What regulates hepcidin in poly-transfused β-Thalassemia Major: Erythroid drive or store drive.
Indian J Pathol Microbiol
;
2014 Jan-Mar 57 (1): 39-42
Article
in English
| IMSEAR
| ID: sea-155965
ABSTRACT
Background:
Hepcidin, a key regulator of iron homeostasis, is increased by iron overload and infl ammation while suppressed by hypoxia. In spite of iron overload in β-Thalassemia Major (β-TM), a paradoxical decrease in hepcidin is observed.Aim:
To assess the opposing effects of enhanced erythropoiesis due to anemia and iron overloading on hepcidin in β-TM patients. Setting andDesign:
This prospective observational study was done at our tertiary care hospital. Materials andMethods:
Eighty-three pediatric polytransfused (> 20 transfusions) patients of β-TM were compared with 70 children who served as controls. Serum assays for ferritin, transferrin receptors (sTfR) and hepcidin were performed. Statisticalanalysis:
Independent Student t test was used to compare variables between both the groups. A Pearson correlation coeffi cient was used to fi nd any correlation between ferritin, sTfR and hepcidin.Results:
The mean value of hepcidin in β-TM children was 13.88±10.68 ng/ml (range, 0.9-60 ng/ml) and showed signifi cant negative correlation with sTfR (r = –0.296, P < 0.0066). However, there was no correlation of hepcidin with ferritin. Ferritin and sTfR were signifi cantly elevated in β-TM children compared to controls (P < 0.001). The mean serum hepcidin/ferritin index in the study group (0.00552) was signifi cantly lower (P value < 0.001) than the controls (0.378) thus indicating inappropriate levels of hepcidin to iron overload.Conclusion:
In polytransfused β-TM children increased iron demand dominates over iron overload in regulating hepcidin. In spite of excessive iron load, the inappropriate hepcidin levels may further contribute to iron overload enhancing iron toxicity.
Full text:
Available
Index:
IMSEAR (South-East Asia)
Type of study:
Observational study
Language:
English
Journal:
Indian J Pathol Microbiol
Year:
2014
Type:
Article
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