Endothelial dysfunction in preeclampsia. Part II: Reducing the adverse consequences of endothelial cell dysfunction in preeclampsia; therapeutic perspectives.

Next to low-dose Aspirin there appear to be several new and promising pharmacologie approaches for reducing the adverse consequences of endothelial cell dysfunction in preeclampsia. Among these are selective thromboxane-A2 synthetase and/or thromboxane-A2 receptor antagonists, stable prostacyclin analogues, selective S(erotonin)2-receptor blockers, nitrovasodilators, glycoprotein IIb/IIIa antagonists, hirudin, and ticlopidine. Early-onset preeclampsia appears to be associated with certain disorders that are likely to provoke an arterial thrombotic process by impairing the normal endothelial cell-platelet interactions. Especially heterozygous hyperhomocysteinemia, protein S deficiency and anticardiolipin antibodies appear to be fairly common. The management of these 3 separate disease entities will be discussed.