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(1) Background: Danaparoid sodium is a heparinoid antithrombotic that has been used for over 40 years for prophylaxis of DVT in non-HIT patients and for the treatment of heparin-induced thrombocytopenia (HIT) with and without thrombosis. This update summarises current information on its pharmacology and reviews danaparoid dose management in a broad spectrum of clinical situations, including off-label indications. (2) Methods: Evidence from published clinical studies, case reports, compassionate use of danaparoid, and spontaneously reported serious adverse events is summarised and analysed by an interdisciplinary expert group to develop a consensus on dosing regimens of danaparoid for complex clinical situations, including vulnerable patient populations.

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A 34-year-old primigravida who had undergone thrombectomy for deep venous thrombosis (DVT) in her leg and exhibited low protein S activity, indicating predisposition to thrombosis, developed DVT of the leg. No pulmonary embolism was detected. After anticoagulant therapy with unfractionated heparin was discontinued because of liver dysfunction, danaparoid treatment was administered in hospital.

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Heparin-induced thrombocytopenia (HIT) is a life and limb-threatening thrombotic complication of heparin, which is the result of platelet activation by anti-PF4/heparin antibodies. With lepirudin and danaparoid no longer available in the US, treatment options are limited to argatroban, fondaparinux (off-label use) and bivalirudin (for patients undergoing percutaneous coronary intervention). Both argatroban and bivalirudin are parenteral drugs and require close monitoring and hospitalization.

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Venous thromboembolism (VTE), encompassing deep venous thrombosis and pulmonary embolism, is a potentially fatal but preventable complication of stroke. Reported rates of VTE after stroke have decreased over the last four decades, possibly due to the implementation of stroke units, early mobilization and hydration, and increased early use of antiplatelets. Additional means of thromboprophylaxis in stroke include mechanical methods (ie, compression stockings) to prevent venous stasis and medical therapy including antiplatelets, heparins, and heparinoids.

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Heparin-induced thrombocytopenia (HIT, type II) is an immune-mediated disorder due to antibodies formed against heparin-platelet factor 4 complexes, usually appearing at days 5 to 14 after initiation of heparin. It is important to recognize HIT because heparin prophylaxis or treatment paradoxically associates with new venous and/or arterial thrombosis. Early clinical suspicion and diagnosis together with proper pharmacotherapy and close laboratory monitoring are the cornerstones for successful management.

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