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Idiopathic Thrombocytopenic Purpura ITP ; is an autoimmune disease in which platelets are erroneously identified as foreign objects by the immune system and are targeted for elimination. Normal proteins located on the surface of the platelets act as antigens in ITP-affected individuals, thus signaling the body's white blood cells to remove the platelets from the bloodstream. The reason why these proteins are suddenly recognized by the body as foreign is not known, hence the word "idiopathic." However, as it is now known that the condition is autoimmune, it is sometimes known as immune rather than idiopathic ; thrombocytopenic purpura. Thrombocytopenia is defined as having too few platelets in the blood and is often characterized by persistent, easy bruising, purpura red or purple areas on the body caused by blood vessel hemorrhages ; , epistaxis nosebleeds ; , and gingival, gastrointestinal, and or central nervous system bleeding. A normal platelet count in a healthy person is between 150, 000 and 400, 000 per cu ml of blood. People with ITP have lower platelet counts that can range from severe cases, with the count at close to zero, to milder cases, where the count stays around 100, 000. A count of 30, 000 is often considered a `safe' count, i.e. one that is high enough to protect against spontaneous bleeding. Platelets are cell fragments that circulate in the blood to prevent blood vessels from leaking. They are produced in the bone marrow by megakaryocytes, which are large, multinucleated cells that undergo cytoplasmic fragmentation i.e. their bodies break into pieces ; to release platelets into the blood. Thrombopoietin, a hormone mainly produced by the liver, activates platelet production by megakaryocytes and can be found bound to circulating platelets. When platelet levels are adequate, unbound thrombopoietin levels remain low; however, when platelet counts drop, the liver is signaled to produce more thrombopoietin, thus increasing bone marrow production of platelets. The circulating lifecycle of a platelet is around 10 days, after which platelets are sequestered in the spleen and broken down. Damaged blood vessels release chemical signals to recruit platelets to the area of injury. Platelets are put into action when they come into contact with chemical signals such as collagen, thrombin, adenosine phosphate ADP ; , receptors on white blood cells or endothelial cells of blood vessels, and other activators. When this contact occurs, platelets release a variety of coagulation factors as well as plateletactivating factors. The platelets attach to each other and to the endothelial cells in the walls of blood vessels, forming a haemostatic plug. Between the platelets and other coagulation factors, the plug acts as a patch while the damaged area heals. When platelet counts are low, as is the case in ITP, the patient suffers from a bleeding diathesis, which is an increased vulnerability to bleeding due to this defect in the coagulation system. Platelet destruction in ITP is initiated by autoantibodies antibodies against self proteins produced by autoreactive B-lymphocytes ; . These antibodies can attach to the platelet antigens opsonization ; , thereby promoting the phagocytosis eating ; of the platelets by white blood cells. Though thrombocytopenia is usually linked with the production of IgG immunoglobulin G ; antiplatelet autoantibodies, which react with platelet glycoproteins IIb IIIa and IB IX protein on the surface of platelets ; , there is no formal proof that any single subset of autoantibodies is responsible for platelet destruction. There are two types of ITP: acute and chronic. Acute ITP usually lasts less than 6 months and mainly occurs in children. It is generally preceded by a viral infection and typically resolves itself within a few weeks or months and does not return. Chronic ITP is longer-lasting and mainly affects adults, specifically women. Treatment for chronic ITP depends on both the severity of the symptoms and the patient's platelet count and
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