Figure 4
From: Serum hepcidin level, iron metabolism and osteoporosis in patients with rheumatoid arthritis
Estimated relationships related to hepcidin in patients with RA. Hepcidin is usually regulated by iron metabolism—iron overload (black arrow) leads to an increase in hepcidin, and iron deficiency (white arrow) leads to a decrease—and is suppressed by erythropoiesis, sex hormones, and growth factors. To maintain iron homeostasis, higher hepcidin levels result in a decrease in serum iron levels, while lower hepcidin levels increase serum iron levels. When inflammation due to RA occurs, production of hepcidin is increased through inflammatory cytokines that cause elevated ferritin levels. In this study, serum iron levels are positively related to serum hepcidin and ferritin levels but negatively related to inflammation due to RA. This unexpected relationship may give arisen because inflammation in most of the patients was well-controlled. Although iron overload and hepcidin may influence osteoporosis, in this study serum iron level was positively related to BMD but serum hepcidin level was not. However, serum 25(OH)D level was positively related to the serum hepcidin level and also positively related to the femoral Z score in this study. According to previous reports, opposite effects of serum iron level on BMD and 25(OH)D on hepcidin are indicated, and further research is needed to determine the mechanism. Serum FGF23 is not directly related to the serum hepcidin level, but serum 25(OH)D level and inflammation are common factors involved in the regulation of both serum hepcidin and FGF23 levels.
