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Antiplatelet therapy with one or more of these drugs decreases the ability of blood clots to form by interfering with the platelet activation process in primary hemostasis. Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another ...
They work by preventing platelet aggregation and thrombus formation. They do so by inhibition of the GpIIb/IIIa receptor on the surface of the platelets. They may also be used to treat acute coronary syndromes, without percutaneous coronary intervention, depending on TIMI risk. They should be given intravenously.
In a phase 1-2 open-label study treatment with CM313, a novel anti-CD38 monoclonal antibody, rapidly boosted platelet levels in adults with ITP by inhibiting antibody-dependent cell-mediated cytotoxicity on platelets; maintained long-term efficacy by clearing plasma cells; and was associated with low-grade toxic effects.
This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots; the platelet count falls as a result, leading to thrombocytopenia. [1] [7] In addition, the reticuloendothelial system (mostly the spleen) removes the antibody-coated platelets, further contributing to the thrombocytopenia.
The limitations of current antiplatelet drugs contain risk of bleeding and interindividual variability of platelet inhibitory response. [6] The aim is to determine the optimal therapeutic window to maximize therapeutic benefits while reducing safety concerns like bleeding. Consequently, the major unmet goal of ADP inhibitors is to develop a ...
An antithrombotic agent is a drug that reduces the formation of blood clots (). [1] [2] Antithrombotics can be used therapeutically for prevention (primary prevention, secondary prevention) or treatment of a dangerous blood clot (acute thrombus).
Low levels of platelets in turn may lead to prolonged or excessive bleeding. It is the most common coagulation disorder among intensive care patients and is seen in a fifth of medical patients and a third of surgical patients. [3] A normal human platelet count ranges from 150,000 to 450,000 platelets/microliter (μL) of blood. [4]
Treating blood clots that have already formed is managed by the use of anti-hemolytic ("clot busters"). Despite its effectiveness, the use of thromboprophylaxis remains under-utilized, though alerts (computer or human) in hospitals are associated with increased prescription and reductions in symptomatic VTE. [ 40 ]