Нарушения структуры и васкуляризации ворсин плаценты при преэклампсии
Нарушения структуры и васкуляризации ворсин плаценты при преэклампсии
Щеголев А.И., Туманова У.Н., Ляпин В.М. Нарушения структуры и васкуляризации ворсин плаценты при преэклампсии. Гинекология. 2018; 20 (4): 12–18.
DOI: 10.26442/2079-5696_2018.4.12-18
________________________________________________
Shchegolev A.I., Tumanova U.N., Lyapin V.M. Disorder of the structure and vascularization of the villi of placenta at the preeclampsia. Gynecology. 2018; 20 (4): 12–18.
DOI: 10.26442/2079-5696_2018.4.12-18
Нарушения структуры и васкуляризации ворсин плаценты при преэклампсии
Щеголев А.И., Туманова У.Н., Ляпин В.М. Нарушения структуры и васкуляризации ворсин плаценты при преэклампсии. Гинекология. 2018; 20 (4): 12–18.
DOI: 10.26442/2079-5696_2018.4.12-18
________________________________________________
Shchegolev A.I., Tumanova U.N., Lyapin V.M. Disorder of the structure and vascularization of the villi of placenta at the preeclampsia. Gynecology. 2018; 20 (4): 12–18.
DOI: 10.26442/2079-5696_2018.4.12-18
Преэклампсия считается одним из наиболее грозных заболеваний беременности, вызывающих серьезные осложнения у матери и плода. Развитие преэклампсии обусловлено нарушением процессов плацентации. Проведен анализ данных литературы, посвященных микроскопическим изменениям структуры и васкуляризации ворсин плаценты при преэклампсии. Показано, что при преэклампсии отмечаются нарушения строения и васкуляризации ворсин плаценты, что, несомненно, указывает на их роль в развитии и прогрессировании данного осложнения беременности. В наблюдениях ранней преэклампсии регистрируются более низкие значения протяженности, площади поверхности и объема ворсин, а также степени их васкуляризации. Имеющаяся в литературе неоднозначность морфометрических и стереометрических показателей ворсин обусловлена, скорее всего, исследованием плацент на разных сроках гестации и различной степенью тяжести преэклампсии. Важным звеном патогенеза преэклампсии и фактором нарушения развития ворсин является изменение уровней проангиогенных и противоангиогенных факторов, главным образом сосудистого эндотелиального фактора роста и его рецепторов. Для полноценного анализа причин и особенностей развития преэклампсии необходимо проведение комплексного макроскопического и микроскопического исследования плаценты.
Preeclampsia is considered one of the most serious diseases of pregnancy and cause serious complications in the mother and fetus. The emergence and development of preeclampsia is due to the violation of placental processes. The literature data on microscopic changes in the structure and vascularization of placental villi in preeclampsia are analyzed. Violations of the structure and vascularization of villi placenta in preeclampsia are noted. This, undoubtedly, indicates their role in the development and progression of this complication of pregnancy. Lower values of the extent, surface area and volume of villi, as well as their degree of vascularization, are registered in observations of early preeclampsia. The ambiguity of the data of morphometric and stereo metric indices of villi, which are available in the literature, is most likely due to the investigation of placentas at various stages of gestation and with varying degrees of severity of preeclampsia. An important link in the pathogenesis of preeclampsia and a factor in violations of the villi development is a change in the levels of pro-angiogenic and anti-angiogenic factors, mainly the vascular endothelial growth factor and its receptors. For a complete analysis of the causes and characteristics of preeclampsia is necessary to conduct a comprehensive macroscopic and microscopic examination of the placenta. Key words: preeclampsia, placenta, villi, vascularization, angiogenic factors.
