期刊论文详细信息
Italian Journal of Pediatrics
Obesity modulate serum hepcidin and treatment outcome of iron deficiency anemia in children: A case control study
Amal Gharib1  Mohammed Osman2  Mohammed Sanad2 
[1]Department of Biochemistry, Faculty of Medicine, Zagazig University, Egypt
[2]Department of Pediatrics, Faculty of Medicine, Zagazig University, Egypt
关键词: Children;    Iron deficiency;    Hepcidin;    Obesity;   
Others  :  829312
DOI  :  10.1186/1824-7288-37-34
 received in 2011-03-18, accepted in 2011-07-19,  发布年份 2011
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【 摘 要 】

Background

Recently, hepcidin expression in adipose tissue has been described and shown to be increased in patients with severe obesity. We tried to assess the effect of obesity on hepcidin serum levels and treatment outcome of iron deficiency anemia in children.

Methods

This was a case control study included 70 children with iron deficiency anemia "IDA" (35 obese and 35 non-obese) and 30 healthy non-obese children with comparable age and sex(control group). Parameters of iron status (Serum iron, ferritin, transferrin, total iron binding capacity and transferrin saturation) and serum hepcidin levels were assessed initially and after 3 months of oral iron therapy for IDA.

Results

Compared to the control group, serum hepcidin was significantly lower in non-obese children with IDA(p < 0.01) and significantly higher in obese children with IDA (p < 0.01). Hepcidin increased significantly in non-obese children with IDA after 3 months of iron therapy (P < 0.01). On the other hand, obese children showed non-significant change in hepcidin level after iron therapy (p > 0.05). Although hepcidin showed significant positive correlations with Hb, serum iron and transferrin saturation in non-obese children with IDA, it showed significant negative correlations with Hb, serum iron and transferrin saturation in obese children with IDA (P < 0.05).

Conclusions

Obesity increased hepcidin levels and was associated with diminished response to oral iron therapy in childhood iron deficiency anemia.

【 授权许可】

   
2011 Sanad et al; licensee BioMed Central Ltd.

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