子宫内膜增生症患者米非司酮治疗前后子宫内膜组织血管内皮生长因子的表达和意义

The change and clinical value of vascular endothelial growth factor and microvessel density in the mifepris-tone treated endometrial hyperplasia

目的探讨米非司酮抑制子宫内膜增生的机制。方法37例子宫内膜增生症（不伴非典型增生）患者，连续口服米非司酮（剂量10mg／a）治疗3个月，刮取治疗前、后子宫内膜组织，进行自身对比；另取10名正常增殖期子宫内膜组织作为对照组进行比较。采用免疫组织化学二步法分别检测血管内皮生长因子（VEGF）及微血管密度（MVD），应用CD34抗体标记微血管并测量MVD。结果子宫内膜增生症治疗前腺上皮VEGF表达（129．6±60．0）略高于正常增殖期子宫内膜（88．5±0．7），差异无统计学意义（P〉0．05）。米非司酮治疗后（61．7±21．8）与治疗前相比，子宫内膜VEGF表达明显下降，差异有统计学意义（P〈0．05）。子宫内膜增生症MVD（16．3±1．9）略高于正常增殖期子宫内膜（11．64-3．8），差异无统计学意义（P〉0．05）。米非司酮治疗后（10．5±2．1）与治疗前相比，MVD明显下降，差异有统计学意义（P〈0．05）。结论米非司酮使子宫内膜VEGF减少从而抑制血管形成，可能是米非司酮抑制子宫内膜增生的机制之一。

Objective To investigate the mechanism of mifepristone in suppressing the emdometrial hypoerplasia. Methods Thirty seven cases with endometrial hyperplasia （without atypical hyperplasia） were pathologically evaluated for the endometrial hyperplasia before and after 3 months＇ treatment with oral mifepristone （ 10 mg,/d）. Normal endometrial iissues in proliferating phase from other 10 healthy women were also evaluated as control. Twostep immunohistochemical staining was adopted to detected the levels of vascular endohtelial growth factor （YEGF） and microvessel density （MVD）. Antibody against CD34 was used as a marker for microvessels. Results VEGF expressed in untreated medometrial hyperplasia was slight higher than that in normal proliferative endometrium [ （ 129. 6 ± 60.0） vs （ 88.5 ± 0. 7） 1, but the difference was not significant （ P 〉 0.05 ）. Compared with that before treatment, VEGF was significantly decreased after mifepristone treatment [ （61.7 ± 21.8 ） vs （ 129.6 ± 60. O） ] （P 〈 0. 05）. MVD in endometrial hyperplasia MVDis slightly higher than that in normal proliferative endometrium （ 16. 3±1.9） vs （ 11.6 ± 3.8 ） （ P 〉 0.05 ）. However, MVD in endometrial hyperplasia was significantly decreased after mifepristone treatment [ （ 10. 5 ±2. 1 ） vs （ 16. 3 ± 1.9） ] （P 〈 O. 05）. Conclusion Mifepristone reduces an- giogenesis in endometrium by supI^ressing VEGF expression, which may be one of its mechanism of inhibiting the endometrial hyperplasia.