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The relationship between Helicobacter pylori infection and iron deficiency: seroprevalence study in 937 pubescent children
  1. Y H Choe1,
  2. S K Kim2,
  3. Y C Hong3
  1. 1Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University, School of Medicine, Seoul, Korea
  2. 2Department of Pediatrics, Inha University Hospital, Incheon, Korea
  3. 3Department of Preventive Medicine, Inha University, College of Medicine, Incheon, Korea
  1. Correspondence to:
    Dr Choe, Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University, School of Medicine, 50 Ilwon-Dong, Kangnam-Gu, Seoul, 135-710, South Korea;
    cyh{at}smc.samsung.co.kr

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Helicobacter pylori infection has been reported to be associated with various unexpected manifestations in childhood. One of them is iron deficiency anaemia at puberty. In 1999, we conducted a double blind, placebo controlled trial in pubescent children with iron deficiency anaemia and coexisting H pylori infection.1 We found that H pylori eradication led to resolution of iron deficiency. We have carried out a study of seroprevalence to examine the epidemiological relationship between H pylori infection and iron deficiency anaemia at puberty. Haemoglobin, serum iron, total iron-binding capacity, serum ferritin, and serum IgG Antibodies to H pylori were measured in 937 Korean children (475 boys and 462 girls). Their ages ranged from 10 to 18 years. The prevalence of H pylori infection was compared between groups, based on the presence or absence of anaemia, hypoferritinemia, iron deficiency, and iron deficiency anaemia. The levels of hemoglobin, serum iron, total iron binding capacity, transferrin saturation, and serum ferritin were obtained according to the presence or absence of H pylori infection.

The prevalences of anaemia, iron deficiency, iron-deficiency anaemia, and H pylori infection were 8.1%, 9.1%, 3.1%, and 20.8%, respectively. The H pylori positive rates in anaemia, hypoferritinemia, and iron deficiency group were 34.2%, 29.5%, and 35.3%, respectively, compared to 19.6% in the non-anaemia group (p=0.003), 19.2% in the non-hypoferritinemia group (p=0.005), and 19.4% in the non-iron deficiency group (p=0.001). The H pylori positive rate in the iron deficiency anaemia group was 44.8% in comparison with 20.0% in the non-iron deficiency anaemia group (p=0.001). Haemoglobin and iron levels did not show any significant differences between the H pylori positive and negative groups. The serum ferritin level was significantly lower in the H pylori infected group (p=0.0002).

The associations between iron status and H pylori were largely restricted to girls rather than boys. We speculate that this is because female adolescents are more vulnerable to iron deficiency. H pylori may affect iron absorption metabolism in the stomach and exacerbate the iron deficit in adolescents, especially girls, whose iron is supplied marginally, with anaemia ensuing promptly.2

We believe that this is the only large scale study in children showing an association between H pylori infection and iron deficiency. When children at puberty are found to have iron deficiency that is refractory to iron supplementation, H pylori infection can be considered to be a possible cause of iron deficiency.

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