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dc.contributor.authorGramstad, Olav Rogde
dc.contributor.authorSchjalm, Camilla
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorNielsen, Erik Waage
dc.date.accessioned2024-01-15T11:43:28Z
dc.date.available2024-01-15T11:43:28Z
dc.date.issued2023-08-10
dc.description.abstractC1 inhibitor (C1Inh) is a serine protease inhibitor involved in the kallikrein-kinin system, the complement system, the coagulation system, and the fibrinolytic system. In addition to the plasma leakage observed in hereditary angioedema (HAE), C1Inh deficiency may also affect these systems, which are important for thrombosis and inflammation. The aim of this study was to investigate the thromboinflammatory load in C1Inh deficiency. We measured 27 cytokines including interleukins, chemokines, interferons, growth factors, and regulators using multiplex technology. Complement activation (C4d, C3bc, and sC5b-C9/TCC), haemostatic markers (β-thromboglobulin (β-TG), thrombin-antithrombin complexes (TAT), prothrombin fragment 1 + 2 (F1 + 2), active plasminogen activator inhibitor-1 (PAI-1), and the neutrophil activation marker myeloperoxidase (MPO) were measured by enzyme immunoassays. Plasma and serum samples were collected from 20 patients with HAE type 1 or 2 in clinical remission and compared with 20 healthy age- and sex-matched controls. Compared to healthy controls, HAE patients had significantly higher levels of tumour necrosis factor (TNF), interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-7, IL-9, IL-12, and IL-17A, chemokine ligand (CXCL) 8, chemokine ligand (CCL) 3, CCL4, IL-1 receptor antagonist (IL-1RA), granulocyte-macrophage colony-stimulating factor (GM-CSF), fibroblast growth factor (FGF) 2 and platelet-derived growth factor (PDGF)-BB. HAE patients also had higher levels of TAT and F1 + 2. Although granulocyte colony-stimulating factor (G-CSF), β-TG and PAI-1 were higher in HAE patients, the differences did not reach statistical significance after correction for multiple testing. In conclusion, C1Inh deficiency is associated with an increased baseline thromboinflammatory load. These findings may reflect that HAE patients are in a subclinical attack state outside of clinically apparent oedema attacks.en_US
dc.identifier.citationGramstad, Schjalm, Mollnes, Nielsen. Increased thromboinflammatory load in hereditary angioedema. Clinical and Experimental Immunology. 2023;214(2):170-181en_US
dc.identifier.cristinIDFRIDAID 2218785
dc.identifier.doi10.1093/cei/uxad091
dc.identifier.issn0009-9104
dc.identifier.issn1365-2249
dc.identifier.urihttps://hdl.handle.net/10037/32493
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.relation.journalClinical and Experimental Immunology
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2023 The Author(s)en_US
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0en_US
dc.rightsAttribution-NonCommercial 4.0 International (CC BY-NC 4.0)en_US
dc.titleIncreased thromboinflammatory load in hereditary angioedemaen_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
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