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.
Dekker
G A
GA
Department of Obstetrics and Gynecology, Free University Hospital, Amsterdam, The Netherlands.
van Geijn
H P
HP
D017153:Antibodies, Anticardiolipin / Q000097:blood; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006710:Homocysteine / Q000097:blood; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011225:Pre-Eclampsia / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D011247:Pregnancy; D018455:Protein S Deficiency / Q000150:complications
D017153:Antibodies, Anticardiolipin; D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors; D006710:Homocysteine; D001241:Aspirin