title: Helicobacter pylori infection and idiopathic thrombocytopenic purpura.
abstract: A treatment strategy for idiopathic thrombocytopenic purpura (ITP) is considered with the aim of cure or management of the bleeding tendency. In 1998, Gasbarrini et al reported a high prevalence of Helicobacter pylori infection in patients with ITP and showed that platelet recovery occurred after eradication therapy in most cases. Since then, many studies were performed to evaluate eradication therapy. This article discusses the incidence of H pylori infection in ITP, characteristic clinical features in H pylori-positive ITP, the effectiveness of eradication on platelet count increase, and the mechanisms of development of ITP by H pylori infection. Overall, there was a positive association between H pylori infection and ITP, and eradication of bacterium was accompanied by a significant increase in platelet counts in more than 50% of H pylori-positive ITP cases. These findings suggest that H pylori infection is involved in the mechanisms of thrombocytopenia in most cases of ITP in middle-aged and older patients. This approach could be beneficial to some ITP patients, but there were some uncertainties raised. To confirm the effectiveness of eradication therapy in H pylori-positive ITP, prospective studies conducted in several countries with a new treatment protocol are required, with a large number of ITP cases and longer follow-up.
authors.affiliation: Graduate School of Biomedical Science, Department of Pharmacotherapy, Division of Hemato/Oncology, Hiroshima University, Hiroshima, Japan. fujimura@hiroshima-u.ac.jp
authors.forename: Kingo
authors.initials: K
authors.lastname: Fujimura
mesh_terms: D001792:Blood Platelets / Q000382:microbiology / Q000473:pathology; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000150:complications* / Q000453:epidemiology / Q000276:immunology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000209:etiology / Q000235:genetics / Q000382:microbiology*