摘要
目的探讨多囊卵巢综合征(PCOS)患者增生期子宫内膜ER、PR含量的变化,为治疗提供理论依据。方法选择PCOS不孕患者32例为实验组,选同期输卵管性不孕患者20例为对照组,在宫腔镜下取子宫内膜标本,行病理学检查,分析免疫组化检测子宫内膜增生早、中、晚期雌激素受体(ER)和孕激素受体(PR)在子宫内膜腺体和间质细胞的细胞核内的表达变化。结果PCOS组中腺体细胞和间质细胞ER和PR的表达在增生早、中、晚期组的免疫组化积分3组间差异均无统计学意义(P〉0.05)。对照组中腺体细胞和间质细胞ER和PR的表达随月经周期子宫内膜增生而逐渐增加,差异均有统计学意义(P〈0.05)。增生早期,ER、PR在腺体细胞和间质细胞表达的免疫组化积分比较,2组差异均无统计学意义(P〉0.05)。但增生中期,ER在腺体细胞和间质细胞表达的免疫组化积分PCOS组均较对照组减少(P〈0.05);增生晚期,ER、PR在腺体细胞和间质细胞表达的免疫组化积分PCOS组均较对照组减少(P〈0.05)。结论PCOS患者的ER、PR缺乏周期性改变;子宫内膜增生中期ER和增生晚期ER、PR含量减少。
Objective To explore the changes of estrogen receptor (ER) and progesterone receptor (PR) in the endometria of proliferative phase in polycystic ovary syndrome (PCOS) patients. Methods Thirty-two patients who suffered PCOS combined with infertilitas feminis were enrolled in this study, and 20 cases of tubal infertilitas feminis having the corresponding time period were selected as controls. The expressions of estrogen receptor (ER) and progesterone receptor (PR) in the endometria were observed by pathological examination and immunohistochemical staining. Results The expressions of ER and PR in the PCOS group in the glands and interstitium of endometrial a- mong three different periods were not significantly different. The expressions of ER and PR in the glands and interstitium of endometrial among three different periods in the control group were significantly different. There was no statistical difference in the expressions of ER, PR in the glands and interstitium of the early endometria between PCOS group and control group. The expressions of ER in the glands and interstitium of the middle endometrial in PCOS group was significantly lower than that of control group. The expressions of ER and PR in the glands and interstitium of the late proliferative endometrial in PCOS group was significantly lower than that of control group. Conclusion ER and PR of endometrial in the PCOS patients decreased. The cyclical of ER and PR in the PCOS patient were irregular.
出处
《中国医师杂志》
CAS
2009年第7期885-888,共4页
Journal of Chinese Physician
基金
湖南省卫生厅科研基金资助项目(C2005-017)