DefinePK

Abstract

The relationship between maternal and foetal iron nutrition has evoked considerable interest and debate. In pregnancy the demand for iron is in­creased by the mother’s need to expand her red cell mass to fulfill the requirements of the developing foetus1. Foetal hon is derived solely from the mother through the active transport function of the placen­ta2, and the quantity transferred might reasonably be supposed to be influenced by how much is avail­able3. Earlier observations suggested that iron defi­cient mothers produce babies who later develop iron deficiency2,4,5. Several subsequent studies us­ing biochemical values reflecting iron nutrition, such as Serum Iron, TIBC and present saturation of transferrin, failed to show this correlation6,7. The advent of sensitive radioimmunoassay for ferritin8,9 offered an additional approach to the problem, which has produced conflicting results. Some wor­kers found that mothers with very low ferritin con­centrations produced infants whose cord serum ferritin concentrations were low1,4,10, while others were unable to demonstrate such a correlation11-13. The rapidly growing human foetus requires a large supply of iron2, which is obtained from the iron stores of the mother. Iron is transported from mother to foetus against a concentration grad­ient2,4,14,16. The placenta plays akey role inregulat­ing the supply of iron in the foetus. The amount of iron passing through the placenta increases as ges­tation progresses15,17. The concentration of mater­nal haemoglobin is also greatly reduced in the latter part of pregnancy even in women who are not anaemic 2. These findings indicate that iron is mobi­lized from the stored iron pooi in the mother as gestation progresses in order to meet the increasing demand of iron for heqiatopoiesis in the foetus and placenta2,3,17. At delivery the umbilical cord blood had a significantly higher content of serum iron than the maternal blood2-4,17. This provides evidence that at least in the terminal stage of gestation iron is actively transported from mother to child against a con­centration gradient. The cord blood also contains a significantly higher amount of serum ferritin than does the maternal blood17. The relationship be­tween maternal and foetal iron stores is controver­sIaL Some found a positive correlation1,3,10,17 while others were unable to do so2,4,11,12,14. Babies born to the mother with low iron stores had a lower amount of storage iron than babies born to the mothers with normal iron stores1,3,4,18, but an over­all correlation between maternal and cord serum was not found1,11,12,17. This suggests that iron stor­age in the mother and iron metabolism in the foetus are not directly related2. The mother and foetus have independent systems for the control of iron metabolism. The foetus and placenta are able to take iron from the maternal circulation in spite of maternal iron deficiency4-7,19,20. Thus, although the mother is iron deficient, foetal iron supply is we­bably adequate. However, there seem to be a level of maternal iron storage, below which the newborn was endowed with decreased iron stores4,19,20.