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Эпигенетические факторы и молекулярные маркеры риска ранних потерь беременности
Эпигенетические факторы и молекулярные маркеры риска ранних потерь беременности
Фролова Н.И., Белокриницкая Т.Е. Эпигенетические факторы и молекулярные маркеры риска ранних потерь беременности. Гинекология. 2019; 21 (3): 9–16.
DOI: 10.26442/20795696.2019.3.190523
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Аннотация
Обоснование. Cамопроизвольный выкидыш является распространенным осложнением беременности. По современным данным, 10–20% клинически диагностированных беременностей заканчиваются прерыванием в ранние сроки. Обзорная статья посвящена современным представлениям об этиологии и патогенезе ранних потерь беременности.
Цель. Оценить роль эпигенетических факторов и молекулярно-генетических детерминант в патогенезе и предикции выкидышей в ранние сроки гестации.
Материалы и методы. Для написания данного обзора был осуществлен поиск отечественных и зарубежных публикаций в российских и международных системах поиска (PubMed, eLibrary и пр.) за последние 10–15 лет. В обзор включены статьи из рецензируемой литературы и клинические протоколы профессиональных сообществ.
Результаты. Во многих исследованиях доказан вклад различных эпигенетических факторов в патогенез самопроизвольных выкидышей и обоснована молекулярно-генетическая детерминированность этого осложнения беременности.
Заключение. Выкидыш в ранние сроки гестации обусловлен суммарным воздействием эпигенетических и молекулярно-генетических факторов, наличием межгенных взаимодействий, в результате которых нарушаются физиологические функции и изменяется течение патологических реакций организма матери в преконцепционном периоде и далее в течение беременности.
Ключевые слова: выкидыш, молекулярные маркеры, эпигенетика.
Aim. Assess the role of epigenetic factors and molecular-genetic markers in the pathogenesis and prediction of early pregnancy losses.
Materials and methods. In order to write this review domestic and foreign publications were searched in Russian and international search systems (PubMed, eLibrary, etc.) for the last 10–15 years. Relevant articles from the peer-reviewed literature and clinical practice guidelines were included.
Results. Many recent studies have proved the contribution of various epigenetic factors to the pathogenesis of spontaneous miscarriages, and the molecular-genetic determination such kinds of pregnancy complication has been confirmed.
Conclusion. The miscarriage in early gestation is driven by combined impact of epigenetic and molecular-genetic factors, as well as the presence of intergenic interactions. It is may lead to deterioration of physiological functions, and maternal pathologenic pathways could be changed as during her periconceptional period as so during the pregnancy.
Key words: miscarriage, molecular markers, epigenetics.
Цель. Оценить роль эпигенетических факторов и молекулярно-генетических детерминант в патогенезе и предикции выкидышей в ранние сроки гестации.
Материалы и методы. Для написания данного обзора был осуществлен поиск отечественных и зарубежных публикаций в российских и международных системах поиска (PubMed, eLibrary и пр.) за последние 10–15 лет. В обзор включены статьи из рецензируемой литературы и клинические протоколы профессиональных сообществ.
Результаты. Во многих исследованиях доказан вклад различных эпигенетических факторов в патогенез самопроизвольных выкидышей и обоснована молекулярно-генетическая детерминированность этого осложнения беременности.
Заключение. Выкидыш в ранние сроки гестации обусловлен суммарным воздействием эпигенетических и молекулярно-генетических факторов, наличием межгенных взаимодействий, в результате которых нарушаются физиологические функции и изменяется течение патологических реакций организма матери в преконцепционном периоде и далее в течение беременности.
Ключевые слова: выкидыш, молекулярные маркеры, эпигенетика.
________________________________________________
Aim. Assess the role of epigenetic factors and molecular-genetic markers in the pathogenesis and prediction of early pregnancy losses.
Materials and methods. In order to write this review domestic and foreign publications were searched in Russian and international search systems (PubMed, eLibrary, etc.) for the last 10–15 years. Relevant articles from the peer-reviewed literature and clinical practice guidelines were included.
Results. Many recent studies have proved the contribution of various epigenetic factors to the pathogenesis of spontaneous miscarriages, and the molecular-genetic determination such kinds of pregnancy complication has been confirmed.
