6 research outputs found
ESTRTOGENE AT EARLY PREGNANCY WITH HERPES-VIRUS EXACERBATION
Decrease of estriol and estradiol concentration, was found, at herpes-viral infection exacerbation, in placenta of pregnant at early stages of gestations. Revealed, change was shown by result of defect of base steroid. β cholesterol content, as well as distribution, of the steroid, hormone syntheses process: low activity of placental 17Ξ²-hydroxysteroid dehydrogenase and. inadequacy steroidogenesis regulating mechanism.
DISTURBANCE OF THE PROGESTERONE AND ITS METABOLITES SYNTHESIS IN THE DEVELOPMENT OF NEUROLOGICAL DISORDERS IN CHILDREN AFTER CYTOMEGALOVIRUS INFECTION DURING PREGNANCY
Cytomegalovirus (CMV) infection is one of the causes of congenital neurological disorders and the virus itself is the mostΒ common viralΒ agent causing an imbalance in the production of placentaΒ progesterone and its neuroactive metabolitesΒ β allopregnenolone and 5Ξ±-dihydroprogesterone. The aim was to evaluate the concentrationΒ of progesterone andΒ its metabolites β 5Ξ±-dihydroprogesterone andΒ allopregnenolone β in placenta during exacerbation of CMV infectionΒ inΒ the first trimester of pregnancy, and the impact of theseΒ disturbances on the development of neurological disorders inΒ children. We examined 30 pregnant women with exacerbation ofΒ CMV infection in the first trimester of pregnancy andΒ 30 pregnantΒ women with latent disease; and later their newborns. The enzymeΒ immunoassay was used to determineΒ concentration of progesteroneΒ in placenta; the histochemical method β to determine 5Ξ±-dihydroprogesterone and allopregnenolone. Newborns underwentΒ neurosonography studies. Exacerbation of CMV infection in the firstΒ trimester of pregnancy decreased progesterone in placenta by 1.3Β times, 5Ξ±-dihydroprogesterone β by 1.73 times and allopregnenolone β by 2 times. Ultrasound examination of the brainΒ showed ventriculomegaly, periventricular ischemia, and pseudocystsΒ in newborns up to one year from mothers with exacerbation of CMVΒ during pregnancy. Later, minimal brain dysfunctions were manifested by motor disorders, increased general, vegetative excitability, and aΒ tendency to digestive and sleep disorders. The data obtainedΒ indicate that the exacerbation of CMV infection in the first trimesterΒ of pregnancy is interrelated with a decrease in the concentration of progesterone and its metabolites (5Ξ±-dihydroprogesterone, allopregnenolone) in the placenta and development of neurological dysfunction in newborns
Effect of Oxidative Stress and Fatty Acids Disbalance on the Development of Apoptosis in the Placenta with Cytomegalovirus Infection in the First Trimester
