Pre-eclampsia (PE) is one of the most widespread complications of pregnancy. The frequency of the disease in Russia is about 20% of all pregnancies. Disturbances in blood circulation constitute the major pathogenic back­ground of typical PE symptoms, which include the classi­cal triad of edema, proteinuria and hypertension. Recent studies have shown that PE is a typical multifactorial dis­order with different pathogenic mechanisms underlying its final clinical manifestation

It is commonly accepted that PE results from the shal­low endovascular cytotrophoblastic invasion into the spiral placental arteries with subsequent reduced placental perfu­sion. The major source of these complications stems from preexisting maternal disorders sometimes not evident be­fore pregnancy such as hypertension, renal disease, obesity and diabetes. All of these predispose to PE through the common mechanism of endothelial dysfunction [1]. The combination of maternal and placental factors is particu­larly devastating. Oxidative stress has also been impli­cated in endothelial damage. One other major gene group of PE concerns intercellular interaction in placental devel­opment. Decidua is composed of cells, which can release bioactive compounds that interact with endothelial cells. This process is usually mediated through cytokines pro­duced by inflammatory cells and activated endothelial cells. Endothelial cell damage enhances the production of thrombin, platelet activating factor and other tissue hor­mones which affect endothelial cell permeability, expres­sion of adhesion molecules, down-regulation of endothe­lial nitric oxide synthetase activity, reduction of plasma fibrinolytic activity due to imbalance of tissue plasmin­ogen activator and its inhibitor.

Taking all these considerations into account, the fol­lowing polymorphic marker loci of genes responsible for predisposition to endothelial dysfunction were studied: tissue plasminogen activator (PLAT) and its inhibitor of type 1 (PAI-1), angiotensin-converting enzyme (ACE), endothelial nitric oxide synthetase (eNOS), cytokine tu­mor necrosis factor-a (TNF-a) and glutathione-S-trans­ferase P1 (GSTP1).