Obstetrics and GynecologyObstetrics and GynecologyАкушерство и гинекология0300-90922412-5679Bionika Media247512ArticlesСтатьиReview ArticlePATHOGENETIC ASPECTS OF PREECLAMPSIAПАТОГЕНЕТИЧЕСКИЕ АСПЕКТЫ ПРЕЭКЛАМПСИИBorisDaiana A.БорисДаяна Амоновна

the resident

клинический ординатор

dayana_boris@mail.ruKanNatalia E.КанНаталья Енкыновна

PhD, MD, the head of the obstetric observation department

д.м.н., зав. акушерским обсервационным отделением

kan-med@mail.ruTyutyunnikVictor L.ТютюнникВиктор Леонидович

PhD, MD, the head of the obstetric physiological department

д.м.н., зав. акушерским физиологическим отделением

tioutiounnik@mail.ruKhovkhaevaPetimat A.ХовхаеваПетимат Ахмедовна

the postgraduate student

аспирант

p_hovhaeva@oparina4.ruResearch Center of Obstetrics, Gynecology, and Perinatology, Ministry of Health of RussiaФГБУ Научный центр акушерства, гинекологии и перинатологии им. академика В.И. Кулакова Минздрава России1512201512NO12 (2015)№12 (2015)111518022023Copyright ©; 2015, Bionika MediaCopyright ©; 2015, ООО «Бионика Медиа»2015Bionika MediaООО «Бионика Медиа»https://journals.eco-vector.com/0300-9092/article/view/247512

Objective. To provide an update on pathogenetic mechanisms for the development of preeclampsia. Material and methods. Literature sources published in the Medline, Pubmed, and other databases were sought. A total of 277 sources on the study of the pathogenesis of preeclampsia at the ultrastructural level were found; 49 of them were included in this review. Results. The preclinical phase of preeclampsia is associated with immunological, molecular, and epigenetic disorders causing structural and functional changes at the cellular and subcellular levels. The study of the problem at the ultrastructural level will be able to diagnose the pathological process at an early stage, to effectively perform prophylaxis, and to reduce maternal and perinatal morbidity rates associated with preeclampsia. Conclusion. The early diagnosis of preeclampsia has not been fully studied. There is a need for further investigation in this area.

Цель исследования. Представить современные данные о патогенетических механизмах развития преэклампсии. Материал и методы. Проведен поиск литературных источников, опубликованных в базе данных Medline, Pubmed и др. Было найдено 277 источников, посвященных изучению патогенеза преэклампсии на ультраструктурном уровне, из которых 49 были включены в данный обзор. Результаты. Доклинический этап развития преэклампсии ассоциирован с иммунологическими, молекулярно-генетическими и эпигенетичесими нарушениями, приводящими к структурным и функциональным изменениям на клеточном и субклеточном уровнях. Изучение проблемы на ультраструктурном уровне позволит диагностировать патологический процесс на раннем этапе, эффективно проводить профилактику и снизить показатели материнской и перинатальной заболеваемости, ассоциированные с преэклампсией. Заключение. Вопрос о ранней диагностике преэклампсии до конца не изучен. Необходимо проводить дальнейшие исследования в этой области.

