Iron Homeostasis in Pregnancy, the Fetus, and the Neonate

Abstract

The master iron regulator, hepcidin, controls maternal-fetal iron metabolism. In the last trimester, fetal liver hepcidin normally signals to the mother to increase maternal iron absorption sixfold to meet needs for fetal growth. Eighty percent of this placental-fetal iron transfer occurs during the last trimester, and preterm infants, without benefit of the third trimester of gestation, have poorer fetal iron endowment. Fifty percent of the iron needed for postnatal infant growth exists at normal term birth, but maternal conditions such as diabetes, obesity, or placental dysfunction can disrupt iron supply, while postnatal phlebotomy volumes promote loss and erythropoietic-stimulating agents increase demand. Delayed umbilical cord clamping improves erythrocyte (and, thus, iron) endowment.