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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 ...
Treatment of thrombotic thrombocytopenic purpura (TTP) is a medical emergency, since the associated hemolytic anemia and platelet activation can lead to kidney failure and changes in the level of consciousness. Treatment of TTP was revolutionized in the 1980s with the application of plasmapheresis.
Thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome [1] Treatment: Directed at the underlying condition [3] Medication: Platelets, cryoprecipitate, fresh frozen plasma, heparin [2] Prognosis: 20–50% risk of death [4] Frequency: 1% of people admitted to hospital [4]
By tradition, the term idiopathic thrombocytopenic purpura is used when the cause is idiopathic, or unknown. However, most cases are now considered to be immune-mediated. [citation needed] Another form is thrombotic thrombocytopenic purpura. [citation needed]
Thrombotic thrombocytopenic purpura (TTP), a TMA, was first described by the Hungarian born, American pathologist and physician Eli Moschcowitz (1879–1964). In 1924, [ 51 ] Moschcowitz first described TTP as a distinct clinicopathologic condition that can mimic the clinical characteristics of Hemolytic–uremic syndrome (HUS).
Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic purpura or immune thrombocytopenia, is an autoimmune primary disorder of hemostasis characterized by a low platelet count in the absence of other causes.
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