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dc.contributor.authorErman, M.
dc.contributor.authorAbalı, H.
dc.contributor.authorOran, B.
dc.contributor.authorHaznedaroğlu, İbrahim C.
dc.contributor.authorCanpınar, H.
dc.contributor.authorKirazlı, S.
dc.contributor.authorÇelik, İ.
dc.date.accessioned2020-02-26T13:20:47Z
dc.date.available2020-02-26T13:20:47Z
dc.date.issued2004
dc.identifier.issn0923-7534
dc.identifier.urihttps://doi.org/10.1093/annonc/mdh437
dc.identifier.urihttp://hdl.handle.net/11655/22217
dc.description.abstractBackground: Current understanding of hemostatic systems enables us to better explore the enigmatic pathobiology of tamoxifen (TAM)-induced thrombotic diathesis. We have therefore aimed to assess the hemostatic changes in breast cancer patients receiving TAM on an adjuvant basis. Patients and methods: The study population consisted of 43 female patients with hormone receptor-positive breast cancer who received TAM 20 mg/day as part of their adjuvant treatment. Mean age was 52+/-12 years (range 25-74). Twenty-one patients (49%) were premenopausal. Plasma samples were collected prior to and following 6 months of TAM therapy and were assayed for total tissue factor pathway inhibitor (TFPI), free TFPI, lipid-bound TFPI, thrombomodulin, D dimer, activated protein C resistance (APC res), factors VIIa, II, V, VII and X, and global fibrinolytic capacity (GFC). Results: Median total TFPI decreased significantly from 48.5 ng/ml to 36.2 ng/ml (P=0.001), free TFPI from 10 to 7.6 ng/ml (P=0.001) and lipid-bound TFPI from 39.1 to 28.7 ng/ml (P=0.001). There were significant decreases in the levels of factor 11 (P=0.03), factor V (P=0.001), factor VII (P=0.06), thrombomodulin (P=0.01) and D dimer (P=0.001). However, APC res times were significantly prolonged (P=0.04). The remaining parameters that we have studied were not significantly affected. Conclusion: Our findings suggest that TAM tends to activate the coagulation pathway by counteracting major molecules involved in coagulation inhibition, namely TFPI and TM. As reflected by unchanged GFC, the drug appears to impair the expected compensatory activation of the fibrinolytic system, which removes fibrin polymers resulting from coagulation activation.tr_TR
dc.language.isoentr_TR
dc.publisherOxford Univ Presstr_TR
dc.relation.isversionof10.1093/annonc/mdh437tr_TR
dc.rightsinfo:eu-repo/semantics/openAccesstr_TR
dc.subjectBreast cancertr_TR
dc.subjectHemostasistr_TR
dc.subjectHypercoagulabilitytr_TR
dc.subjectTamoxifentr_TR
dc.subjectTFPItr_TR
dc.subjectVenous thromboembolismtr_TR
dc.subject.lcshR/W - Tıptr_TR
dc.titleTamoxifen-Induced Tissue Factor Pathway Inhibitor Reduction: A Clue for an Acquired Thrombophilic State?tr_TR
dc.typeinfo:eu-repo/semantics/articletr_TR
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalAnnals Of Oncologytr_TR
dc.contributor.departmentPrevantif Onkolojitr_TR
dc.identifier.volume15tr_TR
dc.identifier.issue11tr_TR
dc.identifier.startpage1622tr_TR
dc.identifier.endpage1626tr_TR
dc.indexingWoStr_TR
dc.indexingScopustr_TR
dc.fundingYoktr_TR


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