Is hepcidin the bridge linking Helicobacter pylori and anemia of chronic infection? A research proposal.

Since the last decade, several studies have reported on the link between chronic Helicobacter pylori (H. pylori) or Helicobacter species (H. species) infection and a variety of extragastric manifestations, comprising iron-deficiency anemia. A crucial question concerns which possible pathogenic mechanism of H. pylori infection may be involved in chronic anemia. Recent findings support the hypothesis that in subjects with H. pylori-positive gastritis, concomitant changes in intragastric pH and ascorbic acid are present that might play a role in impairing alimentary iron absorption with consequent sideropenic anemia. It has also been speculated that H. pylori infected antrum could act as a sequestering focus for iron. The bacterium enhances gastric lactoferrin, which captures iron from transferrin. The iron thus bound to lactoferrin is in turn picked up by the bacterium, by means of its outer membrane receptors, for its own growth. These models, however, are not able to answer why iron-deficiency anemia does not develop in all infected subjects. Recently, a new anti-microbial liver-made peptide, namely hepcidin, has been characterised. The link between hepcidin induction, inflammation and anemia both in humans and in animal models supports its key role as mediator of anemia of inflammation. In the present paper, we highlight the data available on the association between H. pylori and iron-deficiency anemia and, we propose to evaluate a possible mechanism involving hepcidin in a bridging role linking the infection to the anemia.