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One common definition of thrombocytopenia requiring emergency treatment is a platelet count below 50,000/μL. [5] Thrombocytopenia can be contrasted with the conditions associated with an abnormally high level of platelets in the blood – thrombocythemia (when the cause is unknown), and thrombocytosis (when the cause is known).
Thrombotic thrombocytopenic purpura (TTP) is a blood disorder that results in blood clots forming in small blood vessels throughout the body. [2] This results in a low platelet count , low red blood cells due to their breakdown , and often kidney , heart , and brain dysfunction. [ 1 ]
Thrombocytopenic purpura are purpura associated with a reduction in circulating blood platelets which can result from a variety of causes, [1] such as kaposi sarcoma.
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.
Heparin may be used for both prevention and the treatment of thrombosis. It exists in two main forms: an "unfractionated" form that can be injected under the skin (subcutaneously) or through an intravenous infusion, and a "low molecular weight" form that is generally given subcutaneously.
Takeda's Adzynma becomes the first treatment available to patients with congenital thrombotic thrombocytopenic purpura (TTP). Congenital TTP is a life-threatening, rare genetic disorder with ...
The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension, antiphospholipid antibody syndrome, and drug toxicities, e.g. calcineurin inhibitor toxicity. [1]
Immune thrombocytopenic purpura is a condition in which platelets are destroyed by an autoimmune process. Platelets are a component of blood that contribute to the formation of blood clots in the body to prevent bleeding. The syndrome was first described in 1951 by R. S. Evans and colleagues. [1]
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