Objectives Generalised maternal endothelial cell dysfunction appears to be an underlying problem in pre‐eclampsia presumed to be caused, directly or indirectly, by one or more circulating factors derived from the placenta. Recently it has been suggested that tumour necrosis factor (TNF) may play an important role in pre‐eclampsia and contribute to endothelial activation. This study was designed to investigate this proposal. Design Plasma TNF‐α, IL‐6 and both forms of soluble TNF receptors (p55 and p75 TNF‐R) have been measured by ELISA in 31 pre‐eclamptic patients and 31 pregnant controls matched for age, parity and gestational age. Results Levels of IL‐6, TNF‐α and soluble TNF‐R (p55 and p75) were significantly higher in pre‐eclamptic patients, compared with age and gestation matched controls with a wide variation in levels between pre‐eclamptic individuals. There was a correlation between levels of IL‐6 and TNF or TNF‐R and between TNF and TNF‐R levels. However, when the pre‐eclamptic patients were subdivided on the basis of the severity of their disease, the median values of plasma concentrations of IL‐6, TNF‐α and TNF‐R were all higher in the group with lower platelet counts. Conclusions These new findings are consistent with the concept that the maternal syndrome of pre‐eclampsia is associated with endothelial dysfunction and provide evidence that at least part of this dysfunction could arise from excessive release of TNF‐α into the circulation.

No abstract

Objective Design Setting SubjectsTo study associations between established risk factors for pre-eclampsia and different clinical manifestations of the disease.A population-based, nested case-control study.Information from 12,804 consecutive deliveries that took place over three years at a birth clinic, which alone serves a population of nearly 240,000 in Rogaland county, Norway.Cases of pre-eclampsia (n = 323) and healthy controls (n = 650) were selected. Pre-eclampsia was defined as increase in diastolic blood pressure (2 25 mmHg to 2 90 mmHg) and proteinuria (2 1+ by dipstick testing) after 20 weeks of pregnancy.Main study measures Parity, previous pre-eclampsia, blood pressure, maternal weight, and maternal smoking were included as study variables. Women with pre-eclampsia were grouped according to clinical manifestations of the disease (i.e. severity [mild, moderate or severe]) and time of onset (early or late gestation). Associations with the study factors were estimated as relative risks (odds ratio, OR).Both nulliparity and hypertension increased pre-eclampsia risk, with no clear preference for any clinical subtype. High maternal weight was related to a higher risk of mild and moderate, but not severe, pre-eclampsia. Previous pre-eclampsia strongly increased the risk for pre-eclampsia in the current pregnancy, and the risk of early onset disease was especially high (OR 42.4; 95% CI 11.9-151.6). Overall, smoking was associated with a reduced risk for pre-eclampsia (OR 0.6; 95% CI 0.4-0.9). However, no effect of smoking was observed in the early onset disease group and among women with repeated pre-eclampsia. ConclusionNulliparity and hypertension increased the risk for each subgroup of pre-eclampsia, but high maternal weight, previous pre-eclampsia and smoking were not consistently associated with each clinical subtype. This observation may suggest that heterogeneous clinical manifestations of pre-eclampsia may be preceded by different pathological mechanisms.

No abstract

No abstract