1. Савельева Г.М., Ходжаева З.С., Шалина Р.И. Преэклампсия (прежнее название – гестоз), эклампсия. Акушерство: национальное руководство. Под ред. Г.М.Савельевой и др. М.: ГЭОТАР-Медиа, 2016. / Saveleva G.M., Hodzhaeva Z.S., Shalina R.I. Preeklampsiya (prezhnee nazvanie – gestoz), eklampsiya. Akusherstvo: nacionalnoe rukovodstvo. Pod red. G.M.Savelevoj i dr. M.: GEOTAR-Media, 2016. [in Russian]
2. Lowe SA, Brown MA, Dekker G.A et al. Guidelines for the management of hypertensive disorders of pregnancy. Aust New Z J Obstet Gynecol 2009; 49: 242–6.
3. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol 2001; 97: 533–8.
4. Berg CJ, Mackay AP, Qin C, Callaghan WM. Overview of maternal morbidity during hospitalization for labor and delivery in the United States: 1993–1997 and 2001–2005. Obstet Gynecol 2009; 113: 1075–81.
5. Girouard J, Giguere Y, Moutquin J-M, Forest J-C. Previous hypertensive disease of pregnancy is associated with alterations of markers of insulin resistance. Hypertension 2007; 49: 1056–62.
6. Wallis AB, Saftlas AF, Hsia J et al. Secular trends in the rates of pre-eclampsia, eclampsia, and gestational hypertension, United States, 1987–2004. Am J Hypertens 2008; 21: 521–6.
7. Khan KS, Wojdyla D, Say L et al. WHO analysis of causes of maternal death: a systematic review. Lancet 2006; 367 (9516): 1066–74.
8. Myatt L. Role of placenta in pre-eclampsia. Endocrine 2002; 19: 103–11.
9. Lambert G, Brichant JF, Hartstein G et al. Pre-eclampsia: An update. Acta Anaesthesiol Belg 2014; 65: 137–49.
10. Zhou Y, Damsky CH, Chiu K et al. Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts. J Clin Invest 1993; 91: 950–60.
11. Damsky CH, Fitzgerald ML, Fisher SJ. Distribution patterns of extracellular matrix components and adhesion receptors are intricately modulated during first trimester cytotrophoblast differentiation along the invasive pathway, in vivo. J Clin Invest 1992; 89: 210–22.
12. Robertson WB, Brosens I, Dixon G. Uteroplacental vascular pathology. Eur J Obstet Gynecol Reprod Biol 1975; 5: 47–65.
13. Zhou Y, Damsky CH, Fisher SJ. Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype: one cause of defective endovascular invasion in this syndrome? J Clin Invest 1997; 99: 2152–64.
14. Daayana S, Baker P, Crocker I. An image analysis technique for the investigation of variations in placental morphology in pregnancies complicated by preeclampsia with and without intrau-terine growth restriction. J Soc Gynecol Investig 2004; 11: 545–52.
15. Mayhew TM, Wijesekara J, Baker PN, Ong SS. Morphometric evidence that villous development and fetoplacental angiogenesis are compromised by intrauterine growth re-striction but not by pre-eclampsia. Placenta 2004; 25: 829–33.
16. Egbor M, Ansari T, Morris N et al. Pre-eclampsia and fetal growth restriction: How morphometrically different is the placenta? Placenta 2006; 27: 727–34.
17. Corrêa RRM, Gilio DB, Cavellani CL et al. Placental morphometrical and histopathology changes in the different clinical presentations of hypertensive syndromes in pregnancy. Arch Gynecol Obstet 2008; 277: 201–6.
18. Ducray JF, Naicker T, Moodley J. Pilot study of comparative placental morphometry in pre-eclamptic and normotensive pregnancies suggests possible maladaptations of the fetal component of the placenta. Eur J Obstet Gynecol Reprod Biol 2011; 156: 29–34.
19. Odibo AO, Zhong Y, Longtine M et al. First-trimester serum analytes, biophysical tests and the association with pathological morphometry in the placenta of pregnancies with preeclampsia and fetal growth restriction. Placenta 2011; 32: 333–8.
