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dc.contributor.authorSiljan, William Ward
dc.contributor.authorHolter, Jan Cato
dc.contributor.authorNymo, Ståle Haugset
dc.contributor.authorHusebye, Einar
dc.contributor.authorUeland, Thor
dc.contributor.authorAukrust, Pål
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorHeggelund, Lars
dc.date.accessioned2018-07-10T12:29:06Z
dc.date.available2018-07-10T12:29:06Z
dc.date.issued2017-11-24
dc.description.abstractBackground:<br> The inflammatory response to community-acquired pneumonia (CAP) is orchestrated through activation of cytokine networks and the complement system. We examined the association of multiple cytokines and the terminal complement complex (TCC) with microbial aetiology, disease severity and shortterm outcome.<br> Materials and methods: <br>Plasma levels of 27 cytokines and TCC were analysed in blood samples obtained at hospital admission, clinical stabilization and 6-week follow-up from 247 hospitalized adults with CAP. Fourteen mediators were included in final analyses. Adverse short-term outcome was defined as intensive care unit (ICU) admission and 30-day mortality. <br>Results: <br>Cytokine and TCC levels were dynamic in the clinical course of CAP, with highest levels seen at admission for most mediators. Admission levels of cytokines and TCC did not differ between groups of microbial aetiology. High admission levels of IL-6 (odds ratio [OR] 1.47, 95% confidence interval [CI] 1.18-1.84, <i>P</i> = .001), IL-8 (OR 1.79, 95% CI 1.26-2.55, <i>P</i> = .001) and MIP-1b (OR 2.28, 95% CI 1.36-3.81, <i>P</i> = .002) were associated with a CURB-65 severity score of ≥3, while IL-6 (OR 1.37, 95% CI 1.07-1.74, <i>P</i> = .011) and MIP-1b (OR 1.86, 95% CI 1.03-3.36, <i>P</i> = .040) were associated with a high risk of an adverse short-term outcome.<br> Conclusions:<br> In this CAP cohort, admission levels of IL-6, IL-8 and MIP-1b were associated with disease severity and/or adverse short-term outcome. Still, for most mediators, only nonsignificant variations in inflammatory responses were observed for groups of microbial aetiology, disease severity and short-term outcome.en_US
dc.description.sponsorshipVestre Viken Hospital Trusten_US
dc.descriptionSource at: <a href=http://doi.org/10.1111/eci.12865> http://doi.org/10.1111/eci.12865</a>en_US
dc.identifier.citationSiljan, W. W., Holter, J. C., Nymo, S. H., Husebye, E., Ueland, T., Aukrust, P., Mollnes, T. E. & Heggelund L. (2017). Cytokine responses, microbial aetiology and short-term outcome in community-acquired pneumonia. European Journal of Clinical Investigation, 48(1), 1-10. http://doi.org/10.1111/eci.12865en_US
dc.identifier.cristinIDFRIDAID 1567274
dc.identifier.doi10.1111/eci.12865
dc.identifier.issn0014-2972
dc.identifier.issn1365-2362
dc.identifier.urihttps://hdl.handle.net/10037/13211
dc.language.isoengen_US
dc.publisherWileyen_US
dc.relation.journalEuropean Journal of Clinical Investigation
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/SFF/223255/Norway/Centre of Molecular Inflammation Research/CEMIR/en_US
dc.rights.accessRightsopenAccessen_US
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Lungesykdommer: 777en_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Lung diseases: 777en_US
dc.titleCytokine responses, microbial aetiology and short-term outcome in community-acquired pneumoniaen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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