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dc.date.accessioned2018-06-20T08:56:01Z
dc.date.available2018-06-20T08:56:01Z
dc.date.created2017-05-31T20:55:00Z
dc.date.issued2017
dc.identifier.citationShahini, Negar Michelsen, Annika Nilsson, Per Ekholt, Karin Gullestad, Lars Broch, Kaspar Dahl, Christen Peder Aukrust, Pål Ueland, Thor Mollnes, Tom Eirik Yndestad, Arne Louwe, Maria Cornelia . The alternative complement pathway is dysregulated in patients with chronic heart failure. Scientific Reports. 2017, 7
dc.identifier.urihttp://hdl.handle.net/10852/61926
dc.description.abstractThe complement system, an important arm of the innate immune system, is activated in heart failure (HF). We hypothesized that HF patients are characterized by an imbalance of alternative amplification loop components; including properdin and complement factor D and the alternative pathway inhibitor factor H. These components and the activation product, terminal complement complex (TCC), were measured in plasma from 188 HF patients and 67 age- and sex- matched healthy controls by enzyme immunoassay. Our main findings were: (i) Compared to controls, patients with HF had significantly increased levels of factor D and TCC, and decreased levels of properdin, particularly patients with advanced clinical disorder (i.e., NYHA functional class IV), (ii) Levels of factor D and properdin in HF patients were correlated with measures of systemic inflammation (i.e., C-reactive protein), neurohormonal deterioration (i.e., Nt-proBNP), cardiac function, and deteriorated diastolic function, (iii) Low levels of factor H and properdin were associated with adverse outcome in univariate analysis and for factor H, this was also seen in an adjusted model. Our results indicate that dysregulation of circulating components of the alternative pathway explain the increased degree of complement activation and is related to disease severity in HF patients.en_US
dc.languageEN
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleThe alternative complement pathway is dysregulated in patients with chronic heart failureen_US
dc.typeJournal articleen_US
dc.creator.authorShahini, Negar
dc.creator.authorMichelsen, Annika
dc.creator.authorNilsson, Per
dc.creator.authorEkholt, Karin
dc.creator.authorGullestad, Lars
dc.creator.authorBroch, Kaspar
dc.creator.authorDahl, Christen Peder
dc.creator.authorAukrust, Pål
dc.creator.authorUeland, Thor
dc.creator.authorMollnes, Tom Eirik
dc.creator.authorYndestad, Arne
dc.creator.authorLouwe, Maria Cornelia
cristin.unitcode185,53,48,14
cristin.unitnameInstitutt for indremedisinsk forskning
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1473330
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Scientific Reports&rft.volume=7&rft.spage=&rft.date=2017
dc.identifier.jtitleScientific Reports
dc.identifier.volume7
dc.identifier.doihttp://dx.doi.org/10.1038/srep42532
dc.identifier.urnURN:NBN:no-64524
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn2045-2322
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/61926/1/article.pdf
dc.type.versionPublishedVersion


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