Heparin-induced thrombocytopenia is a life-threatening complication of exposure to heparin. Heparin-induced thrombocytopenia results from an autoantibody directed against platelet factor 4 in complex with heparin. Heparin-induced thrombocytopenia is traditionally treated with bivalirudin, argatroban, danaparoid, or fondaparinux. Recently, direct oral anticoagulants administration to treat heparin-induced thrombocytopenia has been reported. Direct oral anticoagulants do not cause platelet activation in the presence of heparin-platelet factor 4 antibodies, nor do they provoke autoantibody production. Direct oral anticoagulants offer advantages such as consistent and predictable anticoagulation, oral administration with good patient compliance, and a good safety profile. We report a case of heparin-induced thrombocytopenia with deep venous thrombosis successfully treated with rivaroxaban and review the current experience with rivaroxaban for the treatment of heparin-induced thrombocytopenia.
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http://dx.doi.org/10.1155/2020/8885256 | DOI Listing |
J Appl Lab Med
January 2025
Department of Pathology, University of Iowa Health Care, Iowa City, IA, United States.
Background: Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening adverse drug reaction with numerous diagnostic challenges. Diagnosis of HIT begins with 4T score clinical assessment, followed by laboratory testing for those not deemed low risk. Laboratory testing for HIT includes screening [enzyme-linked immunosorbent assay (ELISA)] and confirmatory [serotonin release assay (SRA)] assays, wherein SRA testing can be pursued following a positive ELISA result.
View Article and Find Full Text PDFHeparin-induced thrombocytopenia (HIT) is an adverse drug reaction with significant thromboembolic risk. Though there are models for use of non-heparin anticoagulants, heparin remains the preferred anticoagulant in many operative settings, especially cardiovascular surgery and percutaneous cardiac intervention. The natural history of HIT can be stereotyped into phases using HIT laboratory testing to guide clinical management and determine whether heparin re-exposure can be considered.
View Article and Find Full Text PDFJ Thromb Haemost
December 2024
Division of Hematology, Duke University Medical Center, Durham, NC. Electronic address:
Background: IgG antibodies (Abs) to platelet factor 4 complexed to heparin (PF4/H) commonly occur after heparin exposure but cause life-threatening complications of heparin-induced thrombocytopenia (HIT) in only a few patients. Presently, only platelet activation assays reliably distinguish anti-PF4/H Abs that cause disease (HIT Abs) from those likely to be asymptomatic (AAbs).
Objectives: Recent studies indicate that complement activation is an important serologic property of HIT Abs and is essential for FcγRIIA-mediated cellular activation.
J Tehran Heart Cent
January 2024
Department of Cardiac Electrophysiology, Tehran Heart Center, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
Background: The rate of lead extraction has steadily increased alongside the extensive use of cardiovascular implantable electronic devices. Data on the complications and safety of this challenging procedure are limited. We investigated inhospital and midterm outcomes following lead extraction.
View Article and Find Full Text PDFJACC Case Rep
November 2024
Cardiovascular Division, Osaka Police Hospital, Osaka, Japan.
A 66-year-old man presented with chills, exertional dyspnea, and palpitations; he later developed a fever. Because of his elevated cardiac enzymes and electrocardiography and coronary angiography findings, he was diagnosed with acute myocarditis. Given his unstable hemodynamics, an intra-aortic balloon pump was inserted; however, he experienced a hemodynamic collapse due to refractory ventricular fibrillation.
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