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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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タイトル: 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
著者: Ieko, Masahiro 著作を一覧する
Yoshida, Mika 著作を一覧する
Naito, Sumiyoshi 著作を一覧する
Nakabayashi, Toru 著作を一覧する
Kanazawa, Kaoru 著作を一覧する
Mizukami, Kazuhiro 著作を一覧する
Mukai, Masaya 著作を一覧する
Atsumi, Tatsuya 著作を一覧する
Koike, Takao 著作を一覧する
キーワード: Antiphospholipid syndrome
Thrombosis
Thrombin-activatable fibrinolysis inhibitor
Systemic lupus erythematosus
発行日: 2010年 6月
出版者: Springer Japan
誌名: International Journal of Hematology
巻: 91
号: 5
開始ページ: 776
終了ページ: 783
出版社 DOI: 10.1007/s12185-010-0590-0
抄録: 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
資料タイプ: article (author version)
URI: http://hdl.handle.net/2115/43188
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 小池 隆夫

 

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