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Iron deficiency anaemia,helicobacter pylori infection and delayed pubertal growth
  1. L CUOCO,
  2. G CAMMAROTA,
  3. R A JORIZZO,
  4. R CIANCI,
  5. G GASBARRINI
  1. Università Cattolica del Sacro Cuore
  2. Policlinico “A.Gemelli”
  3. Istituto di Medicina Interna e Geriatria
  4. Largo A.Gemelli, 8, 00168 Roma, Italy
  5. gcammarota{at}libero.it

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    We read with great interest the paper by Choe and colleagues which investigated a possible relationship betweenHelicobacter pylori infection, iron deficiency anaemia (IDA), and subnormal growth at puberty.1 The authors concluded that H pylori infection and related IDA, rather than bacterial infection alone, might cause delayed pubertal growth. However, we believe that these results need some consideration.

    H pylori infection may cause IDA in different ways: (a) the bacterium can cause a decrease in the gastric juice of the concentration of ascorbic acid, which is the best promoter of non-heme iron absorption2; (b) H pylori may increase iron demand because iron is an essential bacterial growth factor; (c) H pyloricontains a 19.6 kDA protein resembling ferritin with a binding activity for heme iron in erythrocytes3; (d) acute or chronic blood loss and IDA are associated with typical H pylori related gastroduodenal lesions. In Choe's study, the treatment of H pylori infection with antibiotics (but also with proton pump inhibitors) was probably linked to a more rapid response to oral iron replacement because of the effects of proton pump inhibitors in healing some of the lesions.

    However, IDA, failure to thrive, and delayed pubertal growth are important features of subclinical and silent coeliac disease. Therefore, coeliac disease should be suspected in children or adolescents with these signs, especially when IDA is resistant to oral iron replacement.

    In a recent study,4 IDA seemed to be the most frequent extra-intestinal marker of coeliac disease in both children and adults, followed by short stature for children. Thus, it would be advisable to screen paediatric and juvenile population with IDA, failure to thrive, or delayed pubertal growth for coeliac related antibodies (anti-endomysial, antitransglutaminase, antigliadin) in order to identify coeliac patients who need lifelong gluten withdrawal for recovery of iron, and improved metabolism and growth.

    Finally, it is reasonable that H pyloriinfection may make iron deficiency worse in coeliac patients and subsequently impair growth in children who need a large amount of this essential element.

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