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<unk> globulin G (IgG) type. The Harrington–Hollingsworth experiment established the<unk>  pathogenesis of<unk> . 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<unk> -targeted medications referred to as thrombopoietin receptor agonists. The stimulus for auto-antibody production in<unk>  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.
Immune thrombocytopenic purpura
Drug-induced thrombocytopenic purpura
Thrombotic thrombocytopenic purpura
Heparin-induced thrombocytopenia
Gray platelet syndrome
Quebec platelet disorder
Sticky platelet syndrome
Pseudo gray platelet syndrome