Does Helicobater pylori initiate or perpetuate immune thrombocytopenic purpura?

  • Marc Michel
    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.
  • Nichola Cooper
    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.
  • Christelle Jean
    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.
  • Christine Frissora
    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.
  • 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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<jats:title>Abstract</jats:title> <jats:p>To determine the prevalence of Helicobacter pylori (H pylori) infection in North American patients with immune thrombocytopenic purpura (ITP) and the effect of H pylori eradication on the platelet count, a prospective study was performed. Seventy-four patients aged 10 years and older (mean age of 41 years) with chronic ITP and a platelet count below 60 × 109/L were enrolled. H pylori infection was found in 22% of patients by means of a breath test and could not be predicted by gastrointestinal symptoms. H pylori–positive patients (52.5 years of age) were older than H pylori–negative patients (38.5 years of age; P = .0035). Fifteen of the 16 H pylori–positive patients were treated and the bacteria was eradicated in 14 (93%). After 3 months, a significant response (platelet count &gt; 50 × 109/L and doubling the initial count) was observed in only one patient. After a median follow-up of 11.5 months, none of the 14 patients had responded. Ten H pylori–negative patients treated with the same regimen also did not increase their platelet counts. In conclusion, unlike several previous reports, this study does not implicate H pylori in the pathogenesis of ITP since the prevalence of H pylori infection was low and eradication of H pylori did not positively influence the course of the ITP.</jats:p>

収録刊行物

  • Blood

    Blood 103 (3), 890-896, 2004-02-01

    American Society of Hematology

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