preeclampsiaimmunological tolerancetrophoblast invasionoxidative stressmitochondrial dysfunctionпреэклампсияиммунологическая толерантностьинвазия трофобластаоксидативный стрессмитохондриальная дисфункцияSibai B., Dekker G., Kupferminc M. Pre-eclampsia. Lancet. 2005; 365(9461): 785-99.Genest D.S., Falcao S., Gutkowska J., Lavoie J.L. Impact of exercise training on preeclampsia: potential preventive mechanisms. Hypertension. 2012; 60(5): 1104-9.Mayeur S., Lancel S., Theys N., Lukaszewski M.A., Duban-Deweer S., Bastide B. et al. Maternal calorie restriction modulates placental mito chondrial biogenesis and bioenergetic efficiency: putative involvement in fetoplacental growth defects in rats. Am. J. Physiol. Endocrinol. Metab. 2013; 304(1): Е14-22.Poston L., Igosheva N., Mistry H.D., Seed P.T., Shennan A.H., Rana S. et al. Role of oxidative stress and antioxidant supplementation in pregnancy disorders. Am. J. Clin. Nutr. 2011; 94(6, Suppl.): 1980S-5S.Burton G.J., Jauniaux E. Oxidative stress. Best Pract. Res. Clin. Obstet. Gynaecol. 2011; 25(3): 287-99.Haram K., Svendsen E., Abildgaard U. The HELLP syndrome: clinical issues and management. A review. BMC Pregnancy Childbirth. 2009; 9: 8.Савельева Г.М., Шалина Р.И., Курцер М.А., Штабницкий А.М., Куртенок Н.В., Коновалова О.В. Эклампсия в современном акушерстве. Aкушерство и гинекология. 2010; 6: 4-9.Khong Y., Brosens I. Defective deep placentation. Best Pract. Res. Clin. Obstet. Gynaecol. 2010; 25(3): 301-11.NICE Clinical guideline CG107: Hypertension in Pregnancy: the management of hypertensive disorders during pregnancy. Surveillance proposal GE document, 2015. 71 p. Available at: https://www.nice.org.uk/guidance/cg107/ resources/cg107-hypertension-in-pregnancy-surveillance-review-decision-march-20153Redman C.W., Sargent I.L. Placental stress and pre-eclampsia: a revised view. Placenta. 2009; 30(Suppl.A): S38-42.Ходжаева З.С., Шмаков Р.Г., Коган Е.А., Щеголев А.И., Клименченко Н.И., Акатьева А.С., Вавина О.В., Воднева Д.Н., Романова В.В., Сухих Г.Т. Клинико-анамнестические особенности, плацента и плацентарная площадка при ранней и поздней преэклампсии. Aкушерство и гинекология. 2015; 4: 25-31.Duley L. The global impact of pre-eclampsia and eclampsia. Semin. Perinatol. 2009; 33(3): 130-7.Savaj S., Vaziri N. An overview of recent advances in pathogenesis and diagnosis of preeclampsia. Iran. J. Kidney Dis. 2012; 6(5): 334-8.Bell M.J. Historical overview of preeclampsia-eclampsia. J. Obstet. Gynecol. Neonatal Nurs. 2010; 39(5): 510-8.Huppertz B. Placental origins of preeclampsia: challenging the current hypothesis. Hypertension. 2008; 51(4): 970-5.Patni S., Wynen L.P., Seager A.L., Morgan G., White J.O., Thornton C.A. Expression and activity of Toll-like receptors 1-9 in the human term placenta and changes associated with labor at terme. Biol. Reprod. 2009; 80(2): 243-8.Roberts J.M., Hubel C. The two stage model of preeclampsia: variations on the them. Placenta. 2009; 30(Suppl.A): S32-7.Chandra A., Surti N., Kesavan S., Agarwal A. Significance of oxidative stress in human reproduction. Arch. Med. Sci. 2009; 5(1A): S28-42.Fournier T., Thérond P., Handschuh K., Tsatsaris V., Evain-Brion D. PPARgamma and early human placental development. Curr. Med. Chem. 2008; 15(28): 3011-24.Shah D.M. Preeclampsia: new insights. Curr. Opin. Nephrol. Hypertens. 2007; 16(3): 213-20.Burton G.J., Woods A.W., Jauniaux E., Kingdom J.C. Rheological and physiological consequences of conversion of the maternal spiral arteries for uteroplacental blood flow during human pregnancy. Placenta. 2009; 30(6): 473-82.Geusens N., Verlohren S., Luyten C., Taube M., Hering L., Vercruysse L. et al. Endovascular trophoblast invasion, spiral artery remodelling and uteroplacental haemodynamics in a transgenic rat model of pre-eclampsia. Placenta. 2008; 29(7): 614-23.Espinoza J., Romero R., Mee Kim Y., Kusanovic J.P., Hassan S., Erez O. et al. Normal and abnormal transformation of the spiral arteries during pregnancy. J. Perinat. Med. 2006; 34(6): 447-58.Collins S.L., Stevenson G.N., Noble J.A., Impey L. Developmental changes in spiral artery blood flow in the human placenta observed with colour Doppler ultrasonography. Placenta. 