Pathophysiology of placenta creta: The role of decidua and extravillous trophoblast
Pathophysiology of placenta creta: The role of decidua and extravillous trophoblast
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DOI：
10.1016/j.placenta.2008.04.008
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发表时间：
2008-07-01
期刊：
影响因子：
3.8
通讯作者：
Parast, M. M.
中科院分区：
文献类型：
--
作者：
Tantbirojn, P.;Crum, C. P.;Parast, M. M.
胎盘植入与产后大出血有关，通常导致紧急子宫切除术。虽然胎盘植入的确切发病机制尚不清楚，但提出的假说包括原发性蜕膜缺陷、母体血管重塑异常、滋养层细胞过度侵入或其组合。为了评估这些变化在胎盘植入，我们回顾性分析了49例妊娠子宫切除术，其中38例诊断为胎盘植入，11例未诊断为胎盘植入，收集临床资料，并评估绒毛外滋养细胞的组织病理学。具体而言，我们评估了母体血管的血管内滋养层重塑，以及植入部位间质滋养层的形态和浸润深度。与对照组相比，Creta患者的血管重塑比例降低，许多血管显示部分生理性改变。Creta病例还显示子宫肌层更深处的血管重塑;然而，子宫肌层外大血管的血管重塑仅在Increta和Percreta病例中显示，而在非Creta和Accreta病例中均不存在。如前所述，间质滋养细胞侵入子宫壁的深度在胎盘克雷塔显着更大，但是，有克雷塔亚型之间没有显着差异。最后，Ki-67染色很少观察到绒毛外滋养细胞，除了在滋养细胞列的第一个三个月克瑞塔案件。因此，我们的结论是，胎盘植入的发病机制是多方面的，涉及增加，但不完全的滋养细胞浸润的背景下，没有蜕膜。我们进一步提出胎盘植入和胎盘渗透不是由于绒毛外滋养层进一步侵入子宫壁所致，而可能是继发于瘢痕裂开，导致子宫壁深处存在绒毛膜绒毛，从而使绒毛外滋养层更容易进入子宫深部肌层。(C)2008爱思唯尔有限公司版权所有。
Placenta creta is associated with massive postpartum hemorrhage and commonly leads to emergency hysterectomy. While the exact pathogenesis of placenta creta is unknown, proposed hypotheses include a primary deficiency of decidua, abnormal maternal vascular remodeling, excessive trophoblastic invasion, or a combination thereof. To assess these changes in placenta creta, we retrospectively reviewed 49 cases of gravid hysterectomy, 38 with and 11 without the diagnosis of creta, gathered clinical data, and evaluated histopathology of extravillous trophoblast. Specifically, we evaluated maternal vessels for remodeling by endovascular trophoblast, as well as the morphology and depth of invasion of interstitial trophoblast at the implantation site. Compared to controls, cases with creta had decreased proportion of remodeled vessels, with many vessels displaying partial physiologic change. Cases with creta also demonstrated vascular remodeling deeper in the myometrium; however, vascular remodeling of large outer myometrial vessels was only demonstrated in increta and percreta cases, and was absent in both non-creta and accreta. As previously reported, interstitial trophoblast invaded the uterine wall to a significantly greater depth in placenta creta; however, there was no significant difference between creta subtypes. Finally, Ki-67 staining was rarely observed in extravillous trophoblast, except in the trophoblast columns of first trimester creta cases. We, therefore, conclude that the pathogenesis of placenta creta is multi-dimensional, involving increased, but incomplete trophoblast invasion in a background of absent decidua. We further propose that placenta increta and percreta are not due to a further invasion of extravillous trophoblast in the uterine wall, rather they likely arise secondary to dehiscence of a sear, leading to the presence of chorionic villi deep within the uterine wall, and thus give extravillous trophoblast greater access to the deep myometrium. (C) 2008 Elsevier Ltd. All rights reserved.