The pathogenesis of pre-eclampsia

Syncytiotrophoblast normally sheds redundant placental debris into the maternal circulation, a process, which depends on apoptosis. It is renewed from the underlying mononuclear cytotrophoblast. We propose that the continual clearance of this debris from the maternal circulation causes a systemic inflammatory response that is present in all pregnant women in the third trimester. Pre-eclampsia occurs when the systemic inflammatory response decompensates. This may occur if the burden of the debris is abnormally high, or if the woman's response to the process is excessive. There is evidence that oxidative stress in the placenta could lead to an overload of debris by stimulating apoptosis or necrosis or both. Such stress would be most likely with spiral artery disease either from deficient placentation or acute atherosis, In this model, deficient placentation is not the cause of pre-eclampsia but a powerfully predisposing condition.