Бюллетень сибирской медицины (Jul 2022)
Features of vasoactive substance regulation in chorionic villi in women with spontaneous abortion and active cytomegalovirus infection
Abstract
The aim of the study was to assess the levels of soluble fms-like tyrosine kinase 1 (sFlt1), placental growth factor (PlGF), and vascular endothelial growth factor A (VEGF-A) in tissue extracts in comparison with the histologic examination of the endometrium and chorionic villi in women with spontaneous abortion and active cytomegalovirus (CMV) infection.Materials and methods. 81 women at 7–9 weeks of pregnancy were examined: of them, 51 women were CMVseropositive with active infection and after spontaneous abortion, and 30 patients were CMV-seronegative, healthy women after therapeutic abortion. Immunoglobulins (Ig) M and G to CMV and CMV IgG avidity were measured in the blood plasma; sFlt1, PlGF, and VEGF-A were determined in extracts of chorionic villi by enzyme immunoassay. CMV DNA was detected in mononuclear cells of peripheral blood, urine, and chorionic villi by real-time polymerase chain reaction (PCR). A histologic examination of the endometrium and chorionic villi was carried out.Results. In chorionic villus extracts of women with spontaneous abortion and active CMV infection, the concentration of sFlt1 was 3.25 times higher (p < 0.001), and the levels of PlGF and VEGF-A were 1.31 (p < 0.001) and 2.16 times lower (p < 0.001) than in healthy women. A strong negative correlation was established between the levels of sFlt1 and PlGF (r = –0.702; p < 0.001) and VEGF-A (r = –0.858; p < 0.0005), and a positive correlation was revealed between PlGF and VEGF-A levels (r = 0.860; p < 0.001). According to the data of the histologic examination, a lag in decidual transformation of uterine vessels, trophoblast invasion, growth and differentiation of villi, and formation of fetal circulation was detected.Conclusion. The mechanisms of spontaneous abortion in women with active CMV infection include an imbalance of pro- and anti-angiogenic factors, which causes impaired placental development and uteroplacental circulation.
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