STUDY OF C-786T POLYMORPHISM IN THE NOS3 GENE IN THE DEVELOPMENT OF PREECLAMPSIA

Abstract

Objective: Given the importance of endogenous NO in maintaining normal endothelial function, it is possible that polymorphisms in the gene encoding the enzyme that synthesizes NO may contribute to the development of preeclampsia. The purpose of the work was to determine the role of the C-786T polymorphism in the NOS3 gene in the development of preeclampsia. Design and method: We conducted a study of 90 pregnant women in the II-III trimester, which were divided into two groups: The main group of 53 pregnant women with severe preeclampsia. Control group - 47 pregnant women with a physiological course of the gestational period. The age of the examined women ranged from 19 to 41 years. Samples of pregnant women served as the material for the study. We have identified gene polymorphism - C-786T in the NOS3 gene. Isolation of DNA from blood and PCR analysis were carried out using kits of reagents and test systems from Ampli Prime Ribo-prep. Statistical processing of the results was carried out using statistical programs EpiCalc 2000. Results: There was a trend towards the prevalence of the heterozygous C/T genotype in the group of patients with severe preeclampsia, where it was detected with a frequency of 39.5% (x2-2.23; p-0.15; RR-1.46; 95% CI: 0.54-3.91; OR -1.76.; 95% CI: 0.84-3.69), relative to 27.1% in the control group. The T/T genotype was slightly more common – in 11.6% of cases it was detected among patients with severe preeclampsia (x2-1.08; p-0.30; RR-1.78; 95%CI:0.43-7.32; OR-1.88; 95%CI:0.57- 6.19), while in the control group - with a frequency of 6.5%. The C/C genotype was found in 59.8% of patients with severe preeclampsia (x2-1.04; p-0.31; RR-0.81; 95% CI: 0.37-1.74; OR-0.62) The T allele among patients with severe preeclampsia was detected in 31.4% of cases, which was statistically significantly higher (x2-4.38; p-0.04; RR-1.17; 95%CI:0.79-1.73; OR-1.82; 95%CI:1.04- 3.19) than in the control group. Conclusions: Thus, the results of our study allow us to conclude that the adverse genotypic variants of the C-786T polymorphism of the NOS3 gene (associated with vascular endothelial dysfunction) contribute significantly to the mechanism of preeclampsia.