[Clotting disorders and preeclampsia]

Clotting disorders are associated with the severe, early and complicated forms of PE. Compensated hypercoagulability states associated with a thrombocytopenia (PLT<150k/mm(3)) affect 25 to 50% of severe PE patients. Laboratory markers of platelet and endothelial activation are the early increase of fibronectin levels, the worsening of the thrombocytopenia and the raised platelet turnover. The excessive thrombin formation is physiologically compensated by a rise in thrombin-antithrombin (TAT) complex levels, which is the most specific marker of a PE pregnancy, and a decrease in anti-thrombin (AT) activity. The placenta induced depression of the fibrinolysis appears to contribute towards the hypercoagulable state. The etiological importance of the erythrocyte and leucocyte activation with regards to the abnormal clotting activation is highlighted in the setting of maternal systematic inflammatory disease. The state of compensated coagulopathy found in the PE patient can suffer a pro-coagulatory imbalance because of a quantitative, or a qualitative failure (i.e. thrombophilia) of the physiological coagulation inhibitors, or a combination of both. This disseminated intravascular coagulation, qualified as chronic, is associated with clinically evident signs of foeto-placental unit impairment (i.e. IUGR, foetal death) with or without systemic repercussions in the mother (i.e. renal failure, HELLP syndrome, eclampsia). This set of haemostatic disturbances found in the PE patient is a dynamic phenomenon, which can evolve by the hour therefore requires frequent laboratory investigations. Delivery remains the only curative treatment for these haemostatic disturbances. A better understanding of the aetiology of DIC in PE, an early detection method and a specific identification of the at-risk patients could allow prophylactic and curative treatment.