Abstract
Aim. To determine the pathogenetic role of hepcidin in the development of anemia of inflammation in young children.Materials and methods. The content of hepcidin, ferritin and erythropoietin was studied in young children. The serum total iron-binding capacity, the coefficient of saturation of iron in transferring was determined. The main group consisted of children with acute inflammatory bacterial diseases of the respiratory system: the first subgroup included children with anemia of inflammation, the second group - without anemia. The comparison group included children with iron deficiency anemia without inflammatory manifestations. The control group consisted of conditionally healthy children. The studied groups were age- and sex-representative.Results. Patients with acute bacterial diseases of respiratory tract who developed anemia of inflammation had an elevated level of hepcidin, doubling the control group indicator (2.09 (1.81; 2.24) ng/ml and 1.07 (0.98; 1.17) ng/ml, respectively, P < 0.05). Its increase did not depend on the etiological factor of the disease; however, it increased with the disease severity. Low iron content was found in the first subgroup compared with other groups (P < 0.05), and in the second subgroup, there was an increasing trend in its content (P > 0.05). A high level of ferritin was detected in both subgroups, the concentration of which was 2 times higher than in the control group (P < 0.05). A close direct correlation was established between the serum contents of hepcidin and ferritin in the studied groups of children (r = +0.93, P < 0.01). The coefficient of saturation of iron in transferring was lower in the main group than in the comparison and control groups (P < 0.05). The level of serum total iron-binding capacity was statistically significantly decreased in the first subgroup (P < 0.05), and significantly increased in the second subgroup (P < 0.05), while there was only its downward trend (P > 0.05) in the comparison group. An increase in the content of erythropoietin was observed only in the group of children who were diagnosed with iron deficiency anemia. Its level was statistically significantly higher than the indicators of both subgroups of the main and control groups (P < 0.01).Conclusions. Hepcidin plays a significant pathogenetic role in the development of anemia of inflammation in young children due to the regulatory effect on iron deposition. The increase in its level in response to the development of a bacterial inflammatory process of the respiratory system in young children did not depend on the etiological factor of the disease.
Highlights
MethodsThe content of hepcidin, ferritin and erythropoietin was studied in young children. The serum total iron-binding capacity, the coefficient of saturation of iron in transferring was determined
Patients with acute bacterial diseases of respiratory tract who developed anemia of inflammation had an elevated level of hepcidin, doubling the control group indicator (2.09 (1.81; 2.24) ng/ml and 1.07 (0.98; 1.17) ng/ml, respectively, P < 0.05)
An increase in the content of erythropoietin was observed only in the group of children who were diagnosed with iron deficiency anemia
Summary
The content of hepcidin, ferritin and erythropoietin was studied in young children. The serum total iron-binding capacity, the coefficient of saturation of iron in transferring was determined. The main group consisted of children with acute inflammatory bacterial diseases of the respiratory system: the first subgroup included children with anemia of inflammation, the second group – without anemia. The comparison group included children with iron deficiency anemia without inflammatory manifestations. The main group consisted of 40 children with acute bacterial diseases of the respiratory tract. Bronchitis was diagnosed in 32 (79 %) children, pneumonia – in 8 (21 %) children. Haemophillus influenzae prevailed in 19 (46.6 %) children, Streptococcus pneumoniae – in 12 (30 %) children, Klebsiella pneumo niae – in 4 (10 %). The first subgroup included 20 children with AI, which was determined 4–5 days after the disease onset. The second subgroup consisted of 20 children without anemia.
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