The Evaluation of iron overload through hepcidin level and its related factors in myelodysplastic syndromes

We chose hepcidin and its related factors as evaluating indicators to determine the degrees of iron overload in myelodysplastic syndromes (MDS) patients. A total of 73 patients and 28 healthy volunteers were enrolled in this study. We performed enzyme-linked immunosorbent assay to measure both bone marrow and peripheral blood serum hepcidin. Real-time quantitative polymerase chain reaction was used to determine the gene expression of growth differentiation factor 15 and twisted gastrulation 1. Serum ferritin (SF), C-reactive protein (CRP), and erythropoietin were measured by routine standard laboratory assays. CD4 + and CD19 + lymphocytes and Th polarization were detected by flow cytometry. Twenty-four MDS patients were measured their cardiac and liver iron deposition levels through magnetic resonance imaging (MRI) T2* examination. No significant difference was found between the bone marrow hepcidin levels and peripheral blood hepcidin levels (P = 0.134). Stratified according to different World Health Organization subtypes, refractory anemia with ringed sideroblasts patients had the lowest hepcidin levels (105.40 ± 5.13 ng/ml), while refractory anemia with excess blasts-1 had the highest levels (335.71 ± 25.16 ng/ml). Stratified according to International Prognostic Scoring System and WHO Classification-based Prognostic Scoring System, there was a significant difference of hepcidin levels between low-risk group and high-risk group in two systems, respectively (P = 0.033 and 0.009). The hepcidin levels of CD4 + high-expression group were demonstrated higher than the normal expression groups (P = 0.02), but the CD19 + high-expression group did not show the same result (P = 0.206). Meanwhile, patients with a Th1 polarization trend had a high level of hepcidin versus normal group (P < 0.001). Liver iron concentration (LIC) measured by MRI T2* had a closer correlation (r = 0.582, P < 0.001) to hepcidin than serum ferritin, by stepwise regression. C-reactive protein and LIC seemed to be the key determinants of hepcidin, by multivariate regression. Inflammation plays an important role in the regulation of hepcidin expression. T-lymphocyte activation and Th polarization trend might participate in the regulatory mechanism partly. The capability of organ iron load assessment of MRI T2* seems better than that of SF. It seems that hepcidin with CRP and LIC measured by MRI T2* are potential indicators of iron overload in MDS patients.