Marcie J. Hursting
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Featured researches published by Marcie J. Hursting.
Clinical and Applied Thrombosis-Hemostasis | 2005
Marcie J. Hursting; Bruce E. Lewis; Donald E. Macfarlane
Argatroban, a direct thrombin inhibitor used for thromboprophylaxis or treatment in heparin-induced thrombocytopenia (HIT), is routinely monitored using the activated partial thromboplastin time (aPTT) yet also prolongs the international normalized ratio (INR). Peritransitional INRs, aPTTs, anticoagulant dosing patterns, and outcomes were evaluated in 165 HIT patients who were transitioned, without guidelines, from argatroban to warfarin therapy. Argatroban (median doses: 1.5-2.0 mcg/kg/min) and warfarin (median dose: 5 mg initially with 3.8 mg/day thereafter) overlapped a median 4 days. Median (5-95th percentile) aPTTs (in seconds) and INRs, respectively, were 59.8 (38.8-82.9) and 3.2 (1.7-7.0) during argatroban monotherapy, 68.6 (44.5-104) and 5.3 (2.4-16) maximally during cotherapy, 59.9 (38.7-92.2) and 4.0 (2.2-11.6) immediately before argatroban cessation during cotherapy, and 36.0 (25.6-60.2) and 2.3 (1.3-7.3) within a median 10-12 hours after argatroban cessation. Major bleeding occurred in 1 (0.6%) patient pretransitionally and no patient during or after cotherapy. Eighteen (10.9%) patients experienced 19 peritransitional adverse outcomes (one death, two amputations, 16 new thromboses); these patients had more severe HIT than event-free patients (median baseline platelet count, 39 vs. 83 × 109/L). Of 108 patients with post-transitional INR data, 43 achieved a therapeutic INR (prospectively defined as 1.9-3.5), 34 were subtherapeutic, and 31 were supratherapeutic, with no across-group trend in new thrombosis. Hence in the absence of guidelines, physicians transfer patients from argatroban to warfarin therapy with acceptably low complication rates in HIT, without systematically over- or under-dosing warfarin. Furthermore, INRs greater than 5 commonly occur in HIT patients during argatroban monotherapy and argatroban/warfarin cotherapy, without major bleeding.
Clinical and Applied Thrombosis-Hemostasis | 1997
Richard P. Schwarz; Jean-Claude Becker; R. Lynn Brooks; Marcie J. Hursting; James L. Joffrion; Gary D. Knappenberger; Timothy P. Kogan; Patricia W. Kogan; Anthony Mckinney
Because of the unsatisfactory options available for safe and effective antithrombotic therapy, recent, intense research and development efforts have been focused on direct thrombin inhibitors, also known as site-directed thrombin inhibitors. The intravenous agent Novastan (argatroban) is a small-molecule, reversible, direct thrombin inhibitor that is selective for the catalytic site of the thrombin molecule. Argatrobans molecular properties (small molecule; fast, selective, and reversible inhibition of the thrombin catalytic site; and similar in vitro potency for inhibiting both clot-bound and soluble thrombin) offer the potential for significant antithrombotic efficacy with minimal systemic anticoagulant ef fects. Its clinical pharmacologic properties offer the potential for minimal risk of bleeding, very rapid achievement of therapeutic antithrombotic efficacy, predictable dose-response, and rapid restoration of the hemostatic systems to normal upon termination of intravenous infusion. Argatroban is currently approved for clinical use in Japan for the treatment of peripheral arterial occlusive disease. It is in advanced clinical development in North America, South America, and Western Europe for several clinical indications, including (1) adjunctive therapy to thrombolytic agents in the treatment of acute myocardial infarction and (2) antithrombotic therapy for patients with heparin-induced thrombocytopenia and heparin-induced thrombocytopenia and thrombosis syndrome. Key Words: Molecular properties—Novastan (argatroban)—Pharmacology—Thrombin inhibitor.
Seminars in Thrombosis and Hemostasis | 1997
Marcie J. Hursting; Kenneth Alford; Jean-Claude Becker; R. Brooks; James L. Joffrion; Gary D. Knappenberger; Patricia W. Kogan; Timothy P. Kogan; Anthony Mckinney; Richard P. Schwarz
Clinical Chemistry | 1999
Marcie J. Hursting; James L. Zehnder; James L. Joffrion; Jean-Claude Becker; Gary D. Knappenberger; Richard P. Schwarz
Clinical Chemistry | 1993
Marcie J. Hursting; Andrew G. Stead; Frank V. Crout; Bela Z. Horvath; Bryant M. Moore
Clinical Chemistry | 1993
Marcie J. Hursting; Bryan T. Butman; J P Steiner; Bryant M. Moore; M C Plank; K M Szewczyk; M L Bell; F A Dombrose
Clinical Chemistry | 1992
Marcie J. Hursting; Gregory D. Clark; Vidmantas A. Raisys; Stephen J. Miller; Kent E. Opheim
Archive | 2002
Walenga Jm; Sarfraz Ahmad; D. Hoppensteadt; Omer Iqbal; Marcie J. Hursting; Bruce E. Lewis
Archive | 1999
Marcie J. Hursting; James L. Joffrion; Jean-Claude Becker; Richard P. Schwarz; Texas Bio
Archive | 1992
Bryan T. Butman; Jerald Steiner; Bryant M. Moore; Frederick Dombrose; Marcie J. Hursting