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Blood, 15 January 2002, Vol. 99, No. 2, pp. 526-530
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Plasma levels of endothelial protein C receptor respond to
anticoagulant treatment
Deborah J. Stearns-Kurosawa,
Kandice Swindle,
Armando D'Angelo,
Patrizia Della
Valle,
Annalisa Fattorini,
Nathalie Caron,
Marc Grimaux,
Barry Woodhams, and
Shinichiro Kurosawa
From the Free Radical Biology & Aging Research Program,
Oklahoma Medical Research Foundation, Oklahoma City; the Coagulation
Service and Thrombosis Research Unit, Scientific Institute HS Raffaele,
Milan, Italy; and Serbio (Diagnostica Stago), Gennevilliers, France.
The endothelial protein C receptor (EPCR) facilitates protein C
activation and plays a protective role in the response to Escherichia coli-mediated sepsis in primates. Previously,
a soluble form of EPCR (sEPCR) in human plasma was characterized, and
several studies indicated that generation of sEPCR is regulated by
inflammatory mediators, including thrombin-mediated up-regulation of
surface metalloproteolytic activity in vitro. This study addressed the question of whether plasma sEPCR levels reflect changes in thrombin generation in patients undergoing anticoagulant treatment. The sEPCR
levels in patients treated with coumarin-type oral anticoagulants were
significantly lower than those in healthy asymptomatic adult volunteers
(105.3 ± 70.8 ng/mL [n = 55] versus 165.8 ± 115.8 ng/mL [n = 200]; P < .0001). A similar decline in plasma
sEPCR levels was found in patients treated with unfractionated heparin.
In healthy volunteers, sEPCR levels declined to about 100 ng/mL within 3 days after initiation of an 8-day period of warfarin administration and increased within 2 days after its cessation. Plasma sEPCR levels
returned to pretreatment values within 1 week, and the changes in
plasma sEPCR levels mirrored changes in values for international
normalized ratios. A similar decline in sEPCR levels with time was
observed in 7 patients beginning treatment with warfarin for a
thrombotic disorder. Prothrombin fragment 1 + 2 levels also decreased
in volunteers and patients given warfarin. These results show that
plasma sEPCR levels decline in response to treatment with
anticoagulants whose mechanism of action is known to decrease in vivo
thrombin production.
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