Serum hepcidin levels in Helicobacter pylori-infected children with iron-deficiency anemia: a case-control study
Seham F A Azab1, Asmaa M H Esh
1Department of Pediatrics, Faculty of Medicine, Zagazig University, Zagazig, Egypt, seham_azab@yahoo.com.
Insights
Helicobacter pylori infection increases hepcidin levels in children with iron-deficiency anemia, impairing their response to oral iron therapy. This study highlights hepcidin
Area of Science:
- Pediatric Hematology
- Infectious Diseases
- Iron Metabolism
Background:
- Hepcidin is the master regulator of systemic iron homeostasis, linking iron trafficking with infection response.
- Iron-deficiency anemia (IDA) is a common pediatric condition.
- Helicobacter pylori (H. pylori) infection is prevalent and can affect nutritional status.
Purpose of the Study:
- To investigate the impact of H. pylori infection on serum hepcidin levels in children with IDA.
- To assess the influence of H. pylori infection on the response to oral iron therapy in pediatric IDA.
Main Methods:
- A case-control study involving 60 children with IDA (30 H. pylori infected, 30 noninfected) and 30 healthy controls.
- Assessment of iron parameters (serum iron, ferritin, transferrin, TIBC, transferrin saturation) and serum hepcidin.
- Measurements were taken at baseline and after 3 months of oral iron therapy for IDA.
Main Results:
- Serum hepcidin was lower in noninfected IDA children and higher in H. pylori-infected IDA children compared to controls.
- Hepcidin increased significantly in noninfected IDA children after iron therapy, but showed no significant change in infected children.
- H. pylori infection was associated with altered correlations between hepcidin and iron parameters, and diminished response to oral iron.
Conclusions:
- H. pylori infection upregulates serum hepcidin levels in children with iron-deficiency anemia.
- Elevated hepcidin due to H. pylori infection is linked to a reduced therapeutic response to oral iron supplementation.
- This suggests H. pylori infection complicates iron management in pediatric IDA by modulating hepcidin.
Abstract:
Recently, hepcidin, an antimicrobial-like peptide hormone, has evolved as the master regulator of systemic iron homeostasis. Hepcidin integrates signals from diverse physiological inputs, forming a key connection between iron trafficking and response to infection. In this study, we aimed to investigate whether Helicobacter pylori infection modulates serum hepcidin level and response to oral iron therapy in children with iron-deficiency anemia. This was a case-control study including 60 children with iron-deficiency anemia (IDA; 30 H. pylori infected and 30 H. pylori noninfected) and 30 healthy children with comparable age and gender as the control group. Iron parameters including serum iron, ferritin, transferrin, total iron binding capacity, and transferrin saturation and serum hepcidin levels were assessed initially and after 3 months of oral iron therapy for IDA. Compared to the control group, serum hepcidin was significantly lower in H. pylori-noninfected children with IDA (P < 0.01) and significantly higher in H. pylori-infected children with IDA (P < 0.01). Hepcidin increased significantly in noninfected children with IDA after 3 months of oral iron therapy (P < 0.01). On the other hand, H. pylori-infected children showed nonsignificant change in hepcidin level after oral iron therapy (P > 0.05). Although hepcidin showed significant positive correlations with serum ferritin, hemoglobin (Hb), iron, and transferrin saturation in noninfected children with IDA (P < 0.01), it showed significant negative correlations with serum ferritin, Hb, iron, and transferrin saturation in H. pylori-infected children with IDA (P < 0.05). H. pylori infection upregulates serum hepcidin levels and was associated with diminished response to oral iron therapy in children with iron-deficiency anemia.
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