Endothelial dysfunction in preeclampsia .2. Reducing the adverse consequences of endothelial cell dysfunction in preeclampsia; Therapeutic perspectives

Next to low-dose Aspirin there appear to be several neu and promising pharmacologie approaches for reducing the adverse consequences of endothelial cell dysfunction in preeclampsia. Among these are selective thromboxane-A(2) synthetase and/or thromboxane-A(2) 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 hyperhomocyxteinemia. protein S deficiency and anticardiolipin antibodies appear to be fairly common. The management of these 3 separate disease entities will be discussed.