Conclusion. The miscarriage in early gestation is driven by combined impact of epigenetic and molecular-genetic factors, as well as the presence of intergenic interactions. It is may lead to deterioration of physiological functions, and maternal pathologenic pathways could be changed as during her periconceptional period as so during the pregnancy.
Key words: miscarriage, molecular markers, epigenetics.
Полный текст
Список литературы
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10. Bhattacharya S, Townend J, Bhattacharya S. Recurrent miscarriage: Are three miscarriages one too many? Analysis of a Scottish population-based database of 151,021 pregnancies. Eur J Obstet Gynecol Reprod Biol 2010; 150: 24–7.
11. Lo W, Rai R, Hameed A et al. The effect of body mass index on the outcome of pregnancy in women with recurrent miscarriage. J Family Community Med 2012; 19: 167–71.
12. Prine LW, Paiva P, Menkhorst E et al. Office Management of Early Pregnancy Loss. American Family Physician 2011; 84 (1): 75–82.
13. Pritchard AM, Hendrix PW, Paidas MJ. Hereditary Thrombophilia and Recurrent Pregnancy Loss. Clin Obstet Gynecol 2016; 59 (3): 487–97.
14. Arias-Sosa LA, Acosta ID, Lucena-Quevedo E et al. Genetic and epigenetic variations associated with idiopathic recurrent pregnancy loss.
J Assist Reprod Genet 2018; 35 (3): 355–66.
15. Voskresenskii S.L., Trishina V.L. Soderzhanie progesterona v krovi beremennykh v I i vo II trimestrakh gestatsii pri neblagopriiatnom zavershenii beremennosti. Zhurn. akusherstva i zhenskikh boleznei. 2017; 66 (4): 32–9 (in Russian).
16. Alecsandru D, García-Velasco JA. Immunology and human reproduction. Curr Opin Obstet Gynecol 2015; 27 (3): 231–4.
17. Lash G. Reproductive immunology: Time to look forward. J Reprod Immunol 2017; 119: 61.
18. Belokrinitskaya T.E., Chartorizhskaya N.N., Kazantseva E.V., Frolova N.I. Fetoplacental insufficiency. Chita: Oblastnaia tipografiia, 2009 (in Russian).
19. Su MT, Lee IW, Chen YC, Kuo PL. Association of progesterone receptor polymorphism with idiopathic recurrent pregnancy loss in Taiwanese Han population. J Assist Reprod Genet 2011; 28 (3): 239–43.
20. Bahia W, Finan RR, Al-Mutawa M et al. Genetic variation in the progesterone receptor gene and susceptibility to recurrent pregnancy loss: a case-control study. BJOG 2018; 125 (6): 729–35.
21. Shakhawat A, Shaikly V, Elzatma E et al. Interaction between HLA-G and monocyte/macrophages in human pregnancy. J Reprod Immunol 2010; 85 (1): 40–6.
22. Colucci F. The role of KIR and HLA interactions in pregnancy complications. Immunogenetics 2017; 69 (8–9): 557–65.
23. Meuleman T, Lashley LE, Dekkers OM et al. HLA associations and HLA sharing in recurrent miscarriage: A systematic review and meta-analysis. Hum Immunol 2015; 76 (5): 362–73.
24. Krog MC, Kolte AM, Husby K et al. Recurrent pregnancy loss. Ugeskr Laeger 2017; 179 (17). pii: V11160834. [Article in Danish]. https://www.ncbi.nlm.nih.gov/pubmed/28473031
25. Fan W, Li S, Huang Z, Chen Q. Relationship between HLA-G polymorphism and susceptibility to recurrent miscarriage: a meta-analysis of non-family-based studies. J Assist Reprod Genet 2014; 31 (2): 173–84.
26. Amodio G, Canti V, Maggio L et al. Association of genetic variants in the 3'UTR of HLA-G with Recurrent Pregnancy Loss. Hum Immunol 2016; 77 (10): 886–91.
27. Michita RT, Zambra FMB, Fraga LR et al. A tug-of-war between tolerance and rejection – New evidence for 3'UTR HLA-G haplotypes influence in recurrent pregnancy loss. Hum Immunol 2016; 77 (10): 892–7.
