Does Helicobacter pylori infection cause iron deficiency and IDA?

Evidence from clinical research and mechanistic studies confirms that Helicobacter pylori (H. pylori) infection is a significant contributor to iron deficiency and iron deficiency anemia (IDA) through a combination of impaired absorption and direct competition.

Clinical evidence

H. pylori infection is strongly associated with an increased risk of iron deficiency (ID). A systematic review and meta-analysis of observational studies found that infected individuals have significantly higher odds of developing IDA, with some studies reporting an odds ratio (OR) as high as 3.033 (95% CI: 2.08–4.42). Clinical trials have demonstrated that H. pylori eradication alone, even without iron supplementation, can significantly increase serum ferritin and hemoglobin levels in patients with unexplained or refractory IDA, confirming the infection's causative role in iron depletion.

Mechanistic explanations

The pathogen disrupts iron homeostasis through several distinct biological pathways:

• Impaired Gastric Absorption: The infection often leads to chronic atrophic gastritis, causing the loss of parietal cells. This results in hypochlorhydria (reduced stomach acid), which is critical for converting non-heme iron into a soluble, absorbable form. Furthermore, infection lowers gastric concentrations of ascorbic acid (vitamin C), a key enhancer of iron absorption.
• Direct Bacterial Competition: H. pylori requires iron for survival and has evolved sophisticated systems to sequester it from the host. It utilizes the FeoB ferrous iron transporter and specialized outer membrane proteins (OMPs) to capture iron from host proteins like lactoferrin and transferrin.
• Host Manipulation: The bacterium uses the CagA effector protein to redistribute transferrin receptors to the apical surface of gastric cells, making host iron more accessible for its own uptake. It also possesses internal ferritin (Pfr) stores to thrive even in iron-restricted environments, further depleting host reserves.

Bottom line

H. pylori infection contributes to iron deficiency by both reducing the host's ability to absorb iron (via acid suppression and vitamin C depletion) and by actively sequestering iron for its own metabolic needs through specialized transport systems. Eradication is a key clinical intervention for improving iron status in infected patients.