ITP is an immune-mediated disorder in which platelets are coated with autoantibodies; the spleen subsequently removes the antibody-coated platelets. The autoantibodies are directed against glycoproteins IIb/IIIa (fibrinogen receptor) and the complex GPIb/IX (von Willebrand factor receptor). These glycoproteins are located on the platelet membrane and play an essential role in platelet aggregation, creating a bridge with fibrinogen, and in platelet adhesion.
The pathophysiology of this disorder is unclear. There is speculation that the autoantibodies arise due to a common viral or bacterial infection due to potential similarities between viral or bacterial antigens and platelet glycoprotein receptors in a cross-reaction effect. Another speculation is that there may be a failure of T-regulatory cells.
In addition to increased platelet destruction, platelet production may also be impaired or disrupted to some extent, possibly due to megakaryocyte injury by the autoantibodies.
ITP can be acute or chronic.
Note: Immune Thrombocytopenic Purpura was formerly referred to as Idiopathic Thrombocytopenic Purpura.