Background. Reactivation of cytomegalovirus infection (CMV) during pregnancy is associated with manifestation of oxidative stress, both in the maternal peripheral blood and in the placental tissues. One of the effects of oxidative stress is a disturbance of the metabolism of fatty acids, which leads to the initiation of the apoptotic cascade, the death of trophoblast cells and, as a result, tissue or organ dysfunction, promoting to the development of a pathological condition. However, an analysis of the current literature indicates insufficient information on this problem in the villous chorion of the placenta in CMV infection.Aims. To study the relationship between the oxidative stress development and fatty acid imbalance in apoptosis of trophoblast cells during reactivation of CMV in the first trimester.Material and methods. We examined peripheral blood, urine, a homogenate of the villous chorions from 35 pregnant women with CMV reactivation within 9β11 weeks of pregnancy and from 30 pregnant women without CMV of the same gestation period. We studied levels of IgM and IgG for cytomegalovirus, low-avid IgG antibodies to cytomegalovirus (avidity index), phospholipase A2 content, fatty acid content, number of apoptotic trophoblast cells, fatty acid peroxide content and catalase activity. Sampling and analysis of material from pregnant women was conducted in 2016β2018.Results. The reactivation of CMV in the first trimester of pregnancy led to an increase content in the phospholipase A2 in villous chorion by 2.5 times, by 1.5 times of fatty acid peroxides, 1.5 times arachidonic acid, palmitic acid by 1.3 times, number of trophoblast cells in a state of apoptosis by 4.7 times and decrease catalase activity by 1.44 times.Conclusion. As a result of the study, cytomegalovirus-dependent induction of oxidative stress and imbalance of fatty acids triggering apoptosis of trophoblast cells was identified. Increased apoptosis initiates inflammation and destructive processes in the early placenta
ΠΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ Π²Π°Π·ΠΎΠ°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΡΠ΅Π³ΡΠ»ΡΡΠΈΠΈ Π² Π²ΠΎΡΡΠΈΠ½ΡΠ°ΡΠΎΠΌ Ρ ΠΎΡΠΈΠΎΠ½Π΅ Ρ ΠΆΠ΅Π½ΡΠΈΠ½ Ρ ΡΠ°ΠΌΠΎΠΏΡΠΎΠΈΠ·Π²ΠΎΠ»ΡΠ½ΡΠΌ Π°Π±ΠΎΡΡΠΎΠΌ ΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΡΠΈΡΠΎΠΌΠ΅Π³Π°Π»ΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ
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 7β9 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 = β0.702; p < 0.001) and VEGF-A (r = β0.858; 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.Π¦Π΅Π»Ρ. ΠΡΠ΅Π½ΠΈΡΡ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ ΡΠ°ΡΡΠ²ΠΎΡΠΈΠΌΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅ΠΏΡΠΎΡΠ° fms-ΠΏΠΎΠ΄ΠΎΠ±Π½ΠΎΠΉ ΡΠΈΡΠΎΠ·ΠΈΠ½ΠΊΠΈΠ½Π°Π·Ρ (sFlt1), ΠΏΠ»Π°ΡΠ΅Π½ΡΠ°ΡΠ½ΠΎΠ³ΠΎ ΡΠ°ΠΊΡΠΎΡΠ° ΡΠΎΡΡΠ° (PlGF) ΠΈ Π²Π°ΡΠΊΡΠ»ΠΎΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ°ΠΊΡΠΎΡΠ° ΡΠΎΡΡΠ° (VEGF-Π) Π² ΡΠΊΠ°Π½Π΅Π²ΡΡ
ΡΠΊΡΡΡΠ°ΠΊΡΠ°Ρ
Π² ΡΠΎΠΏΠΎΡΡΠ°Π²Π»Π΅Π½ΠΈΠΈ Ρ Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΠ΅ΠΉ ΡΠ»ΠΈΠ·ΠΈΡΡΠΎΠΉ ΠΎΠ±ΠΎΠ»ΠΎΡΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ ΠΈ Π²ΠΎΡΡΠΈΠ½ΡΠ°ΡΠΎΠ³ΠΎ Ρ