20. Mukherjee R. Morphometric evaluation of preeclamptic placenta using light microscopic images. Bio Med Res Int 2014; 1: 293690. DOI:10.1155/2014/293690
21. Güven D, Altunkaynak BZ, Altun G et al. Histomorphometric changes in the placenta and umbilical cord during complications of pregnancy. Biotech Histochem 2018; 93: 198–210.
22. Mayhew T.M. Fetoplacental angiogenesis during gestation is biphasic, longitudinal and occurs by proliferation and remodelling of vascular endothelial cells. Placenta 2002; 23: 742–50.
23. Stanek J. Acute and chronic placental membrane hypoxic lesions. Virchows Arch 2009; 455: 315–22.
24. Ляпин В.М., Туманова У.Н., Щеголев А.И. Cинцитиальные узелки в ворсинах плаценты при преэклампсии. Соврем. проблемы науки и образования. 2015; 4: 499. / Lyapin V.M., Tumanova U.N., Shegolev A.I. Cincitialnye uzelki v vorsinah placenty pri preeklampsii. Sovrem. problemy nauki i obrazovaniya. 2015; 4: 499. [in Russian]
25. Ляпин В.М., Туманова У.Н., Щеголев А.И. Хорионические кисты в плаценте при преэклампсии. Соврем. проблемы науки и образования. 2015; 5: 163. / Lyapin V.M., Tumanova U.N., Shegolev A.I. Horionicheskie kisty v placente pri preeklampsii. Sovrem. problemy nauki i obrazovaniya. 2015; 5: 163. [in Russian]
26. Щеголев А.И. Современная морфологическая классификация повреждений плаценты. Акушерство и гинекология. 2016; 4: 16–23. / Shegolev A.I. Sovremennaya morfologicheskaya klassifikaciya povrezhdenij placenty. Akusherstvo i ginekologiya. 2016; 4: 16–23. [in Russian]
27. Милованов А.П. Патология системы мать–плацента–плод. М.: Медицина, 1999. / Milovanov A.P. Patologiya sistemy mat–placenta–plod. M.: Medicina, 1999. [in Russian]
28. Silasi M, Cohen B, Karumanchi S, Rana S. Abnormal placentation, angiogenic factors, and the pathogenesis of preeclampsia. Obstet Gynecol Clin N Am 2010; 37: 239–53.
29. Charnock-Jones DS, Kaufmann P, Mayhew TM. Aspects of human fetoplacental vasculogenesis and angiogenesis. I. Molecular regulation. Placenta 2004; 25: 103–13.
30. Павлов К.А., Дубова Е.А., Щеголев А.И. Фетоплацентарный ангиогенез при нормальной беременности: роль сосудистого эндотелиального фактора роста. Акушерство и гинекология. 2011; 3: 11–6. / Pavlov K.A., Dubova E.A., Shegolev A.I. Fetoplacentarnyj angiogenez pri normalnoj beremennosti: rol sosudistogo endotelialnogo faktora rosta. Akusherstvo i ginekologiya. 2011; 3: 11–6. [in Russian]
31. Павлов К.А., Дубова Е.А., Щеголев А.И. Фетоплацентарный ангиогенез при нормальной беременности: роль плацентарного фактора роста и ангиопоэтинов. Акушерство и гинекология. 2010; 6: 10–15. / Pavlov K.A., Dubova E.A., Shegolev A.I. Fetoplacentarnyj angiogenez pri normalnoj beremennosti: rol placentarnogo faktora rosta i angiopoetinov. Akusherstvo i ginekologiya. 2010; 6: 10–15. [in Russian]
32. Kurz H, Wilting J, Sandau K, Christ B. Automated evaluation of angiogenic effects mediated by VEGF and PlGF homo- and heterodimers. Microvasc Res 1998; 55: 92–102.
33. Livingston JC, Chin R, Haddad B et al. Reductions of vascular endothelial growth factor and placental growth factor concentrations in severe preeclampsia. Am J Obstet Gynecol 2000; 183: 1554–7.
