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结构性毛细血管稀疏与子痫前期的发生。

Structural capillary rarefaction and the onset of preeclampsia.

机构信息

Blood Pressure Unit, Department of Clinical Sciences, St George's, University of London, London, United Kingdom.

出版信息

Obstet Gynecol. 2012 May;119(5):967-74. doi: 10.1097/AOG.0b013e31824ea092.

Abstract

OBJECTIVE

To estimate if reduced capillary density (ie, capillary rarefaction) precedes the onset of preeclampsia and if it could play a role in its pathogenesis. Capillary rarefaction is a consistent finding in essential hypertension.

METHODS

In this longitudinal cohort study, we recruited 322 consecutive white women, of whom 305 women completed the study. We used intravital video microscopy to measure basal (ie, functional) and maximal (ie, structural) skin capillary densities according to a well-validated protocol and measured plasma angiogenic and antiangiogenic factors. Women were studied at five consecutive predetermined visits.

RESULTS

Preeclampsia occurred in 16 women (mean onset at 35.6±4.8 weeks of gestation), 272 women had normal pregnancies, eight had hypertension, and nine pregnancies were complicated by intrauterine growth restriction. In women with a normal pregnancy, significant reduction in maximal capillary density occurred at 27-32 weeks but had resolved by the puerperium. In contrast, in women who later developed preeclampsia, structural rarefaction was greater and occurred earlier at 20-24 weeks of gestation and persisted into the puerperium. We also found that the change in soluble Endoglin from 11-16 weeks of gestation to 27-32 weeks of gestation was significantly correlated with the change in structural capillary density.

CONCLUSION

Significant structural capillary rarefaction precedes the onset of preeclampsia and could play a role in its pathogenesis.

LEVEL OF EVIDENCE

II.

摘要

目的

评估毛细血管密度降低(即毛细血管稀疏)是否先于子痫前期的发生,以及它是否在其发病机制中起作用。毛细血管稀疏是原发性高血压的一个一致发现。

方法

在这项纵向队列研究中,我们招募了 322 名连续的白人女性,其中 305 名女性完成了研究。我们使用活体视频显微镜根据经过充分验证的方案测量基础(即功能)和最大(即结构)皮肤毛细血管密度,并测量血浆血管生成和抗血管生成因子。女性在五个连续的预定就诊中接受研究。

结果

16 名女性(平均发病时间为 35.6±4.8 周妊娠)发生子痫前期,272 名女性正常妊娠,8 名患有高血压,9 名妊娠合并宫内生长受限。在正常妊娠的女性中,最大毛细血管密度在 27-32 周时显著降低,但在产褥期已恢复。相比之下,后来发生子痫前期的女性结构稀疏更大,发生在 20-24 周妊娠时更早,并持续到产褥期。我们还发现,从 11-16 周妊娠到 27-32 周妊娠可溶性内皮糖蛋白的变化与结构毛细血管密度的变化显著相关。

结论

显著的结构毛细血管稀疏先于子痫前期的发生,并可能在其发病机制中起作用。

证据水平

II。

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