Abstract

Disturbance of the maternal haemostatic system is a characteristic feature of pre-eclampsia [1]. Microthrombi formation and excess fibrin deposition may affect many maternal organs in pre-eclampsia and contribute to the multisystem dysfunction which characterizes the clinical syndrome. Compared with haemostasis in the healthy adult, fetal haemostasis is characterized by lower circulating levels of coagulation factors and a fetal fibrinolytic system which may be less able to generate plasmin [2]. The effect of pre-eclampsia on haemostasis in the fetal circulation remains unclear. Increased, decreased and unchanged levels of coagulation and fibrinolytic factors have been reported [3,4,5,6]. These studies have focused on activators and inhibitors of the coagulation and fibrinolytic systems. Recent improvements in laboratory methodology allow the study of the end-products of both coagulation (thrombin-antithrombin complex) and fibrinolysis (fibrin-degradation product [D-dimer]). These assays allow the quantification of in vivo thrombin and fibrin production [7,8]. Using this methodology, we have previously observed changes in the levels of thrombin-antithrombin complex and fibrin-degradation products in the uteroplacental circulation of pregnancies complicated by pre-eclampsia [9], suggesting an activation of both the coagulation and fibrinolytic systems.

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