Helicobacter pylori-associated hypochlorhydria in children, and development of iron deficiency
- Paul R Harris1,
- Carolina A Serrano1,
- Andrea Villagrán1,
- Marjorie M Walker2,
- Melanie Thomson3,
- Ignacio Duarte4,
- Henry J Windle5,
- Jean E Crabtree3
- 1Division of Paediatrics, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile
- 2Department of Pathology, Imperial College, London, UK
- 3Molecular Gastroenterology Section, Leeds Institute Molecular Medicine, Leeds, UK
- 4Department of Pathology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile
- 5Institute of Molecular Medicine, Trinity College Dublin, Dublin, Ireland
- Correspondence to Professor Jean E Crabtree, Leeds Institute of Molecular Medicine, St James's University Hospital, Leeds LS9 7TF, UK; j.crabtree{at}leeds.ac.uk
- Received 15 October 2012
- Revised 13 November 2012
- Accepted 15 November 2012
- Published Online First 25 December 2012
Abstract
Aims Acute Helicobacter pylori infection is associated with transient hypochlorhydria. In H pylori-associated atrophy, hypochlorhydria has a role in iron deficiency (ID) through changes in the physiology of iron-complex absorption. The aims were to evaluate the association between H pylori-associated hypochlorhydria and ID in children.
Methods Symptomatic children (n=123) were prospectively enrolled. Blood, gastric juice and gastric biopsies were taken, respectively, for haematological analyses, pH assessment and H pylori determination, and duodenal biopsies for exclusion of coeliac disease. Stool samples were collected for parasitology/microbiology. Thirteen children were excluded following parasitology and duodenal histopathology, and five due to impaired blood analysis.
Results Ten children were hypochlorhydric (pH>4) and 33 were H pylori positive. In H pylori-positive children with pH>4 (n=6) serum iron and transferrin saturation levels % were significantly lower (p<0.01) than H pylori-positive children with pH≤4. No differences in ferritin, or total iron binding capacity, were observed. In H pylori-negative children with pH>4, iron and transferrin saturation were not significantly different from children with pH≤4.
Conclusions Low serum iron and transferrin in childhood H pylori infection is associated with hypochlorhydria. In uninfected children, hypochlorhydria was not associated with altered serum iron parameters, indicating a combination of H pylori infection and/or inflammation, and hypochlorhydria has a role in the aetiology of ID. Although H pylori-associated hypochlorhydria is transient during acute gastritis, this alters iron homeostasis with clinical impact in developing countries with a high H pylori prevalence.








