title: Immune response to CagA protein is associated with improved platelet count after Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura.
abstract: BACKGROUND
  Improvement in platelet counts has been reported after eradication of Helicobacter pylori in patients with idiopathic thrombocytopenic purpura (ITP). We examined the levels of serum markers of gastritis and anti-CagA (cytotoxin-associated gene A) IgG antibody in patients with ITP to investigate whether these factors are associated with the platelet response after H. pylori eradication therapy.
  
  
  METHODS
  One hundred and sixteen consecutive patients with ITP were assessed for H. pylori infection by (13)C-urea breath test and serum H. pylori antibody test. Patients with H. pylori infection received eradication therapy. Before and after eradication therapy, we evaluated serum levels of gastrin, pepsinogen (PG)-I, and PG-II and the anti-CagA IgG antibody titer.
  
  
  RESULTS
  H. pylori infection was found in 67 (58%) of the 116 patients with ITP. Fifty-two infected patients received eradication therapy, which was successful in 44 patients (85%). Twenty-seven patients (62%) showed an increased platelet count and were identified as responders. The duration of ITP was shorter in responders than in nonresponders (p = .017). There was no difference of the levels of gastrin and PGs between responders and nonresponders. Before eradication therapy, the serum anti-CagA antibody titer did not differ significantly between responders and nonresponders. However, reduction in the anti-CagA antibody titer after eradication therapy was significantly greater in responders than in nonresponders (p = .013).
  
  
  CONCLUSIONS
  H. pylori eradication therapy improves the platelet count in H. pylori-positive patients with ITP of short duration. Immune response of hosts to CagA protein of H. pylori may play a role in the pathogenesis of ITP.
authors.affiliation: Department of Medicine and Molecular Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
authors.forename: Michiyo
authors.initials: M
authors.lastname: Kodama
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Kitadai
authors.forename: Masanori
authors.initials: M
authors.lastname: Ito
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Kai
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Masuda
authors.forename: Shinji
authors.initials: S
authors.lastname: Tanaka
authors.forename: Masaharu
authors.initials: M
authors.lastname: Yoshihara
authors.forename: Kingo
authors.initials: K
authors.lastname: Fujimura
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Chayama
mesh_terms: D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000276:immunology*; D001426:Bacterial Proteins / Q000276:immunology*; D005260:Female; D016481:Helicobacter Infections / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D016480:Helicobacter pylori; D006801:Humans; D007564:Japan; D008297:Male; D008875:Middle Aged; D010976:Platelet Count; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000097:blood* / Q000209:etiology; D016896:Treatment Outcome
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori