The old name for the disease, idiopathic thrombocytopenic purpura, is a misnomer. The disease is not idiopathic and most patients do not have purpura.
Though no longer idiopathic its pathogenesis is more complex than once thought. It is a disorder of both peripheral destruction and under production:
ITP is a complex immune process in which cellular and humoral immunity are involved in the destruction of platelets3 as well as impaired platelet production. Several theories have emerged in the last decade to explain this autoimmune process...
The triggering event for antibody initiation in ITP is unknown.3 Autoantibodies (mostly immunoglobulin G [IgG] but sometimes IgM and IgA) are produced against the platelet membrane glycoprotein GPIIb-IIIa. The antibody-coated platelets are rapidly cleared by the reticuloendothelial system in the spleen and liver, in a process mediated by Fc-receptor expression on macrophages and dendritic cells. Autoantibodies may also affect platelet production by inhibiting megakaryocyte maturation and inducing apoptosis.
The review had this updated information on the H pylori association:
The association between H pylori infection and ITP remains uncertain. Eradication of infection appears to completely correct ITP in some places where the prevalence of H pylori is high (eg, Italy and Japan) but not in the United States and Canada, where the prevalence is low.20 The different response may be due not only to the differences in prevalence, but to different H pylori genotypes: most H pylori strains in Japan express CagA, whereas the frequency of CagA-positive strains is much lower in western countries.
Treatment is summarized here.