Labile plasma iron, more practical and more sensitive to iron overload in myelodysplastic syndromes.

OBJECTIVES: In order to gain an insight into labile plasma iron (LPI) in iron metabolism microenvironment in MDS.

METHODS: We performed ELISA, quantitative real-time polymerase chain reaction, flow cytometry, MRI T2* assays to test LPI, iron biochemical parameters, and liver iron concentration (LIC) among 22 MDS patients.

RESULTS: LPI has a statistical difference (P < 0.001 by analysis of variance (ANOVA)), which decreased gradually, among three groups, while no difference was found in adjusted serum ferritin (ASF) (P = 0.086 by ANOVA). After DFO treatment, serum hepcidin expression increased from 301.26 ± 59.78 to 340.33 ± 49.78 µg/l (P = 0.032), while hepcidin/ASF was upregulated gradually from 0.16 ± 0.08 to 0.22 ± 0.03 (P = 0.045). APAF-1 expression (P = 0.047) and erythroid apoptosis rate (P = 0.009) decreased significantly, respectively. No statistical difference was found in EPO (P = 0.247) and GDF15 expression (P = 0.172). LIC dropped from 9.83 ± 4.84 to 6.28 ± 4.01 mg/g dry weight (P < 0.001). No significant difference was found in cardiac T2* (P = 0.594). LPI has a closer connection to LIC than ASF (r = 0.739, P < 0.001 vs. r = 0.321, P = 0.034).

DISCUSSION: LPI seems to be a real-time indicator which reflects body iron loading status instantaneously. Despite the limited knowledge available on LPI speciation in different types and degrees of IO, LPI measurements can be and are in fact used for identifying systemic IO and for initiating/adjusting chelation regimens.