生长分化因子 15 的表达在因志愿献血而导致缺铁的个体中并未升高。
Expression of growth differentiation factor 15 is not elevated in individuals with iron deficiency secondary to volunteer blood donation.
机构信息
Molecular Medicine Branch, NIDDK, Department of Transfusion Medicine, NIH, Bethesda, Maryland 20892, USA.
出版信息
Transfusion. 2010 Jul;50(7):1532-5. doi: 10.1111/j.1537-2995.2010.02601.x. Epub 2010 Feb 26.
BACKGROUND
Low serum hepcidin levels provide a physiologic response to iron demand in patients with iron deficiency (ID). Based on a discovery of suppressed hepcidin expression by a cytokine named growth differentiation factor 15 (GDF15), it was hypothesized that GDF15 may suppress hepcidin expression in humans with ID due to blood loss.
STUDY DESIGN AND METHODS
To test this hypothesis, GDF15 and hepcidin levels were measured in peripheral blood from subjects with iron-deficient erythropoiesis before and after iron supplementation.
RESULTS
Iron variables and hepcidin levels were significantly suppressed in iron-deficient blood donors compared to healthy volunteers. However, ID was not associated with elevated serum levels of GDF15. Instead, iron-deficient subjects' GDF15 levels were slightly lower than those measured in the control group of subjects (307 +/- 90 and 386 +/- 104 pg/mL, respectively). Additionally, GDF15 levels were not significantly altered by iron repletion.
CONCLUSIONS
ID due to blood loss is not associated with a significant change in serum levels of GDF15.
背景
低血清铁调素水平为缺铁（ID）患者对铁需求提供了生理反应。基于细胞因子命名为生长分化因子 15（GDF15）抑制铁调素表达的发现，假设 GDF15 可能由于失血而抑制 ID 患者的铁调素表达。
研究设计与方法
为了验证这一假设，在铁补充前后测量了缺铁性红细胞生成患者外周血中的 GDF15 和铁调素水平。
结果
与健康志愿者相比，缺铁性献血者的铁变量和铁调素水平显著降低。然而，ID 与血清 GDF15 水平升高无关。相反，缺铁患者的 GDF15 水平略低于对照组患者（分别为 307±90 和 386±104pg/ml）。此外，铁补充并没有显著改变 GDF15 水平。
结论
失血引起的 ID 与血清 GDF15 水平的显著变化无关。
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