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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4969-4970.
CORRESPONDENCE To the editor:Helicobacter pylori, iron deficiency, and gastric autoimmunityWe read with interest the article by Hershko et al,1 which reported that the hematologic presentation of autoimmune gastritis (AIG) is age-related and progresses from iron-deficiency to cobalamin depletion. This study is an important contribution to the understanding of the natural history of AIG. We wish to comment on aspects that are related to Helicobacter pylori and may have clinical relevance.The relation between H pylori and AIG is not fully understood. AIG is mediated by CD4+ T cells reactive to the H+K+-ATPase, and H pylori probably triggers the autoimmune process by molecular mimicry.2 Hershko and colleagues1 provide strong epidemiologic evidence in support of this model. In their study, almost 90% of AIG patients younger than 20 years were infected. The low prevalence of infection among old patients with pernicious anemia (12%) does not argue against a relation of H pylori to AIG, but can be explained by the observation that the microenvironment of the atrophic stomach is hostile to the growth and colonization of H pylori, with progressive atrophy leading to a loss of the bacterial niche.3 Indeed, in patients with pernicious anemia an anti–Helicobacter–immunoglobulin G (IgG) seroreversion rate of 6% per year has been observed.3
Although H pylori is potentially involved in the induction of AIG and has its own inhibitory effect on cobalamin absorption,4 there are no recommendations for the management of infection in AIG. The observations of Hershko and colleagues that iron-deficiency anemia (IDA) is the presenting feature in more than 50% of patients with AIG, and that these patients are mainly young and H pylori–positive, provides a basis for new therapeutic considerations. In AIG, IDA develops mainly as a consequence of reduced acid secretion. Acid is indispensable for solubilization, reduction, and subsequent absorption of nonheme dietary iron. Several lines of evidence suggest that AIG patients with IDA would benefit from H pylori eradication: (1) H pylori suppresses acid secretion through induction of interleukin-1 Long-term prospective studies are needed to define the influence of H pylori eradication on the presentation and progression of AIG. Currently available data, however, suggest that at least in AIG patients with IDA, diagnosis and treatment of infection would be beneficial. Finally, the recognition of AIG1 and H pylori10 as possible causes of iron deficiency will probably have a strong impact on the clinical management of unexplained IDA.
Correspondence: Roland Rad, Klinikum Rechts der Isar, Technical University of Munich, 2nd Medical Department, Ismaningerstraße 22, 81675 Munich, Germany; e-mail: roland.rad{at}lrz.tum.de.
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