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dc.contributor.author Füst, György
dc.contributor.author Munthe-Fog L
dc.contributor.author Illés, Zsolt László
dc.contributor.author Széplaki, Gábor
dc.contributor.author Molnár, Tihamér
dc.contributor.author Pusch, Gabriella
dc.contributor.author Hirschberg, Kristóf
dc.contributor.author Szegedi, Róbert
dc.contributor.author Szeplaki, Z
dc.contributor.author Prohászka, Zoltán
dc.contributor.author Skjoedt, MO
dc.contributor.author Garred, P
dc.date.accessioned 2020-05-20T11:27:05Z
dc.date.available 2020-05-20T11:27:05Z
dc.date.issued 2011
dc.identifier 84857193396
dc.identifier.citation pagination=185, 10 pages; journalVolume=8; journalTitle=JOURNAL OF NEUROINFLAMMATION;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/6354
dc.identifier.uri doi:10.1186/1742-2094-8-185
dc.description.abstract Background: A number of data indicate that the lectin pathway of complement activation contributes to the pathophysiology of ischemic stroke. The lectin pathway may be triggered by the binding of mannose-binding lectin (MBL), ficolin-2 or ficolin-3 to different ligands. Although several papers demonstrated the significance of MBL in ischemic stroke, the role of ficolins has not been examined. Methods: Sera were obtained within 12 hours after the onset of ischemic stroke (admission samples) and 3-4 days later (follow-up samples) from 65 patients. The control group comprised 100 healthy individuals and 135 patients with significant carotid stenosis (patient controls). The concentrations of ficolin-2 and ficolin-3, initiator molecules of the lectin complement pathway, were measured by ELISA methods. Concentration of C-reactive protein (CRP) was also determined by a particle-enhanced immunturbidimetric assay. Results: Concentrations of both ficolin-2 and ficolin-3 were significantly (p < 0.001) decreased in both the admission and in the follow-up samples of patients with definite ischemic stroke as compared to healthy subjects. Concentrations of ficolin-2 and ficolin-3 were even higher in patient controls than in healthy subjects, indicating that the decreased levels in sera during the acute phase of stroke are related to the acute ischemic event. Ficolin-3 levels in the follow-up samples inversely correlated with the severity of stroke indicated by NIH scale on admission. In follow-up samples an inverse correlation was observed between ficolin-3 levels and concentration of S100β, an indicator of the size of cerebral infarct. Patients with low ficolin-3 levels and high CRP levels in the follow up samples had a significantly worse outcome (adjusted ORs 5.6 and 3.9, respectively) as measured by the modified Rankin scale compared to patients with higher ficolin-3 and lower CRP concentrations. High CRP concentrations were similarly predictive for worse outcome, and the effects of low ficolin-3 and high CRP were independent. Conclusions: Our findings indicate that ficolin-mediated lectin pathways of complement activation contribute to the pathogenesis of ischemic stroke and may be additive to complement-independent inflammatory processes.
dc.relation.ispartof urn:issn:1742-2094
dc.title Low ficolin-3 levels in early follow-up serum samples are associated with the severity and unfavorable outcome of acute ischemic stroke
dc.type Journal Article
dc.date.updated 2018-09-02T09:01:39Z
dc.language.rfc3066 en
dc.identifier.mtmt 1938405
dc.identifier.wos 000300948800001
dc.identifier.pubmed 22206485
dc.contributor.department SE/AOK/K/III. Sz. Belgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem


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