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Since a report by <jats:italic>Gasbarrini<\/jats:italic> et al. in 1998, an accumulating body of evidence has proposed a pathophysiological link between <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> and chronic <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>elicobacter pylori<\/jats:italic> (<jats:italic>H.\u00a0pylori<\/jats:italic>) infection. Clinical reports have described a spontaneous resolution of <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> symptoms in about 50% of chronic <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> patients following empirical treatment of <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u00a0pylori<\/jats:italic> infection, but response appears to be geography dependent. Studies have also documented that <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> patients in East Asian countries are more likely to express positive antibody titers against <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u00a0pylori<\/jats:italic>\u2010specific cytotoxic\u2010associated gene A (CagA), a virulence factor that is associated with an increased risk for gastric diseases including carcinoma. While a definitive mechanism by which <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u00a0pylori<\/jats:italic> may induce thrombocytopenia remains elusive, proposed pathways include molecular mimicry of CagA by host autoantibodies against platelet surface glycoproteins, as well as perturbations in the phagocytic activity of monocytes. Traditional treatments of <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> have been largely empirical, involving the use of immunosuppressive agents and immunoglobulin therapy. However, based on the findings of clinical reports emerging over the past 20\u00a0years, health organizations around the world increasingly suggest the detection and eradication of <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u00a0pylori<\/jats:italic> as a treatment for <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content>. Elucidating the exact molecular mechanisms of platelet activation in <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u00a0pylori<\/jats:italic>\u2010positive <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> patients, while considering biogeographical differences in response rates, could offer insight into how best to use clinical <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u00a0pylori<\/jats:italic> eradication to treat <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content>, but will require well\u2010designed studies to confirm the suggested causative relationship between bacterial infection and an autoimmune disease state.<\/jats:p>","DOI":"10.1111\/hel.12200","type":"journal-article","created":{"date-parts":[[2015,3,2]],"date-time":"2015-03-02T04:47:26Z","timestamp":1425271646000},"page":"239-251","source":"Crossref","is-referenced-by-count":57,"title":["<i>Helicobacter 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