Preeclampsia is a major complication of pregnancy. Risk factors for preeclampsia include population and regional ethnicity. Chinese women living outside the Chinese mainland have a lower prevalence of preeclampsia than resident Caucasians. We performed a retrospective study to identify potential factors that may be associated with developing preeclampsia in China. A total of 67 746 pregnant women were included in this study from 2002 to 2011. Data included maternal age, maternal body mass index (BMI), age at marriage, parity, gestation and blood pressure at diagnosis, proteinuria, and birth weight. In the study period, 1301 (1.92%) nulliparous women developed preeclampsia. The prevalence of mild or severe preeclampsia was 1.42% or 0.49%, respectively. The average BMI was 21.61 kg m⁻². On the basis of the WHO BMI classification, 78.8% of women were of normal BMI, 18.3% were overweight and 2.9% were obese. A total of 37.8% of preeclamptic women had lived with the same partner for less than 1 year, which was significantly higher than those healthy pregnant women who did not develop preeclampsia (24.2%). The prevalence of preeclampsia in China is low compared with Causcasians, and the contribution to this lower prevalence may be dependent on BMI or lifestyle including period of cohabitation with the partner. Our data suggest that Chinese ethnicity may be a factor responsible for the low risk of developing preeclampsia in the populations studied.

It is hypothesized that preeclampsia is caused by factors from the placenta that induce endothelial cell activation. Trophoblasts are cells that may be shed from the placenta, then deported in the maternal blood, and finally become trapped in the pulmonary capillaries. The ultimate fate of deported trophoblasts is unknown, but to prevent clogging of the pulmonary circulation they must be cleared from the capillary beds. We examined the hypothesis that endothelial cells phagocytose deported trophoblasts and also examined the consequent effects of the trophoblasts on endothelial cells. Fluorescently labeled trophoblast–derived choriocarcinoma cells were induced to become apoptotic or necrotic and exposed to endothelial cell monolayers. Confocal microscopy demonstrated uptake of both apoptotic and necrotic trophoblasts, and this phagocytosis could be inhibited by cytochalasin B. Phagocytosis of necrotic but not apoptotic trophoblasts induced increased endothelial intercellular adhesion molecule 1 (ICAM-1) expression, as well as increased adhesion of monocytes to endothelial cell monolayers. Inhibiting the phosphatidylinositol 3-kinase and p38 mitogen-activated protein kinase pathways blocked both expression of ICAM-1 and phagocytosis, whereas inhibition of the P42/44 mitogen-activated protein kinase pathway blocked only ICAM-1 expression. This work suggests that endothelial cells can phagocytose deported trophoblasts and that the mechanism of trophoblast death (apoptotic or necrotic) could have major effects on the maternal vascular response to shed trophoblasts.

Is the positivity of estrogen receptor or progesterone receptor different between type 1 and type 2 endometrial cancer? Is the positivity of estrogen receptor or progesterone receptor different between type 1 and type 2 endometrial cancer?