GENETIC PREDISPOSITION TO PRE-ECLAMPSIA: POLYMORPHISM OF GENES INVOLVED IN REGULATION OF ENDOTHELIAL FUNCTIONS
Mozgovaia EV, Malysheva OV, Ivashchenko TE, Baranov VS*
*Corresponding Author: Professor Dr. Vladislav S. Baranov, Laboratory of Prenatal Diagnosis of Inherited Disorders, D.O. Ott Research Institute of Obstetrics and Gynecology, Russian Academy of Medical Sciences, Mendeleevskaya line 3, St. Petersburg 199034, Russia; Tel/Fax: +07-812-328-0487; E-mail: baranov@vb2475. spb.edu
page: 19

MATERIALS AND METHODS

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.




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