Indian Journal of Pathology and Microbiology

ORIGINAL ARTICLE
Year
: 2014  |  Volume : 57  |  Issue : 1  |  Page : 39--42

What regulates hepcidin in poly-transfused β-Thalassemia Major: Erythroid drive or store drive?


Richa Chauhan1, Sunita Sharma1, Jagdish Chandra2 
1 Department of Pathology, Lady Hardinge Medical College and Kalawati Saran Children's Hospital,New Delhi, India
2 Department of Pediatrics, Lady Hardinge Medical College and Kalawati Saran Children's Hospital,New Delhi, India

Correspondence Address:
Richa Chauhan
A-1, Parivahan Apts, Vasundhara Sector 5, Ghaziabad - 201 012, Uttar Pradesh
India

Background: Hepcidin, a key regulator of iron homeostasis, is increased by iron overload and inflammation 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 and Design: This prospective observational study was done at our tertiary care hospital. Materials and Methods: 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. Statistical analysis: Independent Student t test was used to compare variables between both the groups. A Pearson correlation coefficient was used to find 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 significant negative correlation with sTfR (r = -0.296, P < 0.0066). However, there was no correlation of hepcidin with ferritin. Ferritin and sTfR were significantly elevated in β-TM children compared to controls (P < 0.001). The mean serum hepcidin/ferritin index in the study group (0.00552) was significantly 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.


How to cite this article:
Chauhan R, Sharma S, Chandra J. What regulates hepcidin in poly-transfused β-Thalassemia Major: Erythroid drive or store drive?.Indian J Pathol Microbiol 2014;57:39-42


How to cite this URL:
Chauhan R, Sharma S, Chandra J. What regulates hepcidin in poly-transfused β-Thalassemia Major: Erythroid drive or store drive?. Indian J Pathol Microbiol [serial online] 2014 [cited 2021 Sep 22 ];57:39-42
Available from: https://www.ijpmonline.org/article.asp?issn=0377-4929;year=2014;volume=57;issue=1;spage=39;epage=42;aulast=Chauhan;type=0