thus, the observed decrease in cardiovascular morbidity in patients treated with TNF-inhibitors might be partly due to its beneficial effect on complement. Trial registration Clinical Trials (NCT00902005), retrospectively registered on the 14th of May 2009.nb_NO
dc.description.abstractTumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational studynb_NO
dc.description.sponsorshipThe first author’s PhD scholarship is funded by The Norwegian Women’s Public Health Association, Grant 14902, URL: https://www. Financial support to the complement analyses was kindly provided by The Norwegian Council on Cardiovascular Disease, The Odd Fellow Foundation and The Simon Fougner Hartmann Family Fund, URL: https://,, and no webpage, respectively. The establishment of PSARA biobank was sponsored by Abbott Laboratories Norway - now Abbvie, URL: https:// The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscriptnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleTumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational studynb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.rights.holder© 2019 Hokstad et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.nb_NO
dc.source.journalPLOS ONEnb_NO
cristin.unitnameDiv Lillehammer

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Navngivelse 4.0 Internasjonal
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