Department of Hematology, Oncology and Clinical Immunology, Heinrich-Heine-University, Moorenstr. 5, 40225, Düsseldorf, Germany,
Ann Hematol. 2013 Dec;92(12):1617-23. doi: 10.1007/s00277-013-1839-5. Epub 2013 Jul 11.
Patients with myelodysplastic syndromes (MDS) often show elevated serum ferritin levels at diagnosis, probably caused by increased intestinal iron uptake attributable to ineffective erythropoiesis. Many patients also develop transfusional iron overload. Hepcidin, a pivotal regulator of iron homeostasis, controls iron uptake in the duodenum as well as iron release from macrophages and is potentially involved in iron distribution to different organs. We measured serum hepcidin, together with other laboratory parameters related to iron metabolism and hematopoiesis (ferritin, transferrin, transferrin saturation, soluble transferrin receptor, erythropoietin, and hemoglobin), and C-reactive protein as marker of inflammation, in 89 MDS patients. Hepcidin levels were measured with two different competitive ELISAs: (a) EIA-4705 as described by Schwarz et al. (J Gastroenterol 46:648-656; 2011) and (b) Hepcidin 25 bioactive ELISA (EIA-5258), which was develop by DRG Diagnostics, Marburg, in 2012. Median hepcidin levels with EIA-5258 were as follows: entire cohort 17.5 ng/ml (n = 89), RA/RARS 5.9 ng/ml (n = 5), RCMD 17.8 ng/ml (n = 38), RS-RCMD 8.7 ng/ml (n = 7), RAEB I/II 29.1 ng/ml (n = 22), CMML I/II 16.9 ng/ml (n = 10), and MDS with del(5q) 26.3 ng/ml (n = 7). Hepcidin levels of the RA/RARS patients were significantly lower than in the other groups except RS-RCMD. RS-RCMD had significantly lower levels than RAEB and 5q- patients. There was a positive correlation between hepcidin levels and serum ferritin and transferrin saturation, and a negative correlation between hepcidin and hemoglobin and transferrin. Malcovati et al. (Blood 112:2676a, 2008), Santini et al. (PLoS One 6:e23109, 2011), and Ambaglio et al. (Haematologica 98:420-423, 2013), using mass spectrometry, reported similar results. We further assessed transfusional status and could show that patients who had been transfused have significantly higher hepcidin levels (median 33.3 versus 8.8 ng/ml (p < 0.001)). A dichotomized hepcidin level correlated with worse survival. EIA-4705 as described by Schwarz showed no correlation with markers of iron metabolism. Measurement of serum hepcidin with an improved ELISA yield results that correlate with other parameters of iron metabolism as well as survival and transfusion needs.
患有骨髓增生异常综合征 (MDS) 的患者在诊断时常表现出血清铁蛋白水平升高，这可能是由于无效性红细胞生成导致肠道铁吸收增加所致。许多患者还会出现输血性铁过载。铁调素是铁稳态的关键调节剂，控制十二指肠中铁的摄取以及巨噬细胞中铁的释放，并且可能参与铁向不同器官的分布。我们测量了 89 例 MDS 患者的血清铁调素，以及与铁代谢和造血相关的其他实验室参数（铁蛋白、转铁蛋白、转铁蛋白饱和度、可溶性转铁蛋白受体、促红细胞生成素和血红蛋白），以及 C 反应蛋白作为炎症标志物。铁调素水平使用两种不同的竞争性 ELISA 进行测量：(a)Schwarz 等人描述的 EIA-4705（J Gastroenterol 46:648-656; 2011）和 (b)2012 年由 DRG Diagnostics，Marburg 开发的 Hepcidin 25 生物活性 ELISA（EIA-5258）。使用 EIA-5258 的铁调素水平中位数如下：整个队列 17.5ng/ml（n=89），RA/RARS 5.9ng/ml（n=5），RCMD 17.8ng/ml（n=38），RS-RCMD 8.7ng/ml（n=7），RAEB I/II 29.1ng/ml（n=22），CMML I/II 16.9ng/ml（n=10），和 MDS 伴 del(5q) 26.3ng/ml（n=7）。RA/RARS 患者的铁调素水平明显低于其他组，除了 RS-RCMD。RS-RCMD 的水平明显低于 RAEB 和 5q-患者。铁调素水平与血清铁蛋白和转铁蛋白饱和度呈正相关，与血红蛋白和转铁蛋白呈负相关。Malcovati 等人（Blood 112:2676a，2008），Santini 等人（PLoS One 6:e23109，2011）和 Ambaglio 等人（Haematologica 98:420-423，2013）使用质谱法报告了类似的结果。我们进一步评估了输血状态，并表明已输血的患者铁调素水平显着升高（中位数 33.3 与 8.8ng/ml（p<0.001）。铁调素水平的二分法与较差的生存相关。Schwarz 描述的 EIA-4705 与铁代谢标志物无相关性。使用改良 ELISA 测量血清铁调素可产生与其他铁代谢参数以及生存和输血需求相关的结果。
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