Objective To investigate trophoblast invasion and vascular changes in placental bed spiral arteries in normal and severe pre‐eclamptic pregnancies.Design A histological and immunohistochemical study of placental bed biopsies containing spiral arteries.Setting The University Hospital, Leuven, Belgium.Subjects Twenty‐one placental bed biopsies from 21 normal pregnancies and 24 placental bed biopsies from 24 severe pre‐eclamptic pregnancies, taken at caesarean section.Observations Histological and immunohistochemical appearance of spiral arteries (stained with haematoxylin and eosin), periodic acid schiff, and a monoclonal antibody to low molecular weight cytokeratin.Results One hundred and twenty‐seven spiral arteries were studied. In the 21 biopsies from clinically normal pregnancies at term, 100% of the decidual spiral arteries and 76% of the myometrial arteries showed trophoblast invasion. In the 24 biopsies from women with severe pre‐eclampsia, trophoblast invasion was seen in 44 % and 18 % of the decidual and myometrial segments, respectively. Endovascular trophoblast invasion was complete, partial or isolated. A variety of morphological features was present not only in different spiral arteries from the same biopsy but also in different segments of the same artery. The vascular change most commonly associated with normal pregnancies was physiological change and subintimal thickening of both segments of the spiral arteries. In pre‐eclampsia medial disorganisation and hyperplasia in the myometrial arteries and acute atherosis in decidual arteries were common.Conclusion Endovascular trophoblast did not show an all or none invasive phenomenon in normal and pre‐eclamptic pregnancies. More decidual than myometrial arteries were invaded in both groups of patients, and there was a gradient in the percentage of decidual and myometrial arteries invaded from normal pregnancy to pre‐eclampsia. Morphological features in one spiral artery may not necessarily be representative of all of those in a placental bed.

Impedance to blood flow through spiral arteries in the second trimester is lower in the central area of the placental bed, and is in agreement with previous histologic data. Physiologic change of the spiral arteries is functionally complete around 17 weeks' gestation.

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SUMMARYPre-eclampsia may develop as a result of an endothelial activation. Tumour necrosis factor-alpha (TNF-n) activates endothelial cells which release soluble E-selectin, a putative circulating marker specific for endothelial damage. A retrospective longitudinal study of maternal blood samples, collected at different gestational ages in pregnancy, was undertaken to determine whether the development of pre-eclampsia is associated with TNF-a-mediated endolhelial activation. This study included 19 women who developed pre-eclampsia and 22 women whose pregnancy outcome was normal. Ten women had blood samples taken before pre-eelampsia was clinically detected and, in all these, TNF-Q was below the immunoassay limit of detection (< 80 pg/ml). Five had further samples taken after pre-eclampsia was clinically diagnosed and, initially, TNF-Q was still below the lower limit of detection in all five pregnancies, but rose later in three (80. 156 and 250 pg/ ml). In nine other patients with diagnosed pre-eclampsia. TNF-a was detected in only two (80 and 650 pg/mi). TNF-Q was identified in only one of the 22 normal pregnancies (80 pg/ml), this being at term. There was no statistical difference in soluble E-selectin levels between normal and preeclamptic pregnancies, neither before nor after pre-eclampsia was diagnosed. Hence, blood TNF-a levels measured by immunoassay can be elevated in approximately 36% of cases of established preeclampsia, but this rise occurs only after the syndrome is detected clinically. Blood concentrations of TNF-a and soluble E-selectin are not related to severity of the disorder. These findings suggest that circulating TNF-a does not contribute to the initiation of endothelial cell activation that may be associated with the development of pre-eclampsia, but may rise as a consequence of the pathological processes of this disorder.

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Maternal serum free beta hCG alone measured in the second trimester is not clinically useful as a screening test for pre-eclampsia in primigravid women. It has, however, some predictive value.

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