Abstract
Anemia often occurs in patients with thyroid dysfunction, and hepcidin plays an important role in this process. As is known, hepcidin is an acute phase protein and a key regulator of iron homeostasis. Hepcidin and ferritin are important biomarkers that reflect the state of iron metabolism in the body. Thyroid dysfunction can affect the levels of these biomarkers, which, in turn, may have clinical significance for the diagnosis and treatment of this category of patients. The aim was to analyze the characteristics of iron me-tabolism indicators, namely: hepcidin, ferritin and serum iron in patients with thyroid dysfunction. Material and methods. The study involved 56 people with thyroid dysfunction. Participants were divided into 3 groups depending on the thyroid pathology: group 1 – hypothyroidism on the background of autoimmune thyroiditis
(n=33, 58.93%, median age 47 [38; 57] years), group 2 – postoperative hypothyroidism (n=18, 32.14%, median age 51.5 [42; 57] years), group 3 – diffuse toxic goiter, thyrotoxicosis (n=5, 8.93%, median age 56 [49; 57] years). All patients underwent determination determination of the levels of the peptide hormone hepcidin, ferritin, iron, thyroid-stimulating hormone, free T4 (fT4), thyroid peroxidase antibodies (TPOAb), as well as an ultrasound examination of the thyroid gland. Results of the analysis of average iron metabolism levels
in adults with thyroid pathology showed that the median hepcidin level was 149.7 [99.4; 187.3] ng/ml, the minimum value was 1.76 ng/ml, the maximum – 342.59 ng/ml. Hepcidin was higher than the norm 40.0 (5.95-81.25) % of adults in group 3, while in groups 1 and 2 there were no patients with such a levels of hepcidin (p<0.05). The median ferritin value was equal to 40.7 [10.7; 79.9] ng/mL (from 3.09 ng/mL to 458.78 ng/mL). Ferritin levels in group 1 were the lowest (32.0 [8.6; 52.9] ng/mL, p=0.03 compared to group 2), which
was also confirmed by the inverse correlation (r=-0.34, p<0.05). Median iron levels were 13.0 [6.8; 27.5] μmol/L and ranged from 2 μmol/L to 44 μmol/L. Median iron levels were the lowest in group 3 (6 [4; 7] μmol/L, r=-0.28, p<0.05), and the highest – in group 2 (20.5 [9; 30.8] μmol/L, p=0.02). In the male group, the levels of ferritin (49.1 [6.8; 75.7] ng/mL) and iron (20.0 [7.8; 31.0] μmol/L) were slightly increased. The value of ferritin indicators directly depended on the level of hepcidin (r=+0.56, p<0.05) and inversely on the level of TPOAb (r=-0.31, p<0.05). Conclusions. According to the obtained data, the level of ferritin had a significant positive correlation with the level of hepcidin (r=+0.56, p<0.05), indicating a direct relationship between iron stores in the body and the regulatory hormone of iron metabolism. At the same time, an inverse correlation was found
between the level of ferritin and TPOAb (r=–0.31, p<0.05). This may indicate the influence of the autoimmune process characteristic of thyroid pathology (including autoimmune thyroiditis) on iron metabolism. An inverse correlation between hepcidin and iron levels was also found (r=–0.28, p<0.05), demonstrating that an elevatedhepcidin level reduces the release of iron from cells into the blood, which leads to a decrease in serum iron level.
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