ITP is an immune-mediated disorder in which platelets are coated with autoantibodies; the antibody-coated platelets are subsequently removed by the spleen. 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 important role in platelet aggregation, in creating a bridge with fibrinogen, and in platelet adhesion.
The pathophysiology for this disorder is unclear. There is speculation that the autoantibodies arise as a result of a common viral or bacterial infection. 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 as a result of megakaryocyte injury by the autoantibodies.
ITP can be acute or chronic.