Increased immunoglobulin E response in acute coronary syndromes

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dc.authoridAltun, Armagan/0000-0002-3233-8263
dc.authorwosidAltun, Armagan/ABB-5844-2020
dc.contributor.authorErdogan, O
dc.contributor.authorGul, C
dc.contributor.authorAltun, A
dc.contributor.authorOzbay, G
dc.date.accessioned2024-06-12T11:17:29Z
dc.date.available2024-06-12T11:17:29Z
dc.date.issued2003
dc.departmentTrakya Üniversitesien_US
dc.description.abstractThe role of inflammation and mast cell activation has been implicated in atherosclerotic plaque destabilization and rupture. To investigate the role of immunoglobulin E (IgE) in acute coronary syndrome, a prospective clinical study was conducted in patients with acute myocardial infarction (AMI), unstable angina pectoris (UAP), stable angina pectoris (SAP), and healthy controls. IgE levels were serially measured and compared in consecutive patients with AMI (n = 16) and UAP (n= 14) on days 1, 3, 7, 21 after admission and 3 months later and only once in stable angina pectoris (n = 15) and healthy controls (n = 14). In addition, blood eosinophil and basophil levels on admission were measured in all groups and compared. Initial IgE levels determined at admission in patients with AMI, UAP, and SAP were significantly higher than levels in the control group (p=0.002). Initial high IgE level in AMI on day I increased to a peak by day 7 (p = 0.024), then gradually decreased by day 21 and at 3 months (p = 0.052). High IgE level in UAP persisted by day 7 and gradually decreased by day 21 and 3 months (p = 0.037 and p = 0.018, respectively). Blood eosinophil count on admission was significantly higher in UAP than in the control group (p = 0.005). Basophil levels of both AMI and UAP groups on admission were found to be elevated as opposed to control group (p = 0.02 and p = 0.012, respectively). This study demonstrates that the level of IgE significantly increased during the acute phase of acute coronary syndromes and gradually decreased, supporting the role of acute inflammatory response and mast cell involvement in plaque rupture.en_US
dc.identifier.doi10.1177/000331970305400109
dc.identifier.endpage79en_US
dc.identifier.issn0003-3197
dc.identifier.issue1en_US
dc.identifier.pmid12593498en_US
dc.identifier.scopus2-s2.0-0037274555en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage73en_US
dc.identifier.urihttps://doi.org/10.1177/000331970305400109
dc.identifier.urihttps://hdl.handle.net/20.500.14551/24729
dc.identifier.volume54en_US
dc.identifier.wosWOS:000180843200009en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWestminster Publ Incen_US
dc.relation.ispartofAngiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectActivated Mast-Cellsen_US
dc.subjectMyocardial-Infarctionen_US
dc.subjectAtherosclerotic Plaquesen_US
dc.subjectAngina-Pectorisen_US
dc.subjectRuptureen_US
dc.subjectIgeen_US
dc.subjectSiteen_US
dc.subjectInfiltrationen_US
dc.subjectDiseaseen_US
dc.subjectErosionen_US
dc.titleIncreased immunoglobulin E response in acute coronary syndromesen_US
dc.typeArticleen_US

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