葡萄胎中的血管生成功能障碍。
Angiogenic dysfunction in molar pregnancy.
机构信息
Department of Obstetrics and Gynecology, The Pritzker School of Medicine, University of Chicago, Chicago, IL, USA.
出版信息
Am J Obstet Gynecol. 2010 Feb;202(2):184.e1-5. doi: 10.1016/j.ajog.2009.09.005.
Abstract
OBJECTIVE
Molar pregnancy is associated with very early-onset preeclampsia. Since excessive circulating antiangiogenic factors may play a pathogenic role in preeclampsia, we hypothesized that molar placentas produce more antiangiogenic proteins than normal placentas.
STUDY DESIGN
This retrospective case-control study used a semiquantitative immunohistochemical technique to compare histologic sections of molar placentas to normal controls. Tissue slides were treated with 2 antisera: one recognized the antiangiogenic markers fms-like tyrosine kinase receptor 1 (Flt1) and its soluble form (sFlt1), while the other recognized vascular endothelial marker CD31. Stain intensity was graded from 1+ (strong focal staining) to 4+ (91-100% staining).
RESULTS
Molar placentas (n = 19) showed significantly more staining than controls (n = 16) for Flt/sFlt1 (P < .0001).
CONCLUSION
There was a significant difference in Flt1/sFlt1 immunostaining intensity when molar placentas were compared to controls. This supports a hypothesis that the phenotype of preeclampsia in molar pregnancy may result from trophoblasts overproducing at least 1 antiangiogenic protein.
摘要
目的
葡萄胎与极早期先兆子痫有关。由于过多的循环抗血管生成因子可能在先兆子痫中起致病作用，我们假设葡萄胎胎盘比正常胎盘产生更多的抗血管生成蛋白。
研究设计
本回顾性病例对照研究使用半定量免疫组织化学技术比较葡萄胎胎盘和正常对照的组织切片。组织载玻片用 2 种抗血清处理：一种识别抗血管生成标记物 fms 样酪氨酸激酶受体 1（Flt1）及其可溶性形式（sFlt1），另一种识别血管内皮标记物 CD31。染色强度从 1+（强局灶性染色）到 4+（91-100%染色）。
结果
葡萄胎胎盘（n = 19）的 Flt/sFlt1 染色强度明显高于对照组（n = 16）（P <.0001）。
结论
与对照组相比，葡萄胎胎盘的 Flt1/sFlt1 免疫染色强度存在显著差异。这支持了这样一种假设，即葡萄胎先兆子痫的表型可能是由于滋养细胞过度产生至少 1 种抗血管生成蛋白所致。
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本文引用的文献
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Elevated serum soluble fms-like tyrosine kinase 1 (sFlt1) level in women with hydatidiform mole.血清可溶性 fms 样酪氨酸激酶 1 水平升高与葡萄胎妇女
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