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The aim of the study was to examine the levels of human β-chorionic gonadotropin (β-hCG) and inhibin A, as prognostic criteria for the development of early pre-eclampsia at 16–18 weeks of pregnancy. Materials and Methods. The prospective study included 60 patients with singlet pregnancies who underwent their first prenatal screening at 11–13 weeks. The patients were selected from 300 patients using continuous sampling method. According to the gestation course and outcome, the patients were divided into 2 groups: group 1 included 45 women with uncomplicated birth, group 2 consisted of 15 women with pre-eclampsia which developed before the 34th week. Based on calculations of the individual pre-eclampsia risks up to the 34th week of pregnancy according to the results of Astraia program (>1:300), women at 16–18 weeks of pregnancy underwent additional examination to determine inhibin A and β-hCG. Results. In both groups, burdened obstetric and somatic anamnesis prevailed. Uterus fibroids and cervical ectopia were significantly more common in women with pre-eclampsia, developed up to the 34th week of pregnancy. Moreover, the threatened miscarriage prevailed in the second trimester. In the group with pre-eclampsia developed up to the 34th week, β-hCG and inhibin A values were, respectively, >35 ng/ml and >260 pg/ml. The indicators were significantly higher than in the uncomplicated birth group. Conclusions. The individual risk of preeclampsia calculated according to the Astraia program up to the 34th week of pregnancy (>1:300) and elevated levels of inhibin A and β-hCG can be considered the predictors of the early pre-eclampsia development. Keywords: early pre-eclampsia, inhibin A, human β-chorionic gonadotropin.

Hypothesis/aims of study. The search for early predictors of preeclampsia currently remains relevant. There is still a need to study maternal factors affecting the development of preeclampsia such as intergenic interactions in a pregnant woman with single nucleotide polymorphisms (SNPs) in genes associated with hemostasis system and folate cycle, as well as predictors. The aim of this study was to assess the role of comorbid pathology and gene polymorphism associated with the hemostasis system and folate cycle in predicting preeclampsia in a pregnant woman. Study design, materials and methods. We examined 158 pregnant women in two study groups, including 92 women with preeclampsia and 66 healthy subjects. Somatic anamnesis of the patients was studied, with the course and outcomes of pregnancy analyzed. The carriage of SNPs in genes involved in hemostasis and the folate cycle was studied once by the method of polymerase chain reaction in real time with amplification of polymorphic loci and restriction analysis using specific endonucleases. The analysis of intergenic interactions was performed using the MDR 3.0.2 program. Results. Seven genes involved in hemostasis and three genes involved in the folate cycle were studied. The highest entropy of the case-control status for preeclampsia is associated with the locus of coagulation factor F7 10976GA 9.49% and that of methylenetetrahydrofolate reductase MTHFR 677CT (A223V) 5.35%. The combination of loci of the tissue plasminogen activator inhibitor-1 gene SERPINE1 (PAI-1) and the platelet glycoprotein integrin 1-2 gene ITGA2 (SERPINE1 (PAI-1) (5G4G) + ITGA2 (807C T)) account for 18.28%, and SERPINE1 (PAI1) (5G4G) + MTHFR (677CT) 14.26% of results. A three-locus synergy model SERPINE1 (PAI-1) (5G4G) + MTHFR (677CT) + ITGA2 (807CT) responsible for the development of preeclampsia was obtained, which has a reproducibility of 10/10 and an accuracy of predictions of 84.3%. Conclusion. Our data indicate a high contribution of the ITGA2, SERPINE1 (PAI-1), and MTHFR mutations combination to the prediction of preeclampsia.