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Obesity modulate serum hepcidin and treatment outcome of iron deficiency anemia in children: a case control study
Mohammed Sanad1, Mohammed Osman, Amal Gharib
1Department of Pediatrics, Faculty of Medicine, Zagazig University, Egypt. zanad_zanad2005@yahoo.com
Insights
Obesity elevates hepcidin levels in children with iron deficiency anemia (IDA), leading to a poorer response to oral iron therapy. This highlights a critical factor in treating pediatric IDA in obese populations.
Area of Science:
- Pediatric Endocrinology
- Hematology
- Nutritional Science
Background:
- Hepcidin expression is elevated in adipose tissue of severely obese individuals.
- Understanding the impact of obesity on hepcidin and iron deficiency anemia (IDA) treatment outcomes in children is crucial.
Purpose of the Study:
- To investigate the effect of obesity on serum hepcidin levels in children with IDA.
- To assess the influence of obesity on the treatment response to oral iron therapy in pediatric IDA.
Main Methods:
- A case-control study involving 70 children with IDA (35 obese, 35 non-obese) and 30 healthy controls.
- Assessed iron status parameters and serum hepcidin levels before and after 3 months of oral iron therapy.
Main Results:
- Serum hepcidin was lower in non-obese IDA children and higher in obese IDA children compared to controls (p < 0.01).
- Non-obese IDA children showed a significant increase in hepcidin after iron therapy (P < 0.01), while obese children did not (p > 0.05).
- Hepcidin correlated positively with Hb, serum iron, and transferrin saturation in non-obese children, but negatively in obese children (P < 0.05).
Conclusions:
- Obesity is associated with increased hepcidin levels in children with iron deficiency anemia.
- Elevated hepcidin in obese children with IDA correlates with a diminished response to oral iron therapy.
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.
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