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Helicobacter pylori and Chronic ITP

Correspondence: Dr. Roberto Stasi, Department of Medical Sciences, Regina Apostolorum Hospital, Via S. Francesco, 50, 00041 Albano Laziale, ITALY; Phone: 01139 06 932989; Fax: 01139 06 233231809; e-mail: roberto.stasi{at}uniroma2.it.

Abstract

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 < 30 x 10⁹/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.

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