Assessment of hepcidin and iron status in children with untreated newly diagnosed graves’ hyperthyroidism

Graves’ disease (GD) is an autoimmune disease causing the overproduction of thyroid hormones from the thyroid gland. Hepcidin is an acute-phase protein and a key regulator of iron homeostasis. This study aimed to assess hepcidin and iron homeostasis parameters in children with newly diagnosed Graves’ disease (GD). Forty-two children with newly diagnosed GD and 42 healthy controls were enrolled. Prior to commencing treatment, both patients and controls underwent assessments for free thyroxine (FreeT4 and FreeT3), thyrotropin receptor antibodies (TRAbs), high-sensitivity C-reactive protein (hs-CRP), iron, ferritin, and hepcidin levels. Children with newly diagnosed GD had higher levels of hsCRP ( p = 0.001), TRAb ( p = 0.001), hepcidin ( p = 0.001), and ferritin ( p = 0.001) and lower serum iron ( p = 0.001). Significant correlations were found between hepcidin and hsCRP ( r = 0.526, p = 0.01), FreeT3 ( r = 0.626, p = 0.001), ferritin ( r = 0.711, p = 0.001), and TRAb ( r = 0.427, p = 0.001). In multivariate regression analysis, the correlation between hepcidin and ferritin (OR = 2.5, 95% CI: 1.17–2.86, p = 0.006), TRAbs (OR = 2.3, 95% CI: 1.16–2.74, p = 0.008), hsCRP (OR = 4.3; 95% CI: 1.19–8.22; p = 0.003), and Free FreeT3 (OR = 3.5, 95% CI: 1.47–3.57, p = 0.001) was confirmed. Higher hepcidin levels and the strong positive correlation between hepcidin and TRAbs in children with newly diagnosed Graves’ disease suggest a possible association between hepcidin and disease activity. However, further studies are needed to clarify whether altered hepcidin levels are a cause or a consequence of the disease process.