How is immune thrombocytopenia (ITP) characterized?

Updated: Nov 30, 2019
  • Author: Perumal Thiagarajan, MD; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP  more...
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Immune thrombocytopenia (ITP) is one of the most common autoimmune disorders. ITP is caused by autoantibodies to platelets. The antigenic target in most patients appears to be the platelet GP IIb/IIIa complex. Platelets with antibodies on their surface are trapped in the spleen, where they are efficiently removed by splenic macrophages.

The mechanism of origin of these antibodies is not known. These antibodies may be directed toward viral antigens and then cross-react with platelet antigens. They persist because of the failure of immune surveillance mechanisms to repress these antibodies.

These antibodies can also react with the developing megakaryocytes in the bone marrow, leading to decreased production of platelets (ineffective thrombopoiesis). The success of thrombopoietin agonist therapy in chronic ITP underscores this mechanism as a major factor in inducing thrombocytopenia.

ITP occurs commonly in otherwise healthy individuals and only rarely as the initial manifestation of lupus and other autoimmune disorders. Human immunodeficiency virus (HIV) infection is often associated with ITP in both adults and children.

ITP occurs in two distinct clinical types: (1) an acute self-limiting form observed almost exclusively in children (five cases per 100,000 persons) and (2) a chronic form, observed mostly in adults (three to five cases per 100,000 persons) and rarely in children. [16, 1, 2, 3]

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