Published online Jan 21, 2014. doi: 10.3748/wjg.v20.i3.714
Revised: November 14, 2013
Accepted: December 3, 2013
Published online: January 21, 2014
Immune thrombocytopenia (ITP) is an autoimmune disease mediated by anti-platelet autoantibodies. There is growing evidence that the eradication of Helicobacter pylori (H. pylori) effectively increases platelet count in a considerable proportion of ITP patients infected with this bacterium. In the majority of ITP patients responding to H. pylori eradication therapy, the anti-platelet autoantibody response is completely resolved with no relapse for more than 7 years, indicating that the disease is cured. Therefore, adult patients with suspected ITP should be examined for H. pylori infection, and eradication therapy is recommended if the infection is present. Notably, however, the efficacy of H. pylori eradication therapy in ITP patients varies widely among countries, with a higher response rate in Japan compared with the United States and European countries other than Italy. The pathogenesis of H. pylori-associated ITP is still uncertain, although the mechanisms are known to involve multiple factors. H. pylori may modulate the Fcγ-receptor balance of monocytes/macrophages in favor of activating Fcγ receptors, and H. pylori components may mimic the molecular makeup of platelet antigens. Further studies of the pathogenic process of H. pylori-associated ITP may be useful for the development of new therapeutic strategies for ITP.
Core tip: In this review, we summarize recent updates on basic and clinical aspects of Helicobacter pylori (H. pylori)-associated immune thrombocytopenia (ITP). We highlight the efficacy of H. pylori eradication in adult and childhood ITP as well as in secondary ITP, variability in the efficacy of eradication in various countries, factors predicting the eradication-related platelet response, and the mechanisms responsible for the development of ITP in association with H. pylori infection. It is apparent that in a distinct subgroup of H. pylori-associated ITP, this bacterial infection is central to the ITP pathogenesis.