Pathophysiology of Placenta in Antiphospholipid Syndrome

A. Bobircă, A. Dumitrache, Cristina Alexandru, A. Florescu, George Ciobotaru, F. Bobircă, R. Sima, C. Poalelungi, M. Bojincă, I. Ancuta
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引用次数: 1

Abstract

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by clinical manifestations caused by arterial or venous thrombosis and pregnancy conditions such as recurrent miscarriage, fetal death, or premature birth in the presence of antiphospholipid antibodies. The obstetrical manifestations are strongly related to the placental alterations. The aim of this review is to summarize the latest data on pathophysiology of obstetrical APS, emphasizing the disturbance of the placentation process. Due to a lack of extravillous trophoblasts to properly reconstruct the spiral arteries, APS causes hypoxic or ischemic injury or high-speed blood flow that damages the placenta. This results in decreased or interrupted maternal blood flow to the placenta and a lack of nutrients for the fetus. Antiphospholipid antibodies can lower the proliferation and infiltration of the extravillous trophoblasts. The placental mal-perfusion causes the release of antiangiogenic substances such as soluble fms-like tyrosine kinase-1 and soluble endoglin. Placental growth factor and vascular endothelial growth factor (VEGF) may be sequestered by sFlt1 and blocked from binding to trophoblast and endothelial cell VEGF receptors, inhibiting their proangiogenic effects. Preeclampsia is the clinical result from a lack of angiogenic factors needed for endothelial vascular homeostasis due to an excess of sFlt1 in the maternal circulation.
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抗磷脂综合征胎盘病理生理学研究
抗磷脂综合征(APS)是一种自身免疫性疾病,其特征是由动脉或静脉血栓形成和妊娠条件引起的临床表现,如反复流产、胎儿死亡或在存在抗磷脂抗体的情况下早产。产科表现与胎盘改变密切相关。这篇综述的目的是总结产科APS的病理生理学的最新数据,强调胎盘形成过程的紊乱。由于缺乏绒毛外滋养层来正确重建螺旋动脉,APS会导致缺氧或缺血性损伤或高速血流损伤胎盘。这导致母亲流向胎盘的血液减少或中断,胎儿缺乏营养。抗磷脂抗体可降低绒毛外滋养层细胞的增殖和浸润。胎盘灌注不良导致抗血管生成物质的释放,如可溶性fms样酪氨酸激酶-1和可溶性endoglin。胎盘生长因子和血管内皮生长因子(VEGF)可被sFlt1隔离,并阻止其与滋养层和内皮细胞VEGF受体结合,抑制其促血管生成作用。先兆子痫是由于母体循环中sFlt1过量而缺乏内皮血管稳态所需的血管生成因子的临床结果。
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