Published online Dec 10, 2012. doi: 10.5317/wjog.v1.i4.40
Revised: August 29, 2012
Accepted: September 12, 2012
Published online: December 10, 2012
Hypertensive disorders in pregnancy continue to be an intriguing and potentially lethal complication in humans and some other primates. In a simplistic way the current hypothesis is that the genesis of preeclampsia starts at 12 to 14 wk gestation with failure of trophoblast invasion in the spiral arteries, resulting in some degree of hypoxemia in the placenta. The hypoperfused placental tissue starts to secrete variable amounts of angiogenic and antiangiogenic factors which eventually cause endothelial damage all over the pregnant women’s body with one of the many signs of preeclampsia as the clinical endpoint. For some incomprehensible reason a major interest has existed for decades concerning the early prediction of preeclampsia, most commonly tested using uterine artery Doppler (the earlier the better) and various serum markers, alone or in combination. Any new model for detection has been welcomed enthusiastically, although nothing has changed in the outcome of women presenting with preeclampsia.