Cause of ITP is -

Idiopathic thrombocytopenic purpura There are two clinical subtypes of primary I.T.P, acute and chronic both are autoimmune disorders in which platelet destruction results from the formation of antiplatelet antibodies. Pathogenesis Chronic ITP is caused by the formation of autoantibodies against platelet membrane glycoproteins most often IIb-IIIa or Ib-IX. In the overwhelming majority of cases, the antiplatelet antibodies are of the IgG class. The mechanism of platelet destruction is similar to that seen in autoimmune hemolytic anemias. Opsonized platelets are rendered susceptible to phagocytosis by the cells of the mononuclear phagocyte system. The spleen is the major site of the destruction of platelets. Pathology The principal morphologic lesions of thrombocytopenic purpura are found in the spleen and bone marrow but they are not diagnostic. The point to stress is that despite the increased destruction of platelets in the spleen, the spleen size remains normal. On histological examination, there is congestion of the sinusoids and hyperactivity and enlargement of the splenic follicles manifested by the formation of prominent germinal centres. Sometimes scattered megakaryocytes are found within the sinuses and sinusoidal walls. This represents a very mild form of extramedullary hematopoiesis. These splenic findings are not sufficiently distinctive to be considered diagnostic. Bone Marrow Bone marrow reveals a modestly increased number of megakaryocytes. These findings are not specific for autoimmune thrombocytopenic purpura but merely reflect accelerated thrombopoiesis, being found in most forms of thrombocytopenia resulting from increased platelet destruction. The importance of bone marrow examination is to rule out thrombocytopenias resulting from bone marrow failure. A decrease in the number of megakaryocytes goes against the diagnosis of I.T.P.