The presence of a H. pylori infection blunted the upregulation of iron-related duodenal proteins in response to anemia.

Helicobacter pylori (H. pylori) infection is often associated with iron-deficiency anemia. The mechanisms that underlie this association are unclear. We attempted to determine whether the presence of a H. pylori infection affected iron homeostasis. Patients with dyspepsia, who underwent an upper gastrointestinal endoscopy, were categorized into those without and with a H. pylori infection. Hematological and iron-related parameters and C-reactive protein (CRP) were estimated in their blood samples. Gene expression of proteins involved in iron absorption (divalent metal transporter 1 [DMT1], duodenal cytochrome B reductase [DCYTB], ferritin [FTN] and ferroportin [FPN]) was determined in duodenal mucosal samples. Hematological and iron-related parameters and CRP levels in blood, and gene expression of duodenal iron-related proteins were not significantly different in those without and with a H. pylori infection. When stratified into quartiles based on hemoglobin values, patients in the lower quartiles (in both groups) showed evidence of a lower iron status. Upregulation of duodenal DMT1 and FPN gene expression in response to anemia (a known physiological phenomenon) was seen in uninfected patients, but not in those with the infection. DYCTB expression was significantly lower in those with the infection, who expressed H. pylori-associated virulence factors, CagA and VacA. H. pylori infection did not significantly affect hematological parameters, blood markers of iron status and gene expression of duodenal proteins involved in iron absorption. However, the physiological response to upregulate DMT1 and FPN gene expression in response to anemia was attenuated in those with the infection.