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Complement activation is a crucial pathogenic factor in catastrophic antiphospholipid syndrome.

dc.contributor.authorBarratt-Due, Andreas
dc.contributor.authorFløisand, Yngvar
dc.contributor.authorLang, Hilde Elisabeth
dc.contributor.authorKvam, Ann Kristin
dc.contributor.authorHolme, Pål Andre
dc.contributor.authorBergseth, Grete
dc.contributor.authorTjønnfjord, Geir Erland
dc.contributor.authorMollnes, Tom Eirik
dc.date.accessioned2017-03-14T12:34:25Z
dc.date.available2017-03-14T12:34:25Z
dc.date.issued2016-04-22
dc.description.abstractCatastrophic antiphospholipid syndrome is associated with excessive complement activation explaining the clinical efficacy of complement inhibitory treatment.en_US
dc.descriptionFull text source is available at: https://doi.org/10.1093/rheumatology/kew040en_US
dc.identifier.citationBarratt-Due A, Fløisand Y, Lang HEL, Kvam AK, Holme PA, Bergseth G, Tjønnfjord GE, Mollnes TE. Complement activation is a crucial pathogenic factor in catastrophic antiphospholipid syndrome. Rheumatology. 2016en_US
dc.identifier.cristinIDFRIDAID 1439398
dc.identifier.doi10.1093/rheumatology/kew040
dc.identifier.issn1462-0324
dc.identifier.issn1462-0332
dc.identifier.urihttps://hdl.handle.net/10037/10654
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.relation.ispartofseriesVolume 55, Issue 7en_US
dc.relation.journalRheumatology
dc.relation.projectIDStiftelsen Kristian Gerhard Jebsen: SKJG-MED-012en_US
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/SFF223255/Norway/CentreofMolecularInflammationResearch/CEMIRen_US
dc.rights.accessRightsopenAccessen_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Rheumatology: 759en_US
dc.subjectCAPSen_US
dc.subjectCatastrophic antiphospholipid syndromeen_US
dc.subjectclinical efficacyen_US
dc.subjecttreatmenten_US
dc.subjectAPSen_US
dc.subjectEculizumaben_US
dc.subjectpathophysiologyen_US
dc.titleComplement activation is a crucial pathogenic factor in catastrophic antiphospholipid syndrome.en_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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