ΠΎΡΠΈΠΎΠ½Π° Ρ ΠΆΠ΅Π½ΡΠΈΠ½ Ρ ΡΠ°ΠΌΠΎΠΏΡΠΎΠΈΠ·Π²ΠΎΠ»ΡΠ½ΡΠΌ Π°Π±ΠΎΡΡΠΎΠΌ ΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΡΠΈΡΠΎΠΌΠ΅Π³Π°Π»ΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ (Π¦ΠΠ) ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π° 81 ΠΆΠ΅Π½ΡΠΈΠ½Π° Π² ΠΏΠ΅ΡΠΈΠΎΠ΄ Ρ 7-ΠΉ ΠΏΠΎ 9-Ρ Π½Π΅Π΄ Π±Π΅ΡΠ΅ΠΌΠ΅Π½Π½ΠΎΡΡΠΈ: 51 Π¦ΠΠ-ΡΠ΅ΡΠΎΠΏΠΎΠ·ΠΈΡΠΈΠ²Π½Π°Ρ Ρ ΡΠ°ΠΌΠΎΠΏΡΠΎΠΈΠ·Π²ΠΎΠ»ΡΠ½ΡΠΌ Π°Π±ΠΎΡΡΠΎΠΌ ΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ ΠΈ 30 ΡΠ΅ΡΠΎΠ½Π΅Π³Π°ΡΠΈΠ²Π½ΡΡ
Π·Π΄ΠΎΡΠΎΠ²ΡΡ
ΠΆΠ΅Π½ΡΠΈΠ½ Ρ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈΠΌ Π°Π±ΠΎΡΡΠΎΠΌ. Π ΠΏΠ»Π°Π·ΠΌΠ΅ ΠΊΡΠΎΠ²ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΈΠΌΠΌΡΠ½ΠΎΠ³Π»ΠΎΠ±ΡΠ»ΠΈΠ½Ρ (Ig) ΠΊΠ»Π°ΡΡΠ° Π ΠΈ G ΠΊ Π¦ΠΠ, Π°Π²ΠΈΠ΄Π½ΠΎΡΡΡ Π¦ΠΠ-IgG; Π² ΡΠΊΡΡΡΠ°ΠΊΡΠ°Ρ
Π²ΠΎΡΡΠΈΠ½ΡΠ°ΡΠΎΠ³ΠΎ Ρ
ΠΎΡΠΈΠΎΠ½Π° β sFlt1, PlGF, VEGF-Π ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅ΡΠΌΠ΅Π½ΡΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΠΈΠ·Π°. Π ΠΌΠΎΠ½ΠΎΠ½ΡΠΊΠ»Π΅Π°ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
ΠΊΡΠΎΠ²ΠΈ, ΠΏΡΠΎΠ±Π°Ρ
ΠΌΠΎΡΠΈ, Π²ΠΎΡΡΠΈΠ½ΡΠ°ΡΠΎΠΌ Ρ
ΠΎΡΠΈΠΎΠ½Π΅ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ°Π·Π½ΠΎΠΉ ΡΠ΅ΠΏΠ½ΠΎΠΉ ΡΠ΅Π°ΠΊΡΠΈΠΈ Π² ΡΠ΅ΠΆΠΈΠΌΠ΅ ΡΠ΅Π°Π»ΡΠ½ΠΎΠ³ΠΎ Π²ΡΠ΅ΠΌΠ΅Π½ΠΈ Π²ΡΡΠ²Π»ΡΠ»ΠΈ ΠΠΠ Π¦ΠΠ. ΠΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠ»ΠΈΠ·ΠΈΡΡΠΎΠΉ ΠΎΠ±ΠΎΠ»ΠΎΡΠΊΠΈ ΠΌΠ°ΡΠΊΠΈ ΠΈ Π²ΠΎΡΡΠΈΠ½ΡΠ°ΡΠΎΠ³ΠΎ Ρ
ΠΎΡΠΈΠΎΠ½Π°.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π ΡΠΊΡΡΡΠ°ΠΊΡΠ°Ρ
Π²ΠΎΡΡΠΈΠ½ΡΠ°ΡΠΎΠ³ΠΎ Ρ
ΠΎΡΠΈΠΎΠ½Π° Ρ ΠΆΠ΅Π½ΡΠΈΠ½ Ρ ΡΠ°ΠΌΠΎΠΏΡΠΎΠΈΠ·Π²ΠΎΠ»ΡΠ½ΡΠΌ Π°Π±ΠΎΡΡΠΎΠΌ ΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ Π¦ΠΠ-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ sFlt-1 Π±ΡΠ»Π° Π²ΡΡΠ΅ Π² 3,25 ΡΠ°Π·Π° (Ρ < 0,001), PlGF ΠΈ VEGF-Π β Π½ΠΈΠΆΠ΅ Π² 1,31 (Ρ < 0,001) ΠΈ 2,16 ΡΠ°Π·Π° (Ρ < 0,001), ΡΠ΅ΠΌ Ρ Π·Π΄ΠΎΡΠΎΠ²ΡΡ
ΠΆΠ΅Π½ΡΠΈΠ½. Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Π° ΡΠΈΠ»ΡΠ½Π°Ρ ΠΎΠ±ΡΠ°ΡΠ½Π°Ρ ΠΊΠΎΡΡΠ΅Π»ΡΡΠΈΠΎΠ½Π½Π°Ρ ΡΠ²ΡΠ·Ρ ΠΌΠ΅ΠΆΠ΄Ρ ΡΡΠΎΠ²Π½ΡΠΌΠΈ sFlt-1 ΠΈ PlGF (r = β0,702; Ρ < 0,001) ΠΈ VEGF-Π (r = β0,858; Ρ < 0,0005), ΠΏΡΡΠΌΠ°Ρ ΡΠ²ΡΠ·Ρ β PlGF ΠΈ VEGF-Π (r = 0,860; Ρ < 0,001). ΠΠΎ Π΄Π°Π½Π½ΡΠΌ Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ, ΠΎΡΠΌΠ΅ΡΠ΅Π½ΠΎ ΠΎΡΡΡΠ°Π²Π°Π½ΠΈΠ΅ Π² Π΄Π΅ΡΠΈΠ΄ΡΠ°Π»ΠΈΠ·Π°ΡΠΈΠΈ ΠΈ ΡΡΠ°Π½ΡΡΠΎΡΠΌΠ°ΡΠΈΠΈ ΠΌΠ°ΡΠΎΡΠ½ΡΡ
ΡΠΎΡΡΠ΄ΠΎΠ², ΠΈΠ½Π²Π°Π·ΠΈΠΈ ΡΡΠΎΡΠΎΠ±Π»Π°ΡΡΠ°, ΡΠΎΡΡΠ° ΠΈ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΠΈ Π²ΠΎΡΡΠΈΠ½, ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠ΅ΡΠ°Π»ΡΠ½ΡΡ
ΡΠΎΡΡΠ΄ΠΎΠ².ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. Π ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠ°ΠΌ ΡΠ°ΠΌΠΎΠΏΡΠΎΠΈΠ·Π²ΠΎΠ»ΡΠ½ΠΎΠ³ΠΎ Π°Π±ΠΎΡΡΠ° Ρ ΠΆΠ΅Π½ΡΠΈΠ½ Ρ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ Π¦ΠΠ-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ ΠΌΠΎΠΆΠ½ΠΎ ΠΎΡΠ½Π΅ΡΡΠΈ Π΄ΠΈΡΠ±Π°Π»Π°Π½Ρ Π°Π½ΡΠΈ- ΠΈ ΠΏΡΠΎΠ°Π½Π³ΠΈΠΎΠ³Π΅Π½Π½ΠΎΠΉ ΡΠ΅Π³ΡΠ»ΡΡΠΈΠΈ, Π²ΡΠ·ΡΠ²Π°ΡΡΠΈΠΉ ΠΎΠ³ΡΠ°Π½ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΏΠ»Π°ΡΠ΅Π½ΡΡ ΠΈ ΠΌΠ°ΡΠΎΡΠ½ΠΎ-ΠΏΠ»Π°ΡΠ΅Π½ΡΠ°ΡΠ½ΠΎΠ³ΠΎ ΠΊΡΠΎΠ²ΠΎΠΎΠ±ΡΠ°ΡΠ΅Π½ΠΈΡ.