28. Shi X, Xie X, Jia Y, Li S. Maternal genetic polymorphisms and unexplained recurrent miscarriage: a systematic review and meta-analysis. Clin Genet 2017; 91 (2): 265–84.
29. Paiva P. Luekemia inhibitory factor and interleukin-11: critical regulators in the establishment of pregnancy. Cytok Growth Factor Rev 2009; 20: 319–28.
30. Li F, Devi Y, Bao L et al. Involvement of cyclin D3, CDKN1A 9h210, and BIRC5 (Survivin) in interleukin 11 stimulation of decidualization in mice. Biol Reprod 2008; 78: 127–33.
31. Jin L, Fan D, Zhang T et al. The costimulatory signal upregulation is associated with Th1 bias at the maternal-fetal interface in human miscarriage. Am J Reprod Immunol 2011; 66: 270–8.
32. Pitirimova L.N., Zagorodneva E.A., Gumilevskii B.Iu. Osobennosti allel'nogo polimorfizma genov interleikinov i tsitokinovyi balans zhenshchin s nevynashivaniem beremennosti. Akusherstvo i ginekologiia. 2014; 3: 33–8 (in Russian).
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35. Pan HT, Ding HG, Fang M et al. Proteomics and bioinformatics analysis of altered protein expression in the placental villous tissue from early recurrent miscarriage patients. Placenta 2018; 61: 1–10.
36. Onda K, Tong S, Beard S et al. J. Proton Pump Inhibitors Decrease Soluble fms-Like Tyrosine Kinase-1 and Soluble Endoglin Secretion, Decrease Hypertension, and Rescue Endothelial Dysfunction. Hypertension 2017; 69 (3): 457–68.
37. Chinni E, Colaizzo D, Tiscia GL et al. Markers of haemostasis and angiogenesis in placentae from gestational vascular complications: impairment of mechanisms involved in maintaining intervillous blood flow. Thromb Res 2010; 125 (3): 267–71.
38. Liu FL, Zhou J, Zhang W, Wang H. Epigenetic regulation and related diseases during placental development. Yi Chuan 2017; 39 (4): 263–75.
39. Wang JM, Gu Y, Zhang Y et al. Deep-sequencing identification of differentially expressed miRNAs in decidua and villus of recurrent miscarriage patients. Arch Gynecol Obstet 2016; 293 (5): 1125–35.
40. Frolova N.I., Belokrinitskaia T.E., Strambovskaia N.N., Belozertseva E.P. Polimorfizm genov, assotsiirovannykh s narusheniiami gemostaza i folatnogo obmena, u patsientok s retsidiviruiushchimi poteriami beremennosti v rannie sroki. Elektronnoe nauchnoe izdanie. Zabaikal'skii med. vestn. 2018; 1: 37–44 (in Russian).
41. Gaiday AN, Tussupkaliyev AB, Bermagambetova SK et al. Effect of homocysteine on pregnancy: A systematic review. Chem Biol Interact 2018; 293: 70–6.
42. Trifonova EA, Swarovskaya MG, Ganzha OA et al. The interaction effect of angiogenesis and endothelial dysfunction-related gene variants increases the susceptibility of recurrent pregnancy loss. J Assist Reprod Genet 2019. DOI: 10.1007/s10815-019-01403-2. https://www.ncbi.nlm.nih.gov/pubmed/30680517
43. Chumanova O.V., Pasman N.M., Voronina E.N., Filipenko M.L. Otsenka roli polimorfizma genov sistemy gemostaza i genov, otvechaiushchikh za formirovanie disfunktsii endoteliia, v razvitii gestatsionnykh oslozhnenii. Med. genetika. 2017; 16 (5): 48–51 (in Russian).
44. McLaughlin K, Audette MC, Parker JD, Kingdom JC. Mechanisms and Clinical Significance of Endothelial Dysfunction in High-Risk Pregnancies. Can J Cardiol 2018; 34 (4): 371–80.
45. López-Jiménez JJ, Porras-Dorantes A, Juárez-Vázquez CI et al. Molecular thrombophilic profile in Mexican patients with idiopathic recurrent pregnancy loss. Genet Mol Res 2016; 15 (4). DOI: 10.4238/gmr.15048728
46. Gumus E. The powerful association of angiotensin-converting enzyme insertion/deletion polymorphism and idiopathic recurrent pregnancy loss. Ginekol Pol 2018; 89 (10): 573–6.
