FGR is characterized by an increase in arachidonic acid both in the placenta and umbilical artery phospolipids, probably reflecting a different mobilization from tissue stores. It is speculated that the different arterial composition could be partially responsible for the increased cardiovascular risk of FGR in adulthood. On the other hand the metabolic status of the placenta concerning polyunsaturated fatty acids was very different in symmetric and asymmetric FGR, suggesting a different pathogenesis.

No abstract