Does endothelial cell activation occur with intrauterine growth restriction?

Abstract

It is possible that in fetal growth restriction without pre-eclampsia endothelial cell activation does not occur. This might be either because there is no release of 'factor X' or because of maternal resistance to its effects. To test this hypothesis, we took blood samples from 26 women with pre-eclampsia (without fetal growth restriction), 13 women with fetal growth restriction (without pre-eclampsia) and 24 normal pregnant controls, and measured the circulating levels of three markers of endothelial cell activation (soluble VCAM, ICAM and E-selectin) and three cytokines [tumour necrosis factor-a (TNF-a), interleukin-6 (IL-6) and -8 (IL-8)]. The levels of the markers of endothelial cell activation were raised in both pre-eclampsia and fetal growth restriction pregnancies compared with controls; however, the levels of TNF-a, IL-6 and IL-8 were significantly raised in pregnancies complicated by pre-eclampsia, but not in fetal growth restriction, compared with controls. These data show that endothelial cell activation is common to both pre-eclampsia and fetal growth restriction, but that the circulating levels of cytokines are elevated only in pre-eclampsia. Thus, it seems likely that endothelial cell activation is a consequence of a failure of trophoblast invasion and that a further step is required, possibly involving cytokine release, for the expression of the full clinical picture of pre-eclampsia.

Free fetal DNA is not increased before 20 weeks in intrauterine growth restriction or pre‐eclampsia

“…The authors postulate that the placental pathology that results in increased fetal DNA trafficking is quite distinct from a second insult at the time of clinical disease that results in widespread endothelial dysfunction (Zhong et al, 2001). Free plasma DNA is a marker of cell death (Fournie et al, 1993) and endothelial cell activation, which may cause endothelial apoptosis, has been documented in IUGR pregnancies (Johnson et al, 2002). Our findings suggest that in our patient population there may be an underlying maternal endothelial dysfunction that may predispose to the development of IUGR and it is interesting to note that women who give birth to small babies have an increased risk of ischaemic heart disease (Smith et al, 2001).…”

Human placental taurine transporter in uncomplicated and IUGR pregnancies: cellular localization, protein expression, and regulation

“…There are contradictory results concerning maternal and fetal cytokine levels in IUGR. Some studies show elevated levels of cytokines, others show reduced levels, and still others show no change in cytokine production in association with IUGR (2,27,51).…”

Changes in the maternal cytokine profile in pregnancies complicated by fetal growth restriction

“…Two studies, Hahn-Zoric et al 11 and Johnson et al 12 considered populations that included FGR, SGA, PET and normal pregnancies.…”