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Abstract
The Two Stage Model of preeclampsia proposes that a poorly perfused placenta (Stage
1) produces factor(s) leading to the clinical manifestations of preeclampsia (Stage
2). Stage 1 is not sufficient to cause the maternal syndrome but interacts with maternal
constitutional factors (genetic, behavioral or environmental) to result in Stage 2.
Recent information indicates the necessity for modifications of this model. It is
apparent that changes relevant to preeclampsia and other implantation disorders can
be detected in the first trimester, long before the failed vascular remodeling necessary
to reduce placental perfusion is completed. In addition, although the factor(s) released
from the placenta has usually been considered a toxin, we suggest that what is released
may also be an appropriate signal from the fetal/placental unit to overcome reduced
nutrient availability that cannot be tolerated by some women who develop preeclampsia.
Further, it is evident that linkage is not likely to be one factor but several, different
for different women. Also although the initial model limited the role of maternal
constitutional factors to the genesis of Stage 2, this does not appear to be the case.
It is evident that the factors increasing risk for preeclampsia are also associated
with abnormal implantation. These several modifications have important implications.
An earlier origin for Stage 1, which appears to be recognizable by altered concentrations
of placental products, could allow earlier intervention. The possibility of a fetal
placental factor increasing nutrient availability could provide novel therapeutic
options. Different linkages and preeclampsia subtypes could direct specific preventive
treatments for different women while the role of maternal constitutional factors to
affect placentation provides targets for prepregnancy therapy. The modified Two Stage
Model provides a useful guide towards investigating pathophysiology and guiding therapy.