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

Ieko, Masahiro; Yoshida, Mika; Naito, Sumiyoshi; Nakabayashi, Toru; Kanazawa, Kaoru; Mizukami, Kazuhiro; Mukai, Masaya; Atsumi, Tatsuya; Koike, Takao

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

Ieko, Masahiro; Yoshida, Mika; Naito, Sumiyoshi et al.

International Journal of Hematology, 2010, 91(5), 776-783

Permalink : https://hdl.handle.net/2115/43188

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アクセス権	open access
URI	https://hdl.handle.net/2115/43188
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 ; Yoshida, Mika ; Naito, Sumiyoshi ; Nakabayashi, Toru ; Kanazawa, Kaoru ; Mizukami, Kazuhiro ; Mukai, Masaya ; Atsumi, Tatsuya ; Koike, Takao
著者名 Ieko, Masahiro
著者名 Yoshida, Mika
著者名 Naito, Sumiyoshi
著者名 Nakabayashi, Toru
著者名 Kanazawa, Kaoru
著者名 Mizukami, Kazuhiro
著者名 Mukai, Masaya
著者名 Atsumi, Tatsuya
e-Rad_Researcher 80146795 著者名 Koike, Takao
言語	英語
キーワード	Antiphospholipid syndrome
	Thrombosis
	Thrombin-activatable fibrinolysis inhibitor
	Systemic lupus erythematosus
発行日	2010-06
出版者	Springer Japan
収録物名	International Journal of Hematology
巻(号)	91(5)
ページ	776-783
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.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	The final publication is available at www.springerlink.com
PISSN	0925-5710
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1007/s12185-010-0590-0