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Heparin‐induced thrombocytopenia from venous thromboembolism treatment
Author(s) -
BEGELMAN S. M.,
HURSTING M. J.,
AGHABABIAN R. V.,
MCCOLLUM D.
Publication year - 2005
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2005.01573.x
Subject(s) - argatroban , medicine , heparin induced thrombocytopenia , heparin , thrombosis , anticoagulant , partial thromboplastin time , venous thrombosis , surgery , anesthesia , platelet , thrombin
. Objectives. We aimed to characterize the clinical experiences of patients in whom heparin‐induced thrombocytopenia (HIT) complicated heparin therapy for venous thromboembolism (VTE) and who switched to argatroban. Design. A retrospective analysis of previously reported prospective, multicentre, historical‐controlled Argatroban‐911 and Argatroban‐915 studies of argatroban therapy in HIT. Setting. Inpatient. Subjects. Patients ( n = 145) administered heparin for VTE and who developed HIT were identified. Interventions. Patients were treated with argatroban 2 mcg kg −1 min −1 for up to 14 days, adjusted to maintain activated partial thromboplastin times 1.5 to three times baseline. Patient characteristics, anticoagulation and outcomes were summarized. The primary end‐point was a composite of death, amputation, or new thrombosis within 37 days of argatroban initiation. Results. During heparin therapy, platelet counts decreased (mean ± SD nadir: 78 ± 67 × 10 9 L −1 ), and 75 (52%) patients developed thrombosis. After heparin was discontinued, patients received argatroban (mean dose 2.1 ± 1.2 mcg kg −1 min −1 ) for 6.8 ± 4.3 days. By day 6 of argatroban therapy, the mean platelet count rose to >150 × 10 9 L −1 . The primary end‐point occurred in 41 (28.3%) patients (values of 26–44% are reported for argatroban therapy of HIT from any heparin indication). Seventeen (11.7%) patients, including 12 who had also experienced thrombosis whilst on heparin, developed new thrombosis after argatroban initiation, typically on the day argatroban was discontinued or later ( n = 10). Seven (4.8%) patients experienced major bleeding. Conclusions. For VTE patients with HIT, argatroban provides effective anticoagulation, with outcomes comparable with those reported for other argatroban‐treated HIT patients. New thrombosis in this setting occurred most often in patients with existing HIT‐associated thrombosis, before HIT recognition or either at/after argatroban discontinuation.