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中华产科急救电子杂志 ›› 2023, Vol. 12 ›› Issue (02) : 65 -70. doi: 10.3877/cma.j.issn.2095-3259.2023.02.001

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妊娠期易栓症的病因学研究
王乐乐, 刘慧姝()   
  1. 510623 广州市妇女儿童医疗中心产科
  • 收稿日期:2022-06-06 出版日期:2023-05-18
  • 通信作者: 刘慧姝

Pathogenesis of thrombophilia in pregnancy

Lele Wang, Huishu Liu()   

  • Received:2022-06-06 Published:2023-05-18
  • Corresponding author: Huishu Liu
引用本文:

王乐乐, 刘慧姝. 妊娠期易栓症的病因学研究[J/OL]. 中华产科急救电子杂志, 2023, 12(02): 65-70.

Lele Wang, Huishu Liu. Pathogenesis of thrombophilia in pregnancy[J/OL]. Chinese Journal of Obstetric Emergency(Electronic Edition), 2023, 12(02): 65-70.

妊娠期易栓症分为遗传性和获得性。遗传性易栓症病因学涉及参与凝血、纤溶过程的因子发生遗传学改变,它与不良妊娠结局间的关系暂不明确;获得性易栓症主要是抗磷脂综合征,抗磷脂抗体谱作为疾病发生的核心因素,能够诱导多种细胞、炎症和补体系统的激活,促进血栓形成及不良妊娠结局的发生。本文就妊娠期易栓症的病因学研究进行论述。

Thrombophilia in pregnancy includes both inherited and acquired. Hereditary thrombophilia involves changes in the factors involved in coagulation and fibrinolysis due to genetic alterations, and their relationship with adverse pregnancy outcomes is still unclear. The acquired thrombophilias are mainly associated with antiphospholipid syndrome, in which the spectrum of antiphospholipid antibodies play a key role in the pathogenesis of the disease, inducing activation of various cells, inflammation and the complement system, leading to the occurrence of thrombosis and adverse pregnancy outcomes. This article reviews the pathogenesis of thrombophilia in pregnancy.

