Abstract
Introduction. Anemia in juvenile idiopathic arthritis (JIA), as a rule, has a multifactorial genesis, which is based on an immune-mediated mechanism: cytokines during inflammation cause changes in iron metabolism, which leads to changes in the production of red blood cells and their precursors, reticulocytes; An increase in hepcidin content causes disturbances in iron metabolism. The purpose of the study was to study hepcidin levels in patients with JIA and determine its prognostic value for the development of anemia. Material and methods. A total of 65 patients with JIA who were undergoing inpatient treatment at the 2nd State Children's Clinical Hospital in Minsk were examined. All patients underwent a general blood test using a hematological analyzer “Sysmex XS-800i” (Japan) with determination of erythrocyte, reticulocyte, and platelet parameters. A biochemical blood test included determination of iron metabolism indicators. The enzyme immunoassay method was used to study the content of cytokines: interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), interleukin-1β (IL-1β) and γ-interferon (γ-IFN). Results. All patients were divided into two groups according to the median hepcidin value. The first group, in which the values were less than 4760.0 pg/ml, included 31 patients, the second group, in which the values were more than 4760.0 pg/ml, included 34 patients. An increase in hepcidin content was accompanied by an increase in the incidence of anemia (χ² = 4.55; p = 0.03). Based on the results of the Pearson correlation analysis (r), a number of statistically significant relationships between the concentration of hepcidin and the level of IL-6 were identified (r = 0.27; p < 0.05); hemoglobin (r= - 0.28; p<0.05); hemoglobin content in the erythrocyte (r = - 0.29; p < 0.05 and erythropoietin (r = 0.32; p < 0.05). Conclusions. In children with juvenile idiopathic arthritis, increased levels of hepcidin in the blood are accompanied by an increased risk of developing anemia. The earliest markers of the development of this anemia are a decrease in the hemoglobin content in the erythrocyte, a decrease in the average volume of the erythrocyte, and an increase in the synthesis of immature forms of reticulocytes. Hepcidin acts as a marker of both the activity of the inflammatory process in children with JIA and affects the distribution of iron between its storage and the functionally active pool.
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