47. Kuznetsova V.L., Solov'eva A.G. Oksid azota: svoystva, biologicheskaya rol', mekhanizmy deystviya. Sovremennye problemy nauki i obrazovaniya. 2015; 4: 462 (in Russian).
48. García-Ortiz A, Serrador JM. Nitric Oxide Signaling in T Cell-Mediated Immunity. Trends Mol Med 2018; 24 (4): 412–27.
49. Osol G, Ko NL, Mandalà M. Altered Endothelial Nitric Oxide Signaling as a Paradigm for Maternal Vascular Maladaptation in Preeclampsia. Curr Hypertens Rep 2017;19 (10): 82.
50. Guttmacher AE, Maddox YT, Spong CY. The Human Placenta Project: placental structure, development, and function in real time. Placenta 2014; 35 (5): 303–4.
51. Sun Y, Chen M, Mao B et al. Association between vascular endothelial growth factor polymorphism and recurrent pregnancyloss: A systematic review and meta-analysis. Eur J Obstet Gynecol Reprod Biol 2017; 211: 169–76.
52. Jung YW, Ahn EH, Kim JO et al. Association of genetic polymorphisms in VEGF-460, -7 and -583 and hematocrit level with the development of idiopathic recurrent pregnancy loss and a meta-analysis. J Gene Med 2018; 20 (9): e3048.
53. Momot A.P., Trukhina D.A., Taranenko I.A., Romanov V.V. Osobennosti sosudisto-trombotsitarnogo gemostaza na raznykh srokakh fiziologicheskoy beremennosti. Med. alfavit. Sovremennaya laboratoriya. 2014; 1: 46–50 (in Russian).
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58. Yang Y, Luo Y, Yuan J et al. Association between maternal, fetal and paternal MTHFR gene C677T and A1298C polymorphisms and risk of recurrent pregnancy loss: a comprehensive evaluation. Arch Gynecol Obstet 2016; 293 (6): 1197–211.
59. Ye Y, Vattai A, Zhang X et al. Role of Plasminogen Activator Inhibitor Type 1 in Pathologies of Female Reproductive Diseases. Int J Mol Sci 2017; 18 (8): 1651.
60. Jeon YJ, Kim YR, Lee BE et al. Genetic association of five plasminogen activator inhibitor-1 (PAI-1) polymorphisms and idiopathic recurrent pregnancy loss in Korean women. Thromb Haemost 2013; 110 (4): 742–50.
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11. Lo W, Rai R, Hameed A et al. The effect of body mass index on the outcome of pregnancy in women with recurrent miscarriage. J Family Community Med 2012; 19: 167–71.
12. Prine LW, Paiva P, Menkhorst E et al. Office Management of Early Pregnancy Loss. American Family Physician 2011; 84 (1): 75–82.
13. Pritchard AM, Hendrix PW, Paidas MJ. Hereditary Thrombophilia and Recurrent Pregnancy Loss. Clin Obstet Gynecol 2016; 59 (3): 487–97.
14. Arias-Sosa LA, Acosta ID, Lucena-Quevedo E et al. Genetic and epigenetic variations associated with idiopathic recurrent pregnancy loss. J Assist Reprod Genet 2018; 35 (3): 355–66.
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17. Lash G. Reproductive immunology: Time to look forward. J Reprod Immunol 2017; 119: 61.
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19. Su MT, Lee IW, Chen YC, Kuo PL. Association of progesterone receptor polymorphism with idiopathic recurrent pregnancy loss in Taiwanese Han population. J Assist Reprod Genet 2011; 28 (3): 239–43.
20. Bahia W, Finan RR, Al-Mutawa M et al. Genetic variation in the progesterone receptor gene and susceptibility to recurrent pregnancy loss: a case-control study. BJOG 2018; 125 (6): 729–35.
21. Shakhawat A, Shaikly V, Elzatma E et al. Interaction between HLA-G and monocyte/macrophages in human pregnancy. J Reprod Immunol 2010; 85 (1): 40–6.
