Pathogenetic significance of vascular endothelial growth factor and prostaglandin F2α in the development of pregnancy loss in cytomegalovirus infection

Introduction. In the past decade, vascular growth factors and prostaglandins have been actively studied in the context of angiogenesis regulation and their role in pregnancy pathologies. A review of the current literature reveals a lack of data proving the involvement of vascular endothelial growth factor (VEGF) A and prostaglandin (PG) F2α in the pathogenesis of early pregnancy loss associated with exacerbation of cytomegalovirus (CMV) infection. Aim. To investigate the levels of VEGF-A and PG F2α in peripheral blood and determine their prognostic significance in pregnancy loss during exacerbation of chronic CMV infection at 6–7 weeks of gestation. Materials and methods. A case-control study was conducted, involving 65 pregnant women. The main group included 35 patients experiencing exacerbation of chronic CMV infection at 6–7 weeks of pregnancy. The control group consisted of 30 practically healthy women at 6–7 weeks of pregnancy. CMV infection was diagnosed by the presence of IgM and IgG antibodies using enzyme-linked immunosorbent assay (ELISA) and the detection of CMV DNA by polymerase chain reaction (PCR). Serum VEGF-A and PG F2α levels were measured using ELISA. Results. During exacerbation of CMV infection at 6–7 weeks of pregnancy, a decrease in VEGF-A concentration to 10.35 ± 0.05 ng/mL was observed, along with an increase in PG F2α levels to 1092 ± 13.33 pg/mL, compared to the control group values (16.56 ± 0.04 ng/mL and 720 ± 9.21 pg/mL, respectively). To analyze the selected evaluation criteria, a discriminant function with a probability of differences of at least 95% was determined. A discriminant equation was derived for this study, which has the form: PI = -231.377 + 13.694 × VEGF-A + 0.052 × PG F2α, where PI is the discriminant function with a threshold value of -32.92. When PI is equal to or greater than the threshold value, it is possible to predict the risk of pregnancy loss at 6–7 weeks of gestation during an exacerbation of cytomegalovirus infection. A PI less than the threshold value indicates the absence of such a risk during this period of pregnancy. Conclusion. The obtained results confirm the pathogenetic significance of VEGF-A and PG F2α dysregulation in the development of pregnancy loss during CMV infection exacerbation at 6–7 weeks. These findings may serve as the basis for expanding diagnostic and therapeutic approaches in this pathology.