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可溶性血管内皮钙黏蛋白水平与重度卵巢过度刺激综合征的临床和生物学特征相关。

Soluble vascular endothelial-cadherin levels correlate with clinical and biological aspects of severe ovarian hyperstimulation syndrome.

作者信息

Villasante A, Pacheco A, Pau E, Ruiz A, Pellicer A, Garcia-Velasco J A

机构信息

Instituto Valenciano de Infertilidad--Madrid, Rey Juan Carlos University, Santiago de Compostela 88, 28035 Madrid, Spain.

出版信息

Hum Reprod. 2008 Mar;23(3):662-7. doi: 10.1093/humrep/dem429. Epub 2008 Jan 23.

Abstract

BACKGROUND

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of ovarian stimulation, and the pathophysiological mechanisms that trigger the syndrome remain unknown. HCG increases serum vascular endothelial growth factor (VEGF) concentrations, and VEGF modulates transendothelial permeability via endothelial adherens junctions, a downstream target for VEGF signalling. We examined whether women with severe OHSS have altered serum levels of soluble vascular endothelial (sVE)-cadherin.

METHODS

We conducted a prospective, case-control study of 28 women with severe OHSS and 34 women undergoing controlled ovarian hyperstimulation (COH) for IVF without developing OHSS. We collected serum samples from both groups on the day of ovum retrieval (Day 0), and on Days 3, 6, 9 and 15. Samples were assayed for sVE-cadherin by enzyme-linked immunosorbent assay.

RESULTS

Women with severe OHSS had significantly higher levels of sVE-cadherin than patients without OHSS (P = 0.001). sVE-cadherin serum levels decreased with clinical improvement; however, they did not reach normal levels in the resolution phase. A positive correlation was demonstrated between sVE-cadherin and serum estradiol levels at the time of HCG administration (r = 0.621; P < 0.001). Serum sVE-cadherin levels were more closely chronologically correlated with corpus luteum function than with biological and clinical aspects of severe OHSS.

CONCLUSIONS

sVE-cadherin may be involved in the pathogenesis of severe OHSS and may possibly serve as an indicator of corpus luteum function after COH.

摘要

背景

卵巢过度刺激综合征(OHSS)是卵巢刺激的一种医源性并发症,引发该综合征的病理生理机制尚不清楚。人绒毛膜促性腺激素(HCG)可增加血清血管内皮生长因子(VEGF)浓度,而VEGF通过内皮黏附连接调节跨内皮通透性,内皮黏附连接是VEGF信号传导的下游靶点。我们研究了重度OHSS患者的血清可溶性血管内皮(sVE)-钙黏蛋白水平是否发生改变。

方法

我们对28例重度OHSS患者和34例接受体外受精(IVF)控制性卵巢刺激(COH)但未发生OHSS的患者进行了一项前瞻性病例对照研究。在取卵日(第0天)以及第3、6、9和15天从两组收集血清样本。通过酶联免疫吸附测定法检测样本中的sVE-钙黏蛋白。

结果

重度OHSS患者的sVE-钙黏蛋白水平显著高于未发生OHSS的患者(P = 0.001)。sVE-钙黏蛋白血清水平随临床症状改善而降低;然而,在缓解期它们并未恢复到正常水平。在注射HCG时,sVE-钙黏蛋白与血清雌二醇水平之间呈正相关(r = 0.621;P < 0.001)。血清sVE-钙黏蛋白水平在时间上与黄体功能的相关性比与重度OHSS的生物学和临床特征的相关性更紧密。

结论

sVE-钙黏蛋白可能参与重度OHSS的发病机制,并且可能作为COH后黄体功能的一个指标。

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