22. Colucci F. The role of KIR and HLA interactions in pregnancy complications. Immunogenetics 2017; 69 (8–9): 557–65.
23. Meuleman T, Lashley LE, Dekkers OM et al. HLA associations and HLA sharing in recurrent miscarriage: A systematic review and meta-analysis. Hum Immunol 2015; 76 (5): 362–73.
24. Krog MC, Kolte AM, Husby K et al. Recurrent pregnancy loss. Ugeskr Laeger 2017; 179 (17). pii: V11160834. [Article in Danish]. https://www.ncbi.nlm.nih.gov/pubmed/28473031
25. Fan W, Li S, Huang Z, Chen Q. Relationship between HLA-G polymorphism and susceptibility to recurrent miscarriage: a meta-analysis of non-family-based studies. J Assist Reprod Genet 2014; 31 (2): 173–84.
26. Amodio G, Canti V, Maggio L et al. Association of genetic variants in the 3'UTR of HLA-G with Recurrent Pregnancy Loss. Hum Immunol 2016; 77 (10): 886–91.
27. Michita RT, Zambra FMB, Fraga LR et al. A tug-of-war between tolerance and rejection – New evidence for 3'UTR HLA-G haplotypes influence in recurrent pregnancy loss. Hum Immunol 2016; 77 (10): 892–7.
28. Shi X, Xie X, Jia Y, Li S. Maternal genetic polymorphisms and unexplained recurrent miscarriage: a systematic review and meta-analysis. Clin Genet 2017; 91 (2): 265–84.
29. Paiva P. Luekemia inhibitory factor and interleukin-11: critical regulators in the establishment of pregnancy. Cytok Growth Factor Rev 2009; 20: 319–28.
30. Li F, Devi Y, Bao L et al. Involvement of cyclin D3, CDKN1A 9h210, and BIRC5 (Survivin) in interleukin 11 stimulation of decidualization in mice. Biol Reprod 2008; 78: 127–33.
31. Jin L, Fan D, Zhang T et al. The costimulatory signal upregulation is associated with Th1 bias at the maternal-fetal interface in human miscarriage. Am J Reprod Immunol 2011; 66: 270–8.
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35. Pan HT, Ding HG, Fang M et al. Proteomics and bioinformatics analysis of altered protein expression in the placental villous tissue from early recurrent miscarriage patients. Placenta 2018; 61: 1–10.
36. Onda K, Tong S, Beard S et al. J. Proton Pump Inhibitors Decrease Soluble fms-Like Tyrosine Kinase-1 and Soluble Endoglin Secretion, Decrease Hypertension, and Rescue Endothelial Dysfunction. Hypertension 2017; 69 (3): 457–68.
37. Chinni E, Colaizzo D, Tiscia GL et al. Markers of haemostasis and angiogenesis in placentae from gestational vascular complications: impairment of mechanisms involved in maintaining intervillous blood flow. Thromb Res 2010; 125 (3): 267–71.
38. Liu FL, Zhou J, Zhang W, Wang H. Epigenetic regulation and related diseases during placental development. Yi Chuan 2017; 39 (4): 263–75.
39. Wang JM, Gu Y, Zhang Y et al. Deep-sequencing identification of differentially expressed miRNAs in decidua and villus of recurrent miscarriage patients. Arch Gynecol Obstet 2016; 293 (5): 1125–35.
40. Фролова Н.И., Белокриницкая Т.Е., Страмбовская Н.Н., Белозерцева Е.П. Полиморфизм генов, ассоциированных с нарушениями гемостаза и фолатного обмена, у пациенток с рецидивирующими потерями беременности в ранние сроки. Электронное научное издание. Забайкальский мед. вестн. 2018; 1: 37–44.
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41. Gaiday AN, Tussupkaliyev AB, Bermagambetova SK et al. Effect of homocysteine on pregnancy: A systematic review. Chem Biol Interact 2018; 293: 70–6.
42. Trifonova EA, Swarovskaya MG, Ganzha OA et al. The interaction effect of angiogenesis and endothelial dysfunction-related gene variants increases the susceptibility of recurrent pregnancy loss. J Assist Reprod Genet 2019. DOI: 10.1007/s10815-019-01403-2. https://www.ncbi.nlm.nih.gov/pubmed/30680517
43. Чуманова О.В., Пасман Н.М., Воронина Е.Н., Филипенко М.Л. Оценка роли полиморфизма генов системы гемостаза и генов, отвечающих за формирование дисфункции эндотелия, в развитии гестационных осложнений. Мед. генетика. 2017; 16 (5): 48–51.
