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 assimilation 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 got poorer fetal iron endowment. Fifty percent of the iron needed for postnatal infant growth exists at normal term birth, but maternal conditions for example diabetes, obesity, or placental dysfunction can disrupt iron supply, while postnatal phlebotomy volumes promote reduction and erythropoietic-stimulating agents increase need. Delayed umbilical cord clamping boosts erythrocyte (and, thus, iron) endowment….
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