Pre-eclampsia and the placenta

Pre-eclampsia is a syndrome that is common, dangerous for both mother and baby, unpredictable in its onset and progression, and untreatable except by terminating the pregnancy. Because its pathogenesis is undefined there is no specific diagnostic test; it is recognized by the concurrence of pregnancy-induced changes that regress after delivery, of which hypertension and proteinuria are both the easiest to recognize and the signs by which it is defined. However the pre-eclamptic syndrome is more polymorphic than the conventional definition implies, with involvement of the liver, and coagulation as well as nervous systems (Redmzn, 1990). The belief that it is primarily or necessarily a hypertensive disorder needs to be questioned because the evidence is compelling that the placenta is the primary cause of the problem. It is axiomatic that pre-eclampsia is a disorder of pregnancy; but it can also complicate some cases of hydatidiform mole (Page, 1939; Scott, 1958; Chun, 1964) where the uterus contains only disordered placental tissue. Thus, a fetus is not necessary, only the placenta. Theories that implicated the placenta as the cause of pre-eclampsia began to be developed around the beginning of the century, at first in relation to the newly discovered process of trophoblast deportation into the maternal circulation by Schmorl(1893), who first reported trophoblast in the lungs of women dying of eclampsia. The finding was later confirmed by others (Bardawil and Toy, 1959; Attwood and Park, 1961). The latter investigators also noted two instances of deportation of whole villi. It was reasonable to propose that the processes of delivery stimulated release of trophoblast into maternal blood; but then deportation was detected antenatally, as early as the first trimester. Some of the earlier theories for the causation of pre-eclampsia assumed that deportation was the cause of eclamptic fits. The later evidence that it is a feature of normal human pregnancy (Douglas et al, 1959; Thomas et al, 1959) -as well as occurring normally in other species (Billington and Weir, 1967) has nullified this supposition. Nevertheless the fact remains that deportation is increased in pre-eclampsia and eclampsia (Attwood and Park, 1961; Jaameri et al, 1965)-an observation that we have confirmed recently using modern methods of labelling to identify the trophoblast in uterine vein blood samples (Chua et al,