Development of complications of gestation in pregnant women with preeclampsia associated with thrombophilia.
In order to determine the impact of acquired, inherited, and combined multigenic thrombophilia in the development of obstetric and perinatal complications in preeclampsia, 133 women in the second and third trimesters of pregnancy were examined. 46 pregnant women with pre-eclampsia and obstetric and/or perinatal complications were included in the main group. Placentae abruption – 8.7%, eclampsia – 2,17%, HELLP- syndrome – 2.17%, FGR – 50.0%, antenatal fetal death – 13.04%, fetal distress during pregnancy – 45.65% were considered as complications. 87 pregnant women with preeclampsia, but without above mentioned complications formed group of comparison. The method of allele-specific polymerase chain reaction was performed to determine polymorphisms in the genes of factor V Leiden 1691 G → A, prothrombin 20210 G → A, plasminogen activator inhibitor type-1 5G / 4G, fibrinogen β 455 G → A, paraoxonase-1 192 Q → R, methylenetetrahydrofolate reductase (MTHFR) 677 C → T and angiotensinogen 235 M → T. To determine the causes of acquired thrombophilia antiphospholipid antibody level and concentration of homocysteine in plasma (ELISA) were studied.There were determined factors that increase relative risk of obstetric and perinatal complications in pregnant women with pre-eclampsia: first delivery, the onset of symptoms of preeclampsia at term less than 28 weeks of pregnancy, severe or moderately severe forms of preeclampsia, the duration of pre-eclampsia more than 5 weeks. Such genotypes as 1691 GA of Factor V Leiden – increases the risk by in 2.9 times (95% CI 1,94-4,33); prothrombin 20210 GA –by 2.36 times (95% CI: 1,54-3,6); prothrombin 20210 AA –by 3.12 times (95% CI 2,4-4,0) a combination of three or more pathologic polymorphisms –by 2.58 times (95% CI 1,64-4,05); pathological level of AFA –by 1.7 times (95% CI 1,08-2,67); combined thrombophilia –by 1.76 times (95% CI 1,12-2,76); homocysteine concentration of more than 15 µmol/l –by 2.31 times (95% CI 1.5-3.5) aremarkers of predisposition to the development of obstetric and perinatal complications in pregnant women with pre-eclampsia
Baranov VS, Ivashchenko TE, Glotov AS. [Defini-tion of genetic predisposition to certain common diseases in preg¬nancy: guidelines]. SPb.: Izdatelstvo N-L, 2009;68. Russian. 2. Makatsariya AD, Bitsadze VO. [Thrombophilia and antithrombotic therapy in obstetric practice]. M.: Triada Kh. 2003;904. Russian. 3. [On approval of clinical protocols for obstetric and gy¬necological care: Order from 31.12.2004 N 676]. Mіnіsterstvo okhoroni zdorov’ya Ukraїni; 2004. Ukrainian. 4. Maksimov SA, Zinchuk SF, Davydova EA, Zin-chuk VG. [Risks and their evaluation in biomedical research: guidelines]. Kemerovo. 2010;28. Russian. 5. Turchin VN. [Probability theory and mathematical statistics. Basic concepts, examples and problems]. Dnepropetrovsk: IMA-PRESS. 2012;576. Russian. 6. Kupferminc M, Rimon E, Ascher-Landsberg J. Perinatal outcome in women with severe pregnancy complications and multiple thrombophilias. J. Perinat Med. 2004;32(3):225-7. 7. Mello G, Paretti E, Marozio L. Thrombophilia is significantly associated with severe preeclampsia. Results of a large scale, case-controlled study. Hypertension. 2005;46:1270-74. 8. Khan KS, Wojdyla D, Say L. WHO analysis of causes of maternal death: a systematic review. Lancet. 2006;367:1066-74. 9. WHO recommendations for Prevention and treat-ment of pre-eclampsia and eclampsia. Geneva. Switzerland: World Health Organization. 2011;38.
GOST Style Citations
1. Gene polymorphism of blood coagulation factors and endothelial dysfunction in early and late preeclampsia.
T. O. Loskutova, T. V. Demchenko, N. V. Kryachkova
Medicni perspektivi (Medical perspectives) Vol: 25 Issue: 2 First page: 66 Year: 2020
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