Eradication of Helicobacter pylori
infection has been variably associated with a platelet response in patients with
immune thrombocytopenic purpura (
ITP). Responses occur in approximately half of
ITP patients infected with this bacterium, more frequently in Japan and Italy than in other countries. For those with severe
ITP (platelet count<30x10(9)/L) and a long duration of disease, eradication
therapy seems to be less effective. Despite extensive efforts, distinctive clinical features and factors predicting the response to eradication
therapy have not been consistently identified. There is no established mechanism to explain how H pylori could be implicated in the pathogenesis of an immune-mediated platelet destruction. Several theories have been proposed to explain the platelet response to anti-H pylori
therapy, including molecular mimicry, platelet aggregation, and the induction of a Th1 phenotype that favors the onset and/or persistence of
ITP. The role of bacterium-related factors, such as the CagA (
cytotoxin-associated gene A)
protein, are still under investigation. Eradication
therapy is simple and inexpensive, with limited toxicity and the advantage of avoiding long-term immunosuppressive treatment for those who respond. Although the evidence and follow-up are limited, it appears reasonable to routinely screen patients with
ITP for H pylori, particularly in those populations with a high background prevalence of H pylori
infection.