34. Tripathi R, Rath G, Ralhan R et al. Soluble and membranous vascular endothelial growth factor receptor-2 in pregnancies complicated by pre-eclampsia. Yonsei Med J 2009; 50: 656–66.
35. Дубова Е.А., Павлов К.А., Ляпин В.М. и др. Фактор роста эндотелия сосудов и его рецепторы в ворсинах плаценты беременных с преэклампсией. Бюл. эксперим. биологии и медицины. 2012; 12: 761–5. / Dubova E.A., Pavlov K.A., Lyapin V.M. i dr. Faktor rosta endoteliya sosudov i ego receptory v vorsinah placenty beremennyh s preeklampsiej. Byul. eksperim. biologii i mediciny. 2012; 12: 761–5. [in Russian]
36. Maynard SE, Min JY, Merchan J et al. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J Clin Invest 2003; 111: 649–58.
37. Ahmad S, Ahmed A. Elevated placental soluble vascular endothelial growth factor receptor-1 inhibits angiogenesis in preeclampsia. Circ Res 2004; 95: 884–91.
38. Ahmad S, Hewett PW, Al-Ani B et al. Autocrine activity of soluble Flt-1 controls endothelial cell function and angiogenesis. Vasc Cell 2011; 3: 15. DOI: 10.1186/2045-824X-3-15
39. Щеголев А.И., Дубова Е.А., Павлов К.А. и др. Морфометрическая характеристика терминальных ворсин плаценты при преэклампсии. Бюл. эксперим. биологии и медицины. 2012; 7: 104–7. / Shegolev A.I., Dubova E.A., Pavlov K.A. i dr. Morfometricheskaya harakteristika terminalnyh vorsin placenty pri preeklampsii. Byul. eksperim. biologii i mediciny. 2012; 7: 104–7. [in Russian]
40. Ihle BU, Long P, Oats J. Early onset preeclampsia: recognition of underlying renal disease. Br Med J 1987; 294: 79–81.
41. Obed SA, Aniteye P. Birth weight and ponderal index in preeclampsia: a comparative study. Ghana Medical J 2006; 40: 8–13.
42. Ходжаева З.С., Шмаков Р.Г., Коган Е.А. и др. Клинико-анамнестические особенности, плацента и плацентарная площадка при ранней и поздней преэклампсии. Акушерство и гинекология. 2015; 4: 25–31. / Hodzhaeva Z.S., Shmakov R.G., Kogan E.A. i dr. Kliniko-anamnesticheskie osobennosti, placenta i placentarnaya ploshadka pri rannej i pozdnej preeklampsii. Akusherstvo i ginekologiya. 2015; 4: 25–31. [in Russian]
43. Dissanayake VH, Samarasinghe HD, Morgan L et al. Morbidity and mortality associated with preeclampsia at two tertiary care hospitals in Sri Lanka. J Obstet Gynecol Res 2007; 33: 56–62.
44. Egbor M, Ansari T, Morris N et al. Morphometric placental villous and vascular abnormalities in early- and late-onset pre-eclampsia with and without fetal growth restriction. BJOG 2006; 113: 580–9.
45. Щеголев А.И., Ляпин В.М., Туманова У.Н. и др. Гистологические изменения плаценты и васкуляризация ее ворсин при ранней и поздней преэклампсии. Арх. патологии. 2016; 1: 13–8. / Shegolev A.I., Lyapin V.M., Tumanova U.N. i dr. Gistologicheskie izmeneniya placenty i vaskulyarizaciya ee vorsin pri rannej i pozdnej preeklampsii. Arh. patologii. 2016; 1: 13–8. [in Russian]
46. Воднева Д.Н., Романова В.В., Дубова Е.А. и др. Клинико-морфологические особенности ранней и поздней преэклампсии. Акушерство и гинекология. 2014; 2: 35–40. / Vodneva D.N., Romanova V.V., Dubova E.A. i dr. Kliniko-morfologicheskie osobennosti rannej i pozdnej preeklampsii. Akusherstvo i ginekologiya. 2014; 2: 35–40. [in Russian]
47. Wikstrom AK, Larrson A, Eriksson UJ et al. Early postpartum changes in circulating pro- and anti-angiogenic factors in early-onset and late-onset preeclampsia. Acta Obstet Gynecol 2008; 87: 146–153.
