In reply. In the past years, eradication of H pylori infection has been associated with the correction of thrombocytopenia in several patients with AITP, suggesting that H pylori could be implicated in AITP pathogenesis.1-4 However, only the study by Emilia et al4 was based on a large series of patients, and, more recently, another group failed to demonstrate a significant improvement in platelet counts after H pylori eradication in 56 patients with chronic AITP.5 Using a different approach, we performed a case-control study and found no evidence for an association between H pylori carriage or past infection and AITP.6 The great variability of H pylori seroprevalence between countries6 raised by Morselli et al cannot be a source of bias in our study since AITP cases and controls were of the same ethnic and geographic origin. Nethertheless, as we have clearly discussed in our article, we did not exclude on this basis that H pylori could be involved in AITP pathogenesis, at least in a subgroup of patients.6 As the aim of our study was not to evaluate the effect of a H pylori eradication therapy on platelet count, we cannot exclude that some of our H pylori–positive patients, who did not report ulcerlike dyspesia, might benefit from such a therapy. We agree with Morselli et al about the limits of the blood antibody detection method used in our study. Indeed, this method does not denote necessarily active H pylori infection. However, this method was the only one that allowed a retrospective analysis of patient's status toward H pylori previous infection or carriage, at the time of AITP diagnosis. Furthermore, other nonendoscopic methods of detection, including the urea breath test and stool antigen testing, although denoting active H pylori infection, bring no additional information about the age of H pylori.7 infection