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Does Helicobater pylori initiate or perpetuate immune thrombocytopenic purpura?
Marc Michel, Nichola Cooper, Christelle Jean, Christine Frissora, and James B. Bussel

From the Department of Pediatrics, Division of Hematology/Oncology, and Department of Medicine, Division of Gastroenterology, Weill Medical College of Cornell University, New York--Presbyterian Hospital, New York, NY.

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The prevalence of 21.6% of H pylori infection found in the 74 patients with ITP was surprisingly low compared with the prevalence of 32.5% assessed by presence of serum IgG antibodies in 7465 healthy adults in the United States.14 The difference in the method of H pylori detection and the ethnic distribution of our patient population are unlikely to explain this low rate of infection. Indeed, in a previous study, the prevalence of H pylori infection among 239 healthy white Americans was 34% using a urea breath test.19 While 25% of children 6 to 19 years old are infected in the United States,15 none of the 11 patients aged of 19 or younger included in the series reported here had a positive breath test. Even eliminating these adolescents, the prevalence of H pylori infection only reached 25.3% in the adults (16/63). These data do not support H pylori initiating ITP in our patient population.

Could H pylori infection be predicted? The questionnaire contained 2 variables that showed a trend toward identifying H pylori infection: heartburn or gas burping. As with the healthy controls, increased age was associated with a higher likelihood of H pylori infection. Therefore, if one wished to test ITP patients, one approach would be to test those older than 50 years of age and those younger than 50 years of age with heartburn or gas burping. In the series reported here, this would have identified 15 of the 16 infected patients while testing only 52 of the total of 74.

Can eradication of H pylori cure ITP? One limitation of previous studies was that at most 25% of the H pylori--positive patients who received the eradication regimen were those with chronic severe thrombocytopenia (ie, platelet count < 30 x 109/L and/or previous splenectomy4; Table 5). By comparison, among the 15 H pylori--positive patients treated in this study, all had chronic ITP with a platelet count less than 55 x 109/L (7 were < 30 x 109/L) and all have been previously treated for their ITP by 2 to 6 different treatments including splenectomy in 5 cases (33%). Therefore, these patients had a very low likelihood of spontaneous improvement and the effectiveness of H pylori eradication on ITP outcome was easier to assess. The eradication rate was 93% since alternative treatment was pursued when the initial regimen was ineffective. However, despite this good rate of eradication and unlike previous studies,2-8 only one of our H pylori--positive patients achieved a significant response 3 months after eradication and this response did not last.

In this study, 3 months was chosen as the time limit for seeing an effect of H pylori eradication. If no response was seen at that time, other therapies were initiated if necessary. Previous studies that provided time frames all demonstrated platelet recovery within 60 days after H pylori eradication.2,6,8 In this study, extending the time beyond 3 months following H pylori eradication did not seem to affect the response since the only platelet changes observed were in those patients who had initiated other therapies. To explain the high rates of response reported by others (Table 5), a nonspecific effect of the drugs used to eradicate the bacteria seems unlikely since in this present study none of the 10 H pylori--negative patients who received the Prevpac experienced a significant improvement in their platelet count.

The striking discrepancies between this report and those from Italy and Japan suggest several hypotheses. One hypothesis is that the response to H pylori infection could be influenced by the host's immunogenetic background.20,21 However, the contradictory findings reported in patients of similar European origin (ie, Spain, France, and Italy)2,3,4,11,12 (Table 5) do not support this hypothesis. Another possibility is that different strains of H pylori, namely those with different cag or vag (cytotoxicity/virulence-associated genes) proteins,20 could exert different immunologic effects on the host T and B cells and hence on ITP. A third hypothesis is that the expression of various Lewis (Le) antigens by H pylori isolates22 and the subsequent production of anti-Le antibodies could play a role in ITP pathogenesis since platelets may adsorb Lewis antigens from the serum.

The management of ITP in adults is complex and may require immunosuppressive therapies and/or splenectomy. One of the challenges for physicians caring for patients with ITP is to find less toxic and more effective approaches. The expectation at the beginning of this study was that a percentage of patients could be "cured" by administration of the Prevpac for 2 weeks. Unexpectedly, in this study there was not a greater prevalence of H pylori in ITP patients. Furthermore, and unlike most of the previous studies, none of the patients substantially improved their platelet count as a result of H pylori eradication. Therefore, even if the success of treatment of the H pylori--infected patients could be predicted by age and questionnaire, it is not obvious from this study that one would choose to test and eradicate infection in them. Future studies performed in this setting should be randomized and controlled and should include large numbers of patients requiring therapy. In addition to tracking the platelet count, other parameters that might be important determinants of response as suggested in the hypotheses considered above should also be studied.


Does Helicobater pylori initiate or perpetuate immune thrombocytopenic purpura?

Submitted March 25, 2003; accepted July 28, 2003.

Prepublished online as Blood First Edition Paper, August 14, 2003; DOI 10.1182/blood-2003-03-0900.

The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.

Reprints: Marc Michel, New York Presbyterian Hospital, Department of Pediatrics, Division of Pediatric Hematology/Oncology, Weill Medical College of Cornell University, 525 East 68th St, New York, NY 10021; e-mail:


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