48. Hernandez-Diaz S, Toh S, Cnattingius S. Risk of preeclampsia in first and subsequent pregnancies: prospective cohort study. BMJ 2009; 338: 1–5.
49. Crispi F, Llurba E, Dominguez C et al. Predictive value of angiogenic factors and uterine artery Doppler for early- versus late-onset preeclampsia and intrauterine growth restriction. Ultrasound Obstet Gynecol 2008; 31: 303–9.
________________________________________________
1. Saveleva G.M., Hodzhaeva Z.S., Shalina R.I. Preeklampsiya (prezhnee nazvanie – gestoz), eklampsiya. Akusherstvo: nacionalnoe rukovodstvo. Pod red. G.M.Savelevoj i dr. M.: GEOTAR-Media, 2016. [in Russian]
2. Lowe SA, Brown MA, Dekker G.A et al. Guidelines for the management of hypertensive disorders of pregnancy. Aust New Z J Obstet Gynecol 2009; 49: 242–6.
3. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol 2001; 97: 533–8.
4. Berg CJ, Mackay AP, Qin C, Callaghan WM. Overview of maternal morbidity during hospitalization for labor and delivery in the United States: 1993–1997 and 2001–2005. Obstet Gynecol 2009; 113: 1075–81.
5. Girouard J, Giguere Y, Moutquin J-M, Forest J-C. Previous hypertensive disease of pregnancy is associated with alterations of markers of insulin resistance. Hypertension 2007; 49: 1056–62.
6. Wallis AB, Saftlas AF, Hsia J et al. Secular trends in the rates of pre-eclampsia, eclampsia, and gestational hypertension, United States, 1987–2004. Am J Hypertens 2008; 21: 521–6.
7. Khan KS, Wojdyla D, Say L et al. WHO analysis of causes of maternal death: a systematic review. Lancet 2006; 367 (9516): 1066–74.
8. Myatt L. Role of placenta in pre-eclampsia. Endocrine 2002; 19: 103–11.
9. Lambert G, Brichant JF, Hartstein G et al. Pre-eclampsia: An update. Acta Anaesthesiol Belg 2014; 65: 137–49.
10. Zhou Y, Damsky CH, Chiu K et al. Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts. J Clin Invest 1993; 91: 950–60.
11. Damsky CH, Fitzgerald ML, Fisher SJ. Distribution patterns of extracellular matrix components and adhesion receptors are intricately modulated during first trimester cytotrophoblast differentiation along the invasive pathway, in vivo. J Clin Invest 1992; 89: 210–22.
12. Robertson WB, Brosens I, Dixon G. Uteroplacental vascular pathology. Eur J Obstet Gynecol Reprod Biol 1975; 5: 47–65.
13. Zhou Y, Damsky CH, Fisher SJ. Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype: one cause of defective endovascular invasion in this syndrome? J Clin Invest 1997; 99: 2152–64.
14. Daayana S, Baker P, Crocker I. An image analysis technique for the investigation of variations in placental morphology in pregnancies complicated by preeclampsia with and without intrau-terine growth restriction. J Soc Gynecol Investig 2004; 11: 545–52.
15. Mayhew TM, Wijesekara J, Baker PN, Ong SS. Morphometric evidence that villous development and fetoplacental angiogenesis are compromised by intrauterine growth re-striction but not by pre-eclampsia. Placenta 2004; 25: 829–33.
16. Egbor M, Ansari T, Morris N et al. Pre-eclampsia and fetal growth restriction: How morphometrically different is the placenta? Placenta 2006; 27: 727–34.
