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Am J Hematol. 2019 Feb;94(2):184-188. doi: 10.1002/ajh.25341. Epub 2018 Nov 26.

Iron homeostasis in pregnancy and spontaneous abortion.

Guo Y1,2,3, Zhang N4, Zhang D2,3, Ren Q1,5, Ganz T6, Liu S1,5, Nemeth E6.

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State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Science, Chinese Academy of Sciences, Beijing, China.
Weifang Medical University, Weifang, China.
Weihai Key Laboratory of Autoimmunity, Weihai Central Hospital, Weihai, China.
Department of Ultrasound, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China.
University of Chinese Academy of Sciences, Beijing, China.
Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California.


During pregnancy, iron requirements are increased to support maternal erythropoietic expansion and fetal growth and development. To meet these requirements, dietary iron absorption increases, and available iron stores are mobilized. These adjustments are thought to be in large part mediated by the iron-regulatory hormone hepcidin, which controls the concentrations of ferroportin, the sole exporter of iron into the extracellular fluid and blood plasma. Hepcidin regulation of iron availability during healthy and abnormal pregnancies is not well understood. In our cross-sectional study, we compared hepcidin, iron and hematological parameters between nonpregnant control women, healthy pregnant women in the first and second trimester, and women with spontaneous abortion in the first trimester. We found that in healthy pregnancy, hepcidin increased in the first trimester compared with nonpregnant women, but then decreased during the second trimester. The second trimester hepcidin levels decreased despite stable serum iron concentrations, suggesting active suppression of hepcidin, presumably to enhance iron availability as iron demand increases. In women with spontaneous abortion during the first trimester, hepcidin, serum iron, and ferritin concentrations were all increased compared with the first trimester healthy pregnancy. Although the specific mechanisms remain to be determined, our findings demonstrate that maternal hepcidin is regulated by signals related to the progression of pregnancy, and that pregnancy loss is associated with profound changes in maternal iron metabolism. These observations highlight the existence of fetoplacental signals that modulate maternal iron homeostasis.

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