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Journal ArticleDOI

Frequent off-label use of fondaparinux in patients with suspected acute heparin-induced thrombocytopenia (HIT)--findings from the GerHIT multi-centre registry study.

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TLDR
There is a wide fondaparinux off-label use (up to 50.3%) for suspected HIT, even in those patients with a high clinical pretest probability, despite the current diagnostic laboratory strategy based on the recommended 2-step strategy.
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This article is published in Thrombosis Research.The article was published on 2014-07-01. It has received 55 citations till now. The article focuses on the topics: Heparin-induced thrombocytopenia & Fondaparinux.

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Citations
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Journal ArticleDOI

Heparin-induced thrombocytopenia

TL;DR: This review will summarize the current understanding of HIT by reviewing pathogenesis, essential clinical and laboratory features, and management.
Journal ArticleDOI

Autoimmune heparin-induced thrombocytopenia.

TL;DR: Non‐APTT‐adjusted therapies with drugs such as danaparoid and fondaparinux, or even direct oral anticoagulants, such as rivaroxaban or apixaban, are suggested therapies, especially for long‐term management of persisting HIT.
Journal ArticleDOI

Pharmacology of Heparin and Related Drugs

TL;DR: A “state of the art” review of the current understanding of the pharmacology of heparin and related drugs and an overview of the status of development of such drugs are provided.
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Guidance for the practical management of the heparin anticoagulants in the treatment of venous thromboembolism

TL;DR: Clinical guidance based on existing guidelines and consensus expert opinion where guidelines are lacking is provided and a concise table of clinical management questions and guidance recommendations is provided to provide a quick reference for the practical management of heparins including low molecular weight heparin and fondaparinux.
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Direct oral anticoagulants for treatment of HIT: update of Hamilton experience and literature review

TL;DR: DOACs offer simplified management of selected patients, as illustrated by a case of persisting (autoimmune) HIT (>2-month platelet recovery with inversely parallel waning of serum-induced heparin-independent serotonin release) with successful outpatient rivaroxaban management of HIT-associated thrombosis.
References
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Journal ArticleDOI

Treatment and prevention of heparin-induced thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.

TL;DR: This article suggests that platelet count monitoring should be performed every 2 or 3 days for patients receiving heparin in whom clinicians consider the risk of HIT to be > 1%, and suggests the use of argatroban or lepirudin or danaparoid over other nonheparin anticoagulants.
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Evaluation of pretest clinical score (4 T's) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings

TL;DR: A low pretest clinical score for HIT seems to be suitable for ruling out HIT in most situations (high‐negative predictive value), and the implications of an intermediate or high score vary in different clinical settings.
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Temporal aspects of heparin-induced thrombocytopenia.

TL;DR: A fall in the platelet count beginning four or more days after the start of heparin therapy occurred in 170 of the 243 patients (70 percent); in these patients, a history of previousHeparin treatment did not influence the timing of the onset of thrombocytope...
Journal ArticleDOI

Treatment and Prevention of Heparin-Induced Thrombocytopenia: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)

TL;DR: In this paper, the recognition, treatment, and prevention of heparin-induced thrombocytopenia (HIT) is part of the Antithrombotic and Thrombolytic Therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).
Journal ArticleDOI

Immunoglobulin G From Patients With Heparin-Induced Thrombocytopenia Binds To a Complex of Heparin and Platelet Factor 4

TL;DR: These studies indicate that heparin and other large, highly sulfated polysaccharides bind to PF4 to form a reactive antigen on the platelet surface and HIT IgG then binds to this complex with activation of platelets through the Platelet Fc receptors.
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