17. Corrêa RRM, Gilio DB, Cavellani CL et al. Placental morphometrical and histopathology changes in the different clinical presentations of hypertensive syndromes in pregnancy. Arch Gynecol Obstet 2008; 277: 201–6.
18. Ducray JF, Naicker T, Moodley J. Pilot study of comparative placental morphometry in pre-eclamptic and normotensive pregnancies suggests possible maladaptations of the fetal component of the placenta. Eur J Obstet Gynecol Reprod Biol 2011; 156: 29–34.
19. Odibo AO, Zhong Y, Longtine M et al. First-trimester serum analytes, biophysical tests and the association with pathological morphometry in the placenta of pregnancies with preeclampsia and fetal growth restriction. Placenta 2011; 32: 333–8.
20. Mukherjee R. Morphometric evaluation of preeclamptic placenta using light microscopic images. Bio Med Res Int 2014; 1: 293690. DOI:10.1155/2014/293690
21. Güven D, Altunkaynak BZ, Altun G et al. Histomorphometric changes in the placenta and umbilical cord during complications of pregnancy. Biotech Histochem 2018; 93: 198–210.
22. Mayhew T.M. Fetoplacental angiogenesis during gestation is biphasic, longitudinal and occurs by proliferation and remodelling of vascular endothelial cells. Placenta 2002; 23: 742–50.
23. Stanek J. Acute and chronic placental membrane hypoxic lesions. Virchows Arch 2009; 455: 315–22.
24. Lyapin V.M., Tumanova U.N., Shegolev A.I. Cincitialnye uzelki v vorsinah placenty pri preeklampsii. Sovrem. problemy nauki i obrazovaniya. 2015; 4: 499. [in Russian]
25. Lyapin V.M., Tumanova U.N., Shegolev A.I. Horionicheskie kisty v placente pri preeklampsii. Sovrem. problemy nauki i obrazovaniya. 2015; 5: 163. [in Russian]
26. Shegolev A.I. Sovremennaya morfologicheskaya klassifikaciya povrezhdenij placenty. Akusherstvo i ginekologiya. 2016; 4: 16–23. [in Russian]
27. Milovanov A.P. Patologiya sistemy mat–placenta–plod. M.: Medicina, 1999. [in Russian]
28. Silasi M, Cohen B, Karumanchi S, Rana S. Abnormal placentation, angiogenic factors, and the pathogenesis of preeclampsia. Obstet Gynecol Clin N Am 2010; 37: 239–53.
29. Charnock-Jones DS, Kaufmann P, Mayhew TM. Aspects of human fetoplacental vasculogenesis and angiogenesis. I. Molecular regulation. Placenta 2004; 25: 103–13.
30. Pavlov K.A., Dubova E.A., Shegolev A.I. Fetoplacentarnyj angiogenez pri normalnoj beremennosti: rol sosudistogo endotelialnogo faktora rosta. Akusherstvo i ginekologiya. 2011; 3: 11–6. [in Russian]
31. Pavlov K.A., Dubova E.A., Shegolev A.I. Fetoplacentarnyj angiogenez pri normalnoj beremennosti: rol placentarnogo faktora rosta i angiopoetinov. Akusherstvo i ginekologiya. 2010; 6: 10–15. [in Russian]
32. Kurz H, Wilting J, Sandau K, Christ B. Automated evaluation of angiogenic effects mediated by VEGF and PlGF homo- and heterodimers. Microvasc Res 1998; 55: 92–102.
33. Livingston JC, Chin R, Haddad B et al. Reductions of vascular endothelial growth factor and placental growth factor concentrations in severe preeclampsia. Am J Obstet Gynecol 2000; 183: 1554–7.
34. Tripathi R, Rath G, Ralhan R et al. Soluble and membranous vascular endothelial growth factor receptor-2 in pregnancies complicated by pre-eclampsia. Yonsei Med J 2009; 50: 656–66.
