Abstract
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. Plasma TNF-alpha, 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. Levels of IL-6, TNF-alpha 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-alpha and TNF-R were all higher in the group with lower platelet counts. 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-alpha into the circulation.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: BJOG: An International Journal of Obstetrics & Gynaecology
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.