1 In patients with beta-thalassaemia intermedia or major, hepcidin was hypothesised to be significantly inhibited by the overexpression of growth differentiation factor 15 (GDF15), a signaling molecule that links erythroid production to iron regulation, 2, 3 and hepcidin is maintained at an extremely low level, which continuously promotes iron absorption to induce or aggravate iron overload.
Iron homeostasis is maintained by the physiological negative feedback regulation of hepcidin, a 25-amino acid peptide produced by hepatocytes. These results suggest that in pregnant women with beta-thalassaemia minor, hepcidin functions normally to maintain iron homeostasis, and that iron supplementation is effective and safe.
After iron supplementation, the routine blood parameters and iron metabolism parameters in the β + IDA group were improved, and the hepcidin content was significantly increased. We found no statistically significant correlation between hepcidin and GDF15 in any group, but a positive correlation was observed between hepcidin and ferritin. In addition, the β + IDA and IDA groups received iron supplementation for four weeks. We compared and analysed routine blood parameters, iron metabolism parameters, the GDF15 levels, and the hepcidin levels among four groups, namely the beta-thalassaemia (β) + IDA, β, IDA, and normal groups.
There have been no studies in pregnant women with beta-thalassaemia minor combined with iron deficiency anaemia (IDA), examining whether hepcidin is inhibited by GDF15, as may occur in patients with beta-thalassaemia intermedia or major, or whether the iron metabolism characteristics and the effect of iron supplementation are consistent with simple IDA in pregnancy. In patients with beta-thalassaemia intermedia or major, hepcidin induces iron overload by continuously promoting iron absorption.
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