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Increase in plasma thrombin-activatable fibrinolysis inhibitor may not contribute to thrombotic tendency in antiphospholipid syndrome because of inhibitory potential of antiphospholipid antibodies toward TAFI activation

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Title: Increase in plasma thrombin-activatable fibrinolysis inhibitor may not contribute to thrombotic tendency in antiphospholipid syndrome because of inhibitory potential of antiphospholipid antibodies toward TAFI activation
Authors: Ieko, Masahiro Browse this author
Yoshida, Mika Browse this author
Naito, Sumiyoshi Browse this author
Nakabayashi, Toru Browse this author
Kanazawa, Kaoru Browse this author
Mizukami, Kazuhiro Browse this author
Mukai, Masaya Browse this author
Atsumi, Tatsuya Browse this author
Koike, Takao Browse this author →KAKEN DB
Keywords: Antiphospholipid syndrome
Thrombosis
Thrombin-activatable fibrinolysis inhibitor
Systemic lupus erythematosus
Issue Date: Jun-2010
Publisher: Springer Japan
Journal Title: International Journal of Hematology
Volume: 91
Issue: 5
Start Page: 776
End Page: 783
Publisher DOI: 10.1007/s12185-010-0590-0
Abstract: Background: The causes of thrombosis in antiphospholipid syndrome (APS) remain unknown, though several hypotheses in regard to hypofibrinolysis have been proposed. Objective: To clarify the mechanism, we measured plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI) in APS patients. Methods and Results: Both the TAFI antigen (TAFI:Ag) level measured with an ELISA, and thrombin-thrombomodulin-dependent TAFI activity (TAFI:Ac) were elevated in 68 APS patients as compared with those in 66 healthy controls, though they were lower than those in 46 patients with autoimmune diseases. As for the influence of antiphospholipid antibodies (aPL) on TAFI levels, the mean TAFI:Ac level in 39 SLE patients positive for APS was significantly lower than that in 27 SLE patients without APS, whereas there was no difference in TAFI:Ag between those groups. Furthermore, purified IgG from patients positive for aPL, and monoclonal aPL (EY2C9 and 23-1D) inhibited the activation of TAFI in a concentration dependent manner. Conclusion: These results suggest that aPL inhibits TAFI activation by affecting the function of thrombomodulin-thrombin complex through phospholipids. Although TAFI in plasma is elevated in autoimmune diseases including APS, we concluded that an elevated level is not likely a risk factor for thrombosis in APS patients, because of the inhibition of TAFI activation by aPL.
Rights: The final publication is available at www.springerlink.com
Type: article (author version)
URI: http://hdl.handle.net/2115/43188
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小池 隆夫

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