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Antiplatelet drugs alter the platelet activation at the site of vascular damage crucial to the development of arterial thrombosis. Aspirin and Triflusal irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA 2 (thromboxane – powerful vasoconstrictor that lowers cyclic AMP and initiates the platelet release ...
Generally, drugs outlined within the ATC code B01AC should be included in this category. Please see WP:PHARM:CAT for more information. Wikimedia Commons has media related to Antiplatelet drugs .
Drug-induced thrombocytopenic purpura is a skin condition result from a low platelet count due to drug-induced anti-platelet antibodies caused by drugs such as heparin, sulfonamides, digoxin, quinine, and quinidine. [1]: 821
(Aspirin can prevent platelets from adhering to clot bleeding.) Some blood centers also prohibit the taking of any non-steroidal anti-inflammatory drug (NSAID) for 36 hours prior. Secondly, platelet donations are allowed anywhere from every 3 to 28 days. This is in contrast to whole-blood donation, which has an eight-week (or longer) waiting ...
Thrombotic thrombocytopenic purpura (TTP) initially presents with a range of symptoms that may include severe thrombocytopenia (platelet count usually < 30,000/mm³), microangiopathic hemolytic anemia (evidenced by schistocytes in the blood smear), and various clinical signs such as petechiae, purpura, neurologic symptoms, myocardial ischemia ...
Anti-platelet effects start within 2 days and reach their maximum by 6 days of therapy. Ticlopidine’s effects persist for 3 days after discontinuing ticlopidine although it may take 1–2 weeks for platelet function to return to normal, as the medication affects platelets irreversibly.
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.
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.