We examined 122 pregnant women with PE and 73 pregnant women without obvious somatic pathology (con­trol group), who were under supervision at the Ott’s Re­search Institute of Obstetrics and Gynecology, St. Peters­burg, Russia. The group of patients was non uniform in severity of PE and in the presence of accompanying back­ground diseases. Forty-six patients did not manifest any accompanying pathology (pure PE), with 31 having mild PE (nephropathia I-II) and 15 having severe PE (nephro­pathia III and real PE). Combined PE was diagnosed in 76 patients. Previous arterial hypertension (AH) was recorded in 49 patients (27 with AH I-II and 22 with AH III), kid­ney disease in 16 and diabetes mellitus in 19.

Genetic Analysis. The relevant polymorphic sites and oligoprimers used for analysis of PLAT, PAI-1, eNOS, ACE, TNF-a and GSTP1 are summarized in Fig. 1. DNA extracted from fresh blood was subjected to polymerase chain reaction (PCR) amplification in a Perkin-Elmer Cetus thermocycler (Norwalk, CT, USA). The products of the PCR amplification were cut with endonucleases such as Bsc4I (PAI-1), Msp1 (TNF-a), BsoMA 1 and BstFN1 (GSTP1) according to the conditions and buffers recom­mended by the manufacturer (Bion, Moscow, Russia). Restriction products were subjected to electrophoresis on a 7.0 % polyacrylamide gel, stained with ethidium bro­mide, visualized under an UV light and scored with the video system of Wilber Laurmant (France).

Statistical Analysis. A standard chi-square test (c²) was used for comparison of genotype frequencies. Relative risk (OR) of disease development for a certain genotype was determined from the standard formula: OR = a/b*d/c, where a and b are the number of patients with illness, having and not having a mutant genotype respectively, c and d are the number of persons in the control group, hav­ing and not having a mutant genotype respectively. We considered values of OR >1 as a risk factor for develop­ment of the given pathology, and OR <1 as a protecting factor.