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. ITP often results in an increased risk of bleeding from mucosal surfaces (such as the nose or gums) or the skin (causing purpura and bruises). Depending on which age group is affected, ITP causes two distinct clinical syndromes: an acute form observed in children and a chronic form in adults. Acute ITP often follows a viral infection and is typically self-limited (resolving within two months), while the more chronic form (persisting for longer than six months) does not yet have a specific identified cause. Nevertheless, the pathogenesis of ITP is similar in both syndromes involving antibodies against various platelet surface antigens such as glycoproteins.

Diagnosis of ITP involves identifying a low platelet count through a complete blood count, a common blood test. However, since the diagnosis relies on excluding other potential causes of a low platelet count, additional investigations, such as a bone marrow biopsy, may be necessary in certain cases.

For mild cases, careful observation may be sufficient. However, in instances of very low platelet counts or significant bleeding, treatment options may include corticosteroids, intravenous immunoglobulin, anti-D immunoglobulin, or immunosuppressive medications. Refractory ITP, which does not respond to conventional treatment or shows constant relapse after splenectomy, requires treatment to reduce the risk of significant bleeding. Platelet transfusions may be used in severe cases with extremely low platelet counts in individuals experiencing bleeding. In some cases, the body may compensate by producing abnormally large platelets.

Signs of ITP include the spontaneous formation of bruises (purpura) and petechiae (tiny bruises), especially on the extremities. Additionally, bleeding from the nostrils and/or gums, as well as menorrhagia (excessive menstrual bleeding), may occur if the platelet count falls below 20,000 per μL. A platelet count below 10,000 per μL can lead to the spontaneous formation of hematomas (blood masses) in the mouth or on other mucous membranes. Furthermore, bleeding time from minor lacerations or abrasions is usually prolonged.^{[citation needed]}

In cases where platelet counts drop to extremely low levels (<5,000 per μL), serious and potentially fatal complications may arise. These complications include subarachnoid or intracerebral hemorrhage (bleeding inside the skull or brain), lower gastrointestinal bleeding, or other internal bleeding. A person with ITP with an extremely low platelet count is susceptible to internal bleeding resulting from blunt abdominal trauma, such as in a motor vehicle crash. These complications are more likely to occur when the platelet count is less than 20,000 per μL.

In approximately 60 percent of cases, antibodies against platelets can be detected. Most often these antibodies are against platelet membrane glycoproteins IIb-IIIa or Ib-IX, and are of the immunoglobulin G (IgG) type. The Harrington–Hollingsworth experiment established the immune pathogenesis of ITP.

The coating of platelets with IgG renders them susceptible to opsonization and phagocytosis by splenic macrophages, as well by Kupffer cells in the liver. The IgG autoantibodies are also thought to damage megakaryocytes, the precursor cells to platelets, although this is believed to contribute only slightly to the decrease in platelet numbers. Recent research now indicates that impaired production of the glycoprotein hormone, thrombopoietin, which is the stimulant for platelet production, may be a contributing factor to the reduction in circulating platelets. This observation has led to the development of a class of ITP-targeted medications referred to as thrombopoietin receptor agonists.

The stimulus for auto-antibody production in ITP is probably abnormal T cell activity. Preliminary findings suggest that these T cells can be influenced by medications that target B cells, such as rituximab.