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44. McLaughlin K, Audette MC, Parker JD, Kingdom JC. Mechanisms and Clinical Significance of Endothelial Dysfunction in High-Risk Pregnancies. Can J Cardiol 2018; 34 (4): 371–80.
45. López-Jiménez JJ, Porras-Dorantes A, Juárez-Vázquez CI et al. Molecular thrombophilic profile in Mexican patients with idiopathic recurrent pregnancy loss. Genet Mol Res 2016; 15 (4). DOI: 10.4238/gmr.15048728
46. Gumus E. The powerful association of angiotensin-converting enzyme insertion/deletion polymorphism and idiopathic recurrent pregnancy loss. Ginekol Pol 2018; 89 (10): 573–6.
47. Кузнецова В.Л., Соловьева А.Г. Оксид азота: свойства, биологическая роль, механизмы действия. Современные проблемы науки и образования. 2015; 4: 462.
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48. García-Ortiz A, Serrador JM. Nitric Oxide Signaling in T Cell-Mediated Immunity. Trends Mol Med 2018; 24 (4): 412–27.
49. Osol G, Ko NL, Mandalà M. Altered Endothelial Nitric Oxide Signaling as a Paradigm for Maternal Vascular Maladaptation in Preeclampsia. Curr Hypertens Rep 2017;19 (10): 82.
50. Guttmacher AE, Maddox YT, Spong CY. The Human Placenta Project: placental structure, development, and function in real time. Placenta 2014; 35 (5): 303–4.
51. Sun Y, Chen M, Mao B et al. Association between vascular endothelial growth factor polymorphism and recurrent pregnancyloss: A systematic review and meta-analysis. Eur J Obstet Gynecol Reprod Biol 2017; 211: 169–76.
52. Jung YW, Ahn EH, Kim JO et al. Association of genetic polymorphisms in VEGF-460, -7 and -583 and hematocrit level with the development of idiopathic recurrent pregnancy loss and a meta-analysis. J Gene Med 2018; 20 (9): e3048.
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[Momot A.P., Trukhina D.A., Taranenko I.A., Romanov V.V. Osobennosti sosudisto-trombotsitarnogo gemostaza na raznykh srokakh fiziologicheskoy beremennosti. Med. alfavit. Sovremennaya laboratoriya. 2014; 1: 46–50 (in Russian).]
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[Galaiko M.V., Rybina O.V., Litvinenko M.S. et al. Trombofiliia i beremennost'. Klinicheskaia onkogematologiia. Fundamental'nye issledovaniia i klinicheskaia praktika. 2017; 10 (3): 409–22 (in Russian).]
55. Klainbart S, Slon A, Kelmer E et al. Global hemostasis in healthy bitches during pregnancy and at different estrous cycle stages: Evaluation of routine hemostatic tests and thromboelastometry. Theriogenology 2017; 97: 57–66.
56. Баймурадова С.М., Слуханчук Е.В. Невынашивание беременности и «критериальная» тромбофилия. Современный взгляд на проблему. Современные проблемы здравоохранения и медицинской статистики. 2018; 2: 94–102.
[Baymuradova S.M., Slukhanchuk E.V. Nevynashivanie beremennosti i “kriterial'naya” trombofiliya. Sovremennyy vzglyad na problemu. Sovremennye problemy zdravookhraneniya i meditsinskoy statistiki. 2018; 2: 94–102 (in Russian).]
57. Kamali M, Hantoushzadeh S, Borna S et al. Association between Thrombophilic Genes Polymorphisms and Recurrent Pregnancy Loss Susceptibility in the Iranian Population: a Systematic Review and Meta-Analysis. Iran Biomed J 2018; 22 (2): 78–89.
58. Yang Y, Luo Y, Yuan J et al. Association between maternal, fetal and paternal MTHFR gene C677T and A1298C polymorphisms and risk of recurrent pregnancy loss: a comprehensive evaluation. Arch Gynecol Obstet 2016; 293 (6): 1197–211.