2012; 33(10): 782-7.Soto E., Romero R., Kusanovic J.P., Ogge G., Hussein Y., Yeo L. et al. Late-onset preeclampsia is associated with an imbalance of angiogenic and anti-angiogenic factors in patients with and without placental lesions consistent with maternal underperfusion. J. Matern. Fetal Neonatal Med. 2012; 25(5): 498-507.Lunghi L., Ferretti M.E., Medici S., Biondi C., Vesce F. Control of human trophoblast function. Reprod. Biol. Endocrinol. 2007; 5: 6.Huppertz B., Kadyrov M., Kingdom J.C. Apoptosis and its role in the trophoblast. Am. J. Obstet. Gynecol. 2006; 195(1): 29-39.Hiden U., Bilban M., Knofler M., Desoye G. Kisspeptins and the placenta: regulation of trophoblast invasion. Rev. Endocr. Metab. Disord. 2007; 8(1): 31-9.Young B.C., Levine R.J., Karumanchi S.A. Pathogenesis of preeclampsia. Annu. Rev. Pathol. 2010; 5: 173-92.Beauséjour A., Bibeau K., Lavoie J.C., St-Louis J., Brochu M. Placental oxidative stress in a rat model of preeclampsia. Placenta. 2007; 28(1): 52-8.Li D., Wen X., Ghali L., Al-Shalabi F.M., Docherty S.M., Purkis P., Iles R.K. hCGß expression by cervical squamous carcinoma - in vivo histological association with tumor invasion and apoptosis. Histopathology. 2008; 53(2): 147-55.Lee J., Romero R., Xu Y., Miranda J., Yoo W., Chaemsaithong P. et al. Detection of anti-HLA antibodies in maternal blood in the second trimester to identify patients at risk of antibody-mediated maternal anti-fetal rejection and spontaneous preterm delivery. Am. J. Reprod. Immunol. 2013; 70(2): 162-75.Redman C.W., Sargent I.L. Immunology of pre-eclampsia. Am. J. Reprod. Immunol. 2010; 63(6): 534-43.Makrigiannakis A., Karamouti M., Drakakis P., Loutradis D., Antsaklis A. Fetomaternal immunotolerance. Am. J. Reprod. Immunol. 2008; 60(6): 482-96.Heyl W., Heintz B., Reister F., Harwig S., Witte K., Lemmer B., Rath W. Increased soluble VCAM-1 serum levels in preeclampsia are not correlated to urinary excretion or circadian blood pressure rhythm. J. Perinat. Med. 2005; 33(2): 144-8.Smith G. First-trimester determination of complications of late pregnancy. JAMA. 2010; 303(6): 561-2.Mehendale R., Hibbard J., Fazleabas A., Leach R. Placental angiogenesis markers sFlt-1 and PlGF: response to cigarette smoke. Am. J. Obstet. Gynecol. 2007; 197(4): 363. e1-5.Shibata E., Rajakumar A., Powers R.W., Larkin R.W., Gilmour C., Bodnar L.M. et al. Soluble fms-like tyrosine kinase 1 is increased in preeclampsia but not in normotensive pregnancies with small-for-gestational-age neonates: relationship to circulating placental growth factor. J. Clin. Endocrinol. Metab. 2005; 90(8): 4895-903.Mutter W.P., Karumanchi S.A. Molecular mechanisms of preeclampsia. Microvasc. Res. 2008; 75(1): 1-8.Wu F.T., Stefanini M.O., Mac Gabhann F., Kontos C.D., Annex B.H., Popel A.S. A systems biology perspective on sVEGFR1: its biological function, pathogenic role and therapeutic use. J. Cell. Mol. Med. 2010; 14(3): 528-52.Myatt L. Reactive oxygen and nitrogen species and functional adaptation of the placenta. Placenta. 2010; 31(Suppl.): 66-9.Crimi M., Rigolio R. The mitochondrial genome, a growing interest inside an organelle. Int. J. Nanomed. 2008; 3(1): 51-7.Wallace D.C. Mitochondrial DNA mutations in disease and aging. Environ. Mol. Mutagen. 2010; 51(5): 440-50.Heazell A.E., Lacey H.A., Jones C.J., Huppertz B., Baker PN., Crocker I.P Effects of oxygen on cell turnover and expression of regulators of apoptosis in human placental trophoblast. Placenta. 2008; 29(2): 175-86.Chen Q., Stone P., Ching L.M., Chamley L. A role for interleukin-6 in spreading endothelial cell activation after phagocytosis of necrotic trophoblastic material: implications for the pathogenesis of pre-eclampsia. J. Pathol. 2009; 217(1): 122-30.Jauniaux E., Hempstock J., Greenwold N., Burton G.J. Trophoblastic oxidative stress in relation to temporal and regional differences in maternal placental blood flow in normal and abnormal early pregnancies. Am. J. Pathol. 2003; 162(1): 115-25.Panda B., Panda A., Ueda I., Abrahams V.M., Norwitz E.R., Stanic A.K. et al. Dendritic cells in the circulation of women with preeclampsia demonstrate a pro-inflammatory bias secondary to dysregulation of TLR receptors. J. Reprod Immunol. 2012; 94(2): 210-5.Burton G.J., Jones C.J. Syncytial knots, sprouts, apoptosis, and trophoblast deportation from the human placenta. Taiwan J. Obstet. Gynecol. 2009; 48(1): 28-37.