Does anti-tnf therapy cause any change in platelet activation in ankylosing spondylitis patients?

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dc.authorwosidTurgut, Burhan/A-2517-2016
dc.contributor.authorOrum, Huseyin
dc.contributor.authorPamuk, Gulsum Emel
dc.contributor.authorPamuk, Omer Nuri
dc.contributor.authorDemir, Muzaffer
dc.contributor.authorTurgut, Burhan
dc.date.accessioned2024-06-12T10:51:48Z
dc.date.available2024-06-12T10:51:48Z
dc.date.issued2012
dc.departmentTrakya Üniversitesien_US
dc.description.abstractRecently, it has been reported that ankylosing spondylitis (AS) was characterised by endothelial dysfunction and the development of atherosclerotic complications. In this study, we evaluated platelet and endothelial activation parameters in AS patients. Fiftynine AS patients and 22 healthy controls were included. The clinical features and acute phase parameters were evaluated. In all patients and healthy controls, platelet-monocyte complexes (PMC), platelet-neutrophil complexes, basal and ADP-stimulated P-selectin (CD62P) expression were determined by flow cytometry; soluble E-selectin (sE-selectin) and soluble CD40L (sCD40L) were determined by ELISA. AS patients were divided into two groups as active and inactive by using BASDAI. In 15 AS patients, the evaluated parameters were assessed before and after 12 weeks of anti-TNF therapy. PMC and sCD40L levels in AS patients were significantly higher than in the control group (P values 0.013 and 0.016). The evaluated variables were similar in active and inactive AS groups (P > 0.05). There were no significant changes in platelet and endothelial activation parameters in AS patients after anti-TNF therapy (P > 0.05). Platelet activation which is reflected by high levels of PMC and sCD40L might be responsible for the increased frequency of atherosclerosis in AS. The platelet activation in our AS patients was not associated with disease activity and did not improve after anti-TNF therapy.en_US
dc.description.sponsorshipTrakya University [TUBAP-870]en_US
dc.description.sponsorshipThis study was supported by the Scientific research projects' fund of Trakya University (Project Number: TUBAP-870).en_US
dc.identifier.doi10.1007/s11239-011-0663-9
dc.identifier.endpage159en_US
dc.identifier.issn0929-5305
dc.identifier.issue2en_US
dc.identifier.pmid22173846en_US
dc.identifier.scopus2-s2.0-84858865771en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage154en_US
dc.identifier.urihttps://doi.org/10.1007/s11239-011-0663-9
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18488
dc.identifier.volume33en_US
dc.identifier.wosWOS:000299775000003en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofJournal Of Thrombosis And Thrombolysisen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAnkylosing Spondylitisen_US
dc.subjectPlatelet-Monocyte Complexesen_US
dc.subjectPlatelet-Neutrophil Complexesen_US
dc.subjectP-Selectinen_US
dc.subjectCD40Len_US
dc.subjectNecrosis-Factor-Alphaen_US
dc.subjectSystemic-Lupus-Erythematosusen_US
dc.subjectAcute Myocardial-Infarction/en_US
dc.subjectIntima-Media Thicknessen_US
dc.subjectRheumatoid-Arthritisen_US
dc.subjectEndothelial Functionen_US
dc.subjectP-Selectinen_US
dc.subjectAtherosclerosisen_US
dc.subjectInflammationen_US
dc.subjectThrombosisen_US
dc.titleDoes anti-tnf therapy cause any change in platelet activation in ankylosing spondylitis patients?en_US
dc.typeArticleen_US

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