NDLI: Antithrombin affects hemostatic response to recombinant activated factor VII in factor VIII deficient plasma.

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Antithrombin affects hemostatic response to recombinant activated factor VII in factor VIII deficient plasma.

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Antithrombin affects hemostatic response to recombinant activated factor VII in factor VIII deficient plasma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Szlam, Fania Taketomi, Taro Sheppard, Chelsea A. Kempton, Christine L. Levy, Jerrold H. Tanaka, Kenichi A.
Description	Country affiliation: United States Author Affiliation: Szlam F ( Department of Anesthesiology, Emory University School of Medicine, 1364 Clifton Rd., NE, Atlanta, GA 30322, USA.)
Abstract	BACKGROUND: Thromboembolic complications can occur with recombinant activated factor VII (rFVIIa) treatment in trauma and surgical patients but they are infrequent in hemophiliacs. Bleeding diathesis in these conditions is often attributed to reduced thrombin generation, which may be improved with rFVIIa. Normally, thrombin that diffuses from local vascular injury sites is quickly inactivated by antithrombin (AT). Evaluating the influence of AT levels on thrombin generation in hypocoagulable FVIII-deficient plasma would be a simple approach to better understand how procoagulant stimuli, such as rFVIIa, might result in postoperative thrombotic complications. We hypothesize that reduced AT concentrations would increase the procoagulant effects of rFVIIa in FVIII-deficient plasma. METHODS: Thrombin generation was evaluated in vitro in FVIII-deficient and AT/FVIII-deficient plasma using thrombelastography and a thrombin generation assay (Thrombinoscope). The effect of added rFVIIa on these variables was evaluated. RESULTS: Delayed thrombus formation based on thrombelastography in FVIII-deficient plasma was predictably reversed by rFVIIa. Improved thrombus formation and responses to rFVIIa were observed when AT levels were 20%-50% of normal. Thrombin generation in FVIII-deficient plasma increased in an inverse relationship to AT levels. Supplemental rFVIIa decreased the lag time of thrombin generation but not the amount of thrombin generated. CONCLUSIONS: Using FVIII-deficient plasma as a model of reduced thrombin generation, we demonstrate that low AT levels enhance in vitro hemostatic responses to rFVIIa. Reduced AT levels in trauma and surgical patients with normal or increased FVIII levels may be considered potentially prothrombotic. Monitoring of AT levels during rFVIIa therapy may thus reduce thrombotic complications in nonhemophiliacs.
File Format	HTM / HTML
ISSN	00032999
Issue Number	3
Volume Number	106
e-ISSN	15267598
Journal	Anesthesia & Analgesia
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2008-03-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Anesthesiology Antithrombins Deficiency Coagulants Pharmacology Factor Viia Hemophilia A Blood Hemostasis Drug Effects Recombinant Proteins Thrombin Metabolism Blood Coagulation Tests Humans In Vitro Techniques Time Factors Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine

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