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Obesity modulate serum hepcidin and treatment outcome of iron deficiency anemia in children: A case control study
Italian Journal of Pediatrics
Obesity modulate serum hepcidin and treatment outcome of iron deficiency anemia in children: A case control study
Mohammed Sanad 0
Mohammed Osman 0
Amal Gharib 1
0 Department of Pediatrics, Faculty of Medicine, Zagazig University , Egypt
1 Department of Biochemistry, Faculty of Medicine, Zagazig University , Egypt
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 nonsignificant 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.
Obesity; Hepcidin; Iron deficiency; Children
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Background
Obesity is associated with low-serum iron
concentrations. The inverse relationship between iron status and
adiposity was first reported in 1962, when Wenzel et al
[1] unexpectedly found a significantly lower mean
serum iron concentration in obese compared with
nonobese adolescents. Most subsequent studies in pediatric
and adult samples have shown similar results [2-5].
The etiology of the hypoferremia of obesity is
uncertain. Among the proposed causes are deficient iron
intake from an iron poor diet [2], and deficient iron
stores owing to greater iron requirements in obese
adults because of their larger blood volume [6].
Recently, fat mass was described as a significant negative
predictor of serum iron and this hypoferremia seemed
not to be explained by differences in iron intake [7].
Adipose tissue is a very active endocrine organ
secreting numerous hormones and cytokines associated with
important systemic effects on different metabolic
processes [8]. Recently, hepcidin expression in adipose tissue
has been described and shown to be increased in patients
with severe obesity [9]. Hepcidin is a small, cysteine-rich
cationic peptide produced by hepatocytes [10,11],
secreted into plasma, and excreted in urine. Hepcidin
expression is induced by iron stores and inflammation
[11] and is suppressed by hypoxia and anemia [12].
Hepcidin is proposed to be a key regulator of iron
metabolism and its discovery has changed our understanding of
the pathophysiology of iron disorders [10]. Adipose tissue
of obese patients produced increased amount of
proinflammatory cytokines contributing to the
development of a low-grade systemic inflammation in these
patients [13].
At present, regulatory pathways that are generally
thought to control liver hepcidin production include: (i)
iron store-related regulation (ii) erythropoietic activity
driven regulation, and (iii) inflammation related
regulation. All are found to interact with liver cells to initiate
the production of sufficient hepcidin for correct
maintenance of iron homeostasis [14-17]. The aim of this
study was to assess the effect of obesity on hepcidin
serum levels and its relation to treatment outcome of
iron deficiency anemia in children.
Methods
This was a prospective case control study performed in
Zagazig University Children Hospital and Outpatient
Clinics in the same Hospital from April 2009 to August
2010. Informed parental consent was obtained for
enrollment into the study. The study was done
according to the rules of the local ethics committee of Faculty
of medicine, Zagazig University. The study included 70
children with iron deficiency anemia [35 obese with
BMI 95thcentile for age and sex and 35 non-obese
with BMI < 85thcentile for age and sex]. 30 healthy
nonobese children of comparable age and sex served as a
control group.
Iron deficiency was defined as presence of one or
more abnormal age-corrected iron parameters (iron,
ferritin, transferrin and transferrin saturation). IDA
was defined as concurrent iron deficiency and anemia
[18].
We excluded from the study all patients with
(...truncated)