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Blood, 15 August 2000, Vol. 96, No. 4, pp. 1594-1595
BRIEF REPORT
Coagulation and fibrinolytic activities in 2 siblings with
 2-glycoprotein I deficiency
Rie Takeuchi,
Tatsuya Atsumi,
Masahiro Ieko,
Hiroyuki Takeya,
Shinsuke Yasuda,
Kenji Ichikawa,
Akito Tsutsumi,
Koji Suzuki, and
Takao Koike
From the Department of Medicine II, Hokkaido
University School of Medicine, Sapporo; the Health Sciences University
of Hokkaido, Tobetsu; and the Department of Molecular Pathobiology, Mie
University School of Medicine, Tsu, Japan.
 2-Glycoprotein I (2GPI) is a
major antigen for antiphospholipid antibodies, and its multiple in
vitro functions have been reported. This glycoprotein not only
down-regulates thrombin formation by inhibiting contact activation or
prothrombinase activity, but also up-regulates coagulation by reducing
protein C anticoagulant activity. However, the in vivo roles of
2GPI remain obscure. Coagulation and fibrinolytic
characteristics were investigated in individuals with
2GPI deficiency. An apparently healthy woman and her
brother are homozygotes for 2GPI deficiency. In these patients, Russell viper venom time was shortened (40.4 seconds; normal
range, 47.8 ± 4.95 seconds), but all markers of thrombin generation
and fibrin turnover were within normal ranges. Exogenous activated
protein C adequately prolonged the clotting time of the
2GPI-deficient plasma, and euglobulin lysis time was
also normal. Thus, elevated thrombin generation, enhancement of
activated protein C response, and an altered fibrinolytic system were
not found in congenitally 2GPI-deficient plasma.
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