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Blood, 1 December 2007, Vol. 110, No. 12, pp. 3833-3841.
Prepublished online as a Blood First Edition Paper on July 24, 2007; DOI 10.1182/blood-2006-12-063222.
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Submitted December 15, 2006
Accepted July 16, 2007
Helicobacter pylori infection and chronic immune thrombocytopenic purpura: long-term results of bacterium eradication and association with bacterium virulence profiles
Giovanni Emilia*, Mario Luppi, Patrizia Zucchini, Monica Morselli, Leonardo Potenza, Fabio Forghieri, Francesco Volzone, Gordana Jovic, Giovanna Leonardi, Amedea Donelli, and Giuseppe Torelli
Department of Oncology and Hematology, Section of Hematology, University of Modena and Reggio Emilia, Modena, Italy
* Corresponding author; email: emilia.giovanni{at}unimore.it.
Eradication of Helicobacter pylori (H.Pylori) may lead to improvement of chronic immune thrombocytopenic purpura (ITP), although its efficacy over time is uncertain. We report the results of H.pylori screening and eradication in 75 consecutive adult patients with ITP. We also used molecular methods to investigate lymphocyte clonality and H.pylori genotypes in the gastric biopsies from 10 H.pylori positive ITP and 19 H.pylori positive non ITP patients with chronic gastritis. Active H.pylori infection was documented in 38 (51%) and successfully eradicated in 34 (89%) patients. After a median follow-up of 60 months, a persistent platelet response in 23 (68%) of eradicated patients was observed; one relapse occurred. No differences in mucosal B or T cell clonalities were observed between ITP patients and controls. Of note, the frequency of H.pylori cagA gene (P= 0.02) and the frequency of concomitant H.pylori cagA, vacAs1 and iceA genes (triple positive strains) (P= 0.015) resulted statistically higher in ITP than in controls. All aymptomatic H.pylori positive ITP patients were suffering from chronic gastritis. Our data suggest a sustained platelet recovery in a proportion of ITP patients, by H.pylori eradication alone. Over-representation of specific H.pylori genotypes in ITP suggests a possible role for bacterium-related factors in the disease pathogenesis.
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