Abstract
Hepcidin, a major regulator of iron metabolism and homeostasis, is regulated by inflammation. Recent studies have suggested that hepcidin and iron metabolism are involved in osteoporosis, and the aim of this study was to determine whether serum hepcidin levels are correlated with the degree of osteoporosis in patients with rheumatoid arthritis (RA). A total of 262 patients with RA (67.5 ± 11.4 years; 77.5% female) were enrolled. Serum iron, ferritin, and hepcidin levels were positively correlated each other. Multiple regression analyses revealed that the serum iron level was positively correlated with femoral T and Z scores, whereas the serum hepcidin level was not. Serum hepcidin level was correlated with the serum 25-hydroxy vitamin D level, which was in turn positively related to the femoral Z score. Serum hepcidin and serum iron were indirectly and directly related to osteoporosis in patients with RA.
Highlights
Hepcidin, a major regulator of iron metabolism and homeostasis, is regulated by inflammation
As the mechanism linking inflammation and Fibroblast growth factor 23 (FGF23) has been studied with regard to iron metabolism[3,4], IL-15β, and IL-66, here we focused on hepcidin as a factor associated with rheumatoid arthritis (RA) inflammation, iron metabolism and systemic osteoporosis
The results of this study indicate that the serum iron level is positively related to bone mineral density (BMD) and serum hepcidin and ferritin levels are positively related to the 25(OH)D level, which is positively related to the femoral Z score
Summary
A major regulator of iron metabolism and homeostasis, is regulated by inflammation. Recent studies have suggested that hepcidin and iron metabolism are involved in osteoporosis, and the aim of this study was to determine whether serum hepcidin levels are correlated with the degree of osteoporosis in patients with rheumatoid arthritis (RA). Ferritin, and hepcidin levels were positively correlated each other. Serum hepcidin and serum iron were indirectly and directly related to osteoporosis in patients with RA. As the mechanism linking inflammation and FGF23 has been studied with regard to iron metabolism[3,4], IL-15β, and IL-66, here we focused on hepcidin as a factor associated with RA inflammation, iron metabolism and systemic osteoporosis. In one study, lower serum hepcidin levels and higher serum iron levels were reported in patients with osteoporosis than healthy controls[14].
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