Hepcidin profile of anemic adolescent schoolgirls in Indonesia at the end of 12 weeks of iron supplementation.

Background: Iron deficiency is still the major nutritional problem in the developing world, and iron supplementation remains one of the most effective intervention strategies. Hepcidin, a newly discovered iron regulatory hormone, is an acute phase protein, and its role in iron supplementation has not been well explored.

Objective: To investigate the hepcidin profiles of anemic adolescent girls who had received weekly iron supplementation.

Methods: A cross-sectional study was conducted at the end of iron supplementation among adolescent schoolgirls (n = 83) in Pramuka Island, Indonesia. All the girls were anemic at the beginning and received 60 mg of elemental iron twice weekly for 12 weeks. Hemoglobin, hepcidin, serum ferritin, and red cell parameters were measured, together with inflammation markers.

Results: At the end of the 12-week supplementation, 65.1% (n = 64) of the girls were no longer anemic, but 43.4% (n = 36) were still iron deficient. The rate of subclinical inflammation, measured by C-reactive protein (CRP) and alpha-1-acid glycoprotein (AGP), was 38.6% (n = 32). Hepcidin was not correlated with either ferritin or red cell parameters. There was no association between hepcidin and the inflammatory markers CRP and AGP. The mean hepcidin concentration was 42.9 +/- 17.9 ng/mL and was not significantly different between anemic and nonanemic girls (44.2 +/- 14.9 and 42.3 +/- 19.2 ng/mL, respectively; p = .708). However, hepcidin concentration was slightly higher in the iron replete-group than in the iron-deficient group (45.2 +/- 20.0 and 39.3 +/- 13.5 ng/mL, respectively), a suggestive trend that did not reach statistical significance (p = .218).

Conclusions: Hepcidin concentrations tended to be higher among the subset of girls who responded poorly to iron supplementation as a consequence of increased subclinical inflammation. A longitudinal study should be conducted to explore the role of hepcidin in iron supplementation.