sels invaded by the trophoblasts rapidly contract,
controlling maternal placental bed hemorrhage
(24). This process fails in PP and commonly leads
to severe post-partum hemorrhage in these cases.
It has been shown that abnormal decidua formation
at the time of placental implantation, specifically
imperfect development of the fibrinoid
(Nitabuch's) layer is more common when there is
an abnormal site of placental implantation like
previa (25). Kanfer studied the placentas of PE
using stereological method and showed that the
volume of villous surface fibrin increased in PE
group compared to the controls. They stated that
antifibrinolytic potential increased in pregnancyinduced
hypertension and preeclampsia. This
change and the association of the highest PAI-2
placental concentrations with the lowest concentrations
of thrombomodulin, may contribute to
prethrombotic state and to the excessive placental
perivillous fibrin deposition observed in these situations
(25-27). The studies of Ducray et al. using
an image analysis method on PE patients’ placentas
also indicated that there was an increase of
placental volume of villous surface fibrin (15, 27).
According to the protective effect of PP on PE,
the opposite results are justifiable