35. Dubova E.A., Pavlov K.A., Lyapin V.M. i dr. Faktor rosta endoteliya sosudov i ego receptory v vorsinah placenty beremennyh s preeklampsiej. Byul. eksperim. biologii i mediciny. 2012; 12: 761–5. [in Russian]
36. Maynard SE, Min JY, Merchan J et al. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J Clin Invest 2003; 111: 649–58.
37. Ahmad S, Ahmed A. Elevated placental soluble vascular endothelial growth factor receptor-1 inhibits angiogenesis in preeclampsia. Circ Res 2004; 95: 884–91.
38. Ahmad S, Hewett PW, Al-Ani B et al. Autocrine activity of soluble Flt-1 controls endothelial cell function and angiogenesis. Vasc Cell 2011; 3: 15. DOI: 10.1186/2045-824X-3-15
39. Shegolev A.I., Dubova E.A., Pavlov K.A. i dr. Morfometricheskaya harakteristika terminalnyh vorsin placenty pri preeklampsii. Byul. eksperim. biologii i mediciny. 2012; 7: 104–7. [in Russian]
40. Ihle BU, Long P, Oats J. Early onset preeclampsia: recognition of underlying renal disease. Br Med J 1987; 294: 79–81.
41. Obed SA, Aniteye P. Birth weight and ponderal index in preeclampsia: a comparative study. Ghana Medical J 2006; 40: 8–13.
42. Hodzhaeva Z.S., Shmakov R.G., Kogan E.A. i dr. Kliniko-anamnesticheskie osobennosti, placenta i placentarnaya ploshadka pri rannej i pozdnej preeklampsii. Akusherstvo i ginekologiya. 2015; 4: 25–31. [in Russian]
43. Dissanayake VH, Samarasinghe HD, Morgan L et al. Morbidity and mortality associated with preeclampsia at two tertiary care hospitals in Sri Lanka. J Obstet Gynecol Res 2007; 33: 56–62.
44. Egbor M, Ansari T, Morris N et al. Morphometric placental villous and vascular abnormalities in early- and late-onset pre-eclampsia with and without fetal growth restriction. BJOG 2006; 113: 580–9.
45. Shegolev A.I., Lyapin V.M., Tumanova U.N. i dr. Gistologicheskie izmeneniya placenty i vaskulyarizaciya ee vorsin pri rannej i pozdnej preeklampsii. Arh. patologii. 2016; 1: 13–8. [in Russian]
46. Vodneva D.N., Romanova V.V., Dubova E.A. i dr. Kliniko-morfologicheskie osobennosti rannej i pozdnej preeklampsii. Akusherstvo i ginekologiya. 2014; 2: 35–40. [in Russian]
47. Wikstrom AK, Larrson A, Eriksson UJ et al. Early postpartum changes in circulating pro- and anti-angiogenic factors in early-onset and late-onset preeclampsia. Acta Obstet Gynecol 2008; 87: 146–153.
48. Hernandez-Diaz S, Toh S, Cnattingius S. Risk of preeclampsia in first and subsequent pregnancies: prospective cohort study. BMJ 2009; 338: 1–5.
49. Crispi F, Llurba E, Dominguez C et al. Predictive value of angiogenic factors and uterine artery Doppler for early- versus late-onset preeclampsia and intrauterine growth restriction. Ultrasound Obstet Gynecol 2008; 31: 303–9.
Авторы
А.И.Щеголев*, У.Н.Туманова, В.М.Ляпин
ФГБУ «Национальный медицинский исследовательский центр акушерства, гинекологии и перинатологии им. акад. В.И.Кулакова» Минздрава России. 117997, Россия, Москва, ул. Академика Опарина, д. 4
*ashegolev@oparina4.ru
________________________________________________
A.I.Shchegolev*, U.N.Tumanova, V.M.Lyapin
V.I.Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Akademika Oparina, d. 4
*ashegolev@oparina4.ru