Background: The present paper gives an overview of recent research on mechanisms underlying pre-eclampsia. Special attention is paid to immune reactions at the feto-maternal site and genetics linked to maternal susceptibility.
Results: The pathogenesis of pre-eclampsia may be seen as a two-stage process. Deficient trophoblast invasion and artery remodelling may underlie subsequent placental hypoperfusion. Impaired trophoblast invasion may either be caused by abnormal biology of the trophoblast, or increased cytotoxicity of maternal immunocompetent cells, or a combination of both. The placental hypoxia/ischaemia (step 1 of the pathogenesis) is associated with release of products into the maternal circulation, and maternal responses evoked may imply endothelial activation (step 2). The linkage between the placental disease and the maternal syndrome is still a matter of discussion, but more oxidative stress and/or elevated maternal inflammatory response has been hypothesised. Maternal susceptibility for endothelial activation, hence development of pre-eclampsia, seems to be determined by genetic factors. According to recent family linkage studies of the whole human genome, a region on chromosome 2 seems to be involved.
Conclusion: Pre-eclampsia develops in the interaction between the placental disease and maternal responses. Immune responses appear to underlie the placental disease, whereas genetic arrangements determine maternal susceptibility.