59. Ye Y, Vattai A, Zhang X et al. Role of Plasminogen Activator Inhibitor Type 1 in Pathologies of Female Reproductive Diseases. Int J Mol Sci 2017; 18 (8): 1651.
60. Jeon YJ, Kim YR, Lee BE et al. Genetic association of five plasminogen activator inhibitor-1 (PAI-1) polymorphisms and idiopathic recurrent pregnancy loss in Korean women. Thromb Haemost 2013; 110 (4): 742–50.
61. Salazar Garcia MD, Sung N, Mullenix TM et al. Plasminogen Activator Inhibitor-1 4G/5G Polymorphism is Associated with Reproductive Failure: Metabolic, Hormonal, and Immune Profiles. Am J Reprod Immunol 2016; 76 (1): 70–81.
62. Barut MU, Bozkurt M, Kahraman M et al. Thrombophilia and Recurrent Pregnancy Loss: The Enigma Continues. Med Sci Monit 2018; 24: 4288–94.
63. Gao H, Tao FB. Prothrombin G20210A mutation is associated with recurrent pregnancy loss: a systematic review and meta-analysis update. Thromb Res 2015; 135 (2): 339–46.
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54. Galaiko M.V., Rybina O.V., Litvinenko M.S. et al. Trombofiliia i beremennost'. Klinicheskaia onkogematologiia. Fundamental'nye issledovaniia i klinicheskaia praktika. 2017; 10 (3): 409–22 (in Russian).
55. Klainbart S, Slon A, Kelmer E et al. Global hemostasis in healthy bitches during pregnancy and at different estrous cycle stages: Evaluation of routine hemostatic tests and thromboelastometry. Theriogenology 2017; 97: 57–66.
56. Baymuradova S.M., Slukhanchuk E.V. Nevynashivanie beremennosti i “kriterial'naya” trombofiliya. Sovremennyy vzglyad na problemu. Sovremennye problemy zdravookhraneniya i meditsinskoy statistiki. 2018; 2: 94–102 (in Russian).
57. Kamali M, Hantoushzadeh S, Borna S et al. Association between Thrombophilic Genes Polymorphisms and Recurrent Pregnancy Loss Susceptibility in the Iranian Population: a Systematic Review and Meta-Analysis. Iran Biomed J 2018; 22 (2): 78–89.
58. Yang Y, Luo Y, Yuan J et al. Association between maternal, fetal and paternal MTHFR gene C677T and A1298C polymorphisms and risk of recurrent pregnancy loss: a comprehensive evaluation. Arch Gynecol Obstet 2016; 293 (6): 1197–211.
59. Ye Y, Vattai A, Zhang X et al. Role of Plasminogen Activator Inhibitor Type 1 in Pathologies of Female Reproductive Diseases. Int J Mol Sci 2017; 18 (8): 1651.
60. Jeon YJ, Kim YR, Lee BE et al. Genetic association of five plasminogen activator inhibitor-1 (PAI-1) polymorphisms and idiopathic recurrent pregnancy loss in Korean women. Thromb Haemost 2013; 110 (4): 742–50.
61. Salazar Garcia MD, Sung N, Mullenix TM et al. Plasminogen Activator Inhibitor-1 4G/5G Polymorphism is Associated with Reproductive Failure: Metabolic, Hormonal, and Immune Profiles. Am J Reprod Immunol 2016; 76 (1): 70–81.
62. Barut MU, Bozkurt M, Kahraman M et al. Thrombophilia and Recurrent Pregnancy Loss: The Enigma Continues. Med Sci Monit 2018; 24: 4288–94.
63. Gao H, Tao FB. Prothrombin G20210A mutation is associated with recurrent pregnancy loss: a systematic review and meta-analysis update. Thromb Res 2015; 135 (2): 339–46.
Авторы
Н.И. Фролова*, Т.Е. Белокриницкая
ФГБОУ ВО «Читинская государственная медицинская академия» Минздрава России, Чита, Россия
*taasyaa@mail.ru
Chita State Medical Academy, Chita, Russia
*taasyaa@mail.ru
ФГБОУ ВО «Читинская государственная медицинская академия» Минздрава России, Чита, Россия
*taasyaa@mail.ru
________________________________________________
Chita State Medical Academy, Chita, Russia
*taasyaa@mail.ru
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