OBJECTIVE: To explore the application value of detection of Hepcidin together with indicator of iron overload on clinical diagnosis and treatment of MDS with iron overload by measuring Hepcidin and iron load indices of transfusion dependent myelodysplastic syndrome (MDS) patients. METHODS: Enzyme-linked immunosorbent assay (ELISA), radioimmunoassay and colorimetry were used to determine the Hepcidin, serum ferritin (SF) and serum iron (SI) levels of 106 serum samples from 68 cases of transfusion dependent MDS patients, 30 serum samples of MDS patients without transfusion and 60 serum samples of controls. RESULTS: For MDS group, Hepcidin level in blood transfusion < 9 U subgroup was significantly higher than that in control group [(583 ± 50) µg/L vs (175 ± 35) µg/L] and there was a strong positive correlation between Hepcidin levels and SF (r = 0.976), but no correlation between Hepcidin and SI (r = 0.284); Both Hepcidin and SF level in transfusion 9 ∼ 24 U subgroup was significantly higher than those in control group [(665 ± 80) µg/L vs (175 ± 35) µg/L; (1445 ± 275) µg/L vs (112 ± 26)µg/L]; whereas for SI level, there was no difference between transfusion 9 ∼ 24 U subgroup and the control group. Hepcidin did not correlate with SF or SI; For blood transfusion > 24 U group, all of Hepcidin, SF and SI levels were higher than those in control groups [(703 ± 64) µg/L vs (175 ± 35) µg/L; (2587 ± 352) µg/L vs (112 ± 26)µg/L; (20 ± 4) µg/L vs (14 ± 4) µmol/L], Hepcidin negatively correlated with SF and SI (r = -0.536; r = -0.456). Hepcidin levels of RARS patients were significantly lower than RAEB patients [(260 ± 40) µg/L vs (442 ± 51) µg/L], and there was no significant difference between RARS group and control group regardless of the number of blood transfusion. CONCLUSION: Both Hepcidin and SF levels in MDS patients regardless of transfusion dependent or not, or the number of blood transfused were higher than those of normal controls, the increase of Hepcidin can not synchronize with the increase of SF level due to the increased blood transfusion, when blood transfusion > 24 U, Hepcidin level showed a negative relationship with SF and SI, reflecting the decreased ability of Hepcidin to inhibit body iron absorption during the increase of blood transfusion, which finally would lead to iron overload. We can predict the occurrence of iron overload in transfusion dependent MDS patients by dynamic monitoring concentration of Hepcidin.