[1]
中华医学会血液学分会血栓与止血学组. 易栓症诊断与防治中国指南(2021年版)[J]. 中华血液学杂志202142(11):881-888.
[2]
Lefkou E, Parmar K, Mamopoulos A, et al. Peripartum Haemostatic Changes in Women in Labour[J]. Blood2008112(11):1-2.
[3]
American College of Obstetricians and Gynecologists′ Committee on Practice Bulletins-Obstetrics. ACOG practice bulletin No. 197: inherited thrombophilias in pregnancy[J]. Obstet Gynecol2018132(1):e18-e34.
[4]
Herrmann FH, Koesling M, Schrǒder W, et al. Prevalence of factor V Leiden mutation in various populations[J]. Genet Epidemiol199714(4):403-411.
[5]
Tam WH, Ng MH, Yiu AK, et al. Thrombophilia among Chinese women with venous thromboembolism during pregnancy[J]. Gynecol Obstet Invest201273 (3):183-188.
[6]
Shen MC, Lin JS, Tsay W. High prevalence of antithrombin Ⅲ,protein C and protein S deficiency, but no factor V Leiden mutation in venous thrombophilic Chinese patients in Taiwan[J]. Thromb Res199787 (4):377-385.
[7]
Stenflo J. A new vitamin K-dependent protein: purification from bovine plasma and preliminary characterization[J]. J Biol Chem1976251(2):355-363.
[8]
Dinarvand P, Moser KA. Protein C deficiency[J]. Arch Pathol Lab Med2019143(10):1281-1285.
[9]
Di Scipio RG, Hermodson MA, Yates SG, et al. A comparison of human prothrombin, factor IX (Christmas factor), factor X (Stuart factor), and protein S[J]. Biochemistry197716(4):698-706.
[10]
Gierula M, Ahnström J. Anticoagulant protein S-New insights on interactions and functions[J]. J Thromb Haemost202018 (11):2801-2811.
[11]
中华医学会围产医学分会. 产科抗磷脂综合征诊断与处理专家共识[J]. 中华围产医学杂志202023(8):517-522.
[12]
Esteve-Valverde E, Ferrer-Oliveras R, Alijotas-Reig J. Obstetric antiphospholipid syndrome[J]. Rev Clin Esp2015216(3):135-145.
[13]
Knight JS, Kanthi Y. Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome[J]. Semin Immunopathol202244 (3):347-362.
[14]
Cervera R, Serrano R, Pons-Estel GJ, et al. Morbidity and mortality in the antiphospholipid syndrome during a 10-year period: a multicentre prospective study of 1000 patients[J]. Ann Rheum Dis201574 (6):1011-1018.
[15]
Jørgensen M, Broholm R, Bækgaard N. Pregnancy after catheter-directed thrombolysis for acute iliofemoral deep venous thrombosis[J]. Phlebology201328 Suppl 1:34-38.
[16]
Antovic A, Bruzelius M. Impaired fibrinolysis in the antiphospholipid syndrome[J]. Semin Thromb Hemost202147(5):506-511.
[17]
Zhang W, Gao F, Lu D, et al. Anti-β2 glycoproteinⅠantibodies in complex with β2 glycoproteinⅠinduce platelet activation via two receptors: apolipoprotein E receptor 2′ and glycoproteinⅠbα[J]. Front Med201610(1):76-84.
[18]
Bondanza A, Sabbadini MG, Pellegatta F, et al. Anti-β2 glycoproteinⅠantibodies prevent the De-activation of platelets and sustain their phagocytic clearance[J]. J Autoimmun200015(4):469-477.
[19]
Engelmann B, Massberg S. Thrombosis as an intravascular effector of innate immunity[J]. Nat Rev Immunol201313(1):34-45.
[20]
Tambralli A, Gockman K, Knight JS. NETs in APS: current knowledge and future perspectives[J]. Curr Rheumatol Rep202022(10):1-12.
[21]
Yalavarthi S, Gould TJ, Rao AN, et al. Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome[J]. Arthritis Rheumatol201567 (11):2990-3003.
[22]
Sule G, Kelley WJ, Gockman K, et al. Increased adhesive potential of antiphospholipid syndrome neutrophils mediated by beta-2 integrin Mac-1[J]. Arthritis Rheumatol202072(1):114-124.
[23]
Branch DW, Dudley DJ, Mitchell MD, et al. Immunoglobulin G fractions from patients with antiphospholipid antibodies cause fetal death in BALB/c mice: a model for autoimmune fetal loss[J]. Am J Obstet Gynecol1990163(1 Pt 1):210-216.
[24]
Oku K, Atsumi T, Bohgaki M, et al. Complement activation in patients with primary antiphospholipid syndrome[J]. Ann Rheum Dis200968(6):1030-1035.
[25]
Ritis K, Doumas M, Mastellos D, et al. A novel C5a receptor-tissue factor cross-talk in neutrophils links innate immunity to coagulation pathways[J]. J Immunol2006177(7):4794-4802.
[26]
Wolberg AS, Roubey RA. Mechanisms of autoantibody-induced monocyte tissue factor expression[J]. Thromb Res2004114(5-6):391-396.
[27]
Müller-Calleja N, Ritter S, Hollerbach A, et al. Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies[J]. Blood Adv20182(9):979-986.
[28]
Sciascia S, Amigo MC, Roccatello D, et al. Diagnosing antiphospholipid syndrome: 'extra-criteria’ manifestations and technical advances[J]. Nat Rev Rheumatol201713(9):548-560.
[29]
Di Simone N, Meroni PL, de Papa N, et al. Antiphospholipid antibodies affect trophoblast gonadotropin secretion and invasiveness by binding directly and through adhered β2-glycoproteinⅠ[J]. Arthritis Rheum200043(1):140-150.
[30]
Carroll TY, Mulla MJ, Han CS, et al. Modulation of trophoblast angiogenic factor secretion by antiphospholipid antibodies is not reversed by heparin[J]. Am J Reprod Immunol201166(4):286-296.
[31]
Di Simone N, Di Nicuolo F, D′Ippolito S, et al. Antiphospholipid antibodies affect human endometrial angiogenesis[J]. Biol Reprod201083(2):212-219.
[32]
Quenby S, Mountfield S, Cartwright JE, et al. Antiphospholipid antibodies prevent extravillous trophoblast differentiation[J]. Fertil Steril200583(3):691-698.
[33]
Mulla MJ, Brosens JJ, Chamley LW, et al. Antiphospholipid antibodies induce a pro-inflammatory response in first trimester trophoblast via the TLR4/MyD88 pathway[J]. Am J Reprod Immunol200962(2):96-111.
[34]
Gysler SM, Mulla MJ, Guerra M, et al. Antiphospholipid antibody-induced miR-146a-3p drives trophoblast interleukin-8 secretion through activation of Toll-like receptor 8[J]. Mol Hum Reprod201622(7):465-474.
[35]
Mulla MJ, Weel IC, Potter JA, et al. Antiphospholipid antibodies inhibit trophoblast Toll-like receptor and inflammasome negative regulators[J]. Arthritis Rheumatol201870(6):891-902.
[36]
Ramesh S, Morrell CN, Tarango C, et al. Antiphospholipid antibodies promote leukocyte-endothelial cell adhesion and thrombosis in mice by antagonizing eNOS via β2GPI and apoER2[J]. J Clin Invest2010121(1):120-131.
[37]
Kim MY, Guerra MM, Kaplowitz E, et al. Complement activation predicts adverse pregnancy outcome in patients with systemic lupus erythematosus and/or antiphospholipid antibodies[J]. Ann Rheum Dis20187(4):549-555.
[38]
Cohen D, Buurma A, Goemaere NN, et al. Classical complement activation as a footprint for murine and human antiphospholipid antibody-induced fetal loss[J]. J Pathol2011225(4):502-511.
[39]
Holers VM, Girardi G, Mo L, et al. Complement C3 activation is required for antiphospholipid antibody-induced fetal loss[J]. J Exp Med2002195(2):211-220.
[40]
Girardi G, Berman J, Redecha P, et al. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome[J]. J Clin Invest2003112(11):1644-1654.
[41]
Marder W, Knight JS, Kaplan MJ, et al. Placental histology and neutrophil extracellular traps in lupus and pre-eclampsia pregnancies[J]. Lupus Sci Med20163(1):1-9.
[42]
Lu Y, Dong Y, Zhang Y, et al. Antiphospholipid antibody-activated NETs exacerbate trophoblast and endothelial cell injury in obstetric antiphospholipid syndrome[J]. J Cell Mol Med202024(12):6690-6703.
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