CAJ | 학술논문

目的探讨子宫内膜息肉切除术后放置左炔诺孕酮宫内缓释系统( LNG-IUS)后子宫内膜的改变.方法对21例宫腔镜下子宫内膜息肉切除术后患者,放置LNG-IUS,随访1年后提取内膜组织,对内膜组织雌激素受体(ER)、孕激素受体(PR)、Ki-67与bcl-2、bax进行免疫组化半定量分析；连续随访3年,观察使用LNG-IUS后子宫内膜厚度、子宫重量的改变情况.结果使用LNG-IUS后,子宫内膜厚度和子宫重量呈持续性下降,子宫内膜厚度从术前的(9.8±1.2) mm降至(3.5±1.0) mm,子宫重量从术前的(98.8±8.6)g降至(66.6±9.8)g,子宫内膜组织雌激素受体(ER)、孕激素受体(PR)、Ki-67表达较治疗前息肉周边内膜组织明显降低(P＜0.05),bcl-2、bax表达较治疗前息肉周边内膜组织明显增高(P＜0.05).结论 LNG-IUS可能通过抑制ER、PR、Ki-67表达,诱导子宫内膜凋亡促进子宫内膜萎缩以预防子宫内膜息肉的复发.
목적 탐토자궁내막식육절제술후방치좌결낙잉동궁내완석계통( LNG-IUS)후자궁내막적개변.방법 대21례궁강경하자궁내막식육절제술후환자,방치LNG-IUS,수방1년후제취내막조직,대내막조직자격소수체(ER)、잉격소수체(PR)、Ki-67여bcl-2、bax진행면역조화반정량분석；련속수방3년,관찰사용LNG-IUS후자궁내막후도、자궁중량적개변정황.결과 사용LNG-IUS후,자궁내막후도화자궁중량정지속성하강,자궁내막후도종술전적(9.8±1.2) mm강지(3.5±1.0) mm,자궁중량종술전적(98.8±8.6)g강지(66.6±9.8)g,자궁내막조직자격소수체(ER)、잉격소수체(PR)、Ki-67표체교치료전식육주변내막조직명현강저(P＜0.05),bcl-2、bax표체교치료전식육주변내막조직명현증고(P＜0.05).결론 LNG-IUS가능통과억제ER、PR、Ki-67표체,유도자궁내막조망촉진자궁내막위축이예방자궁내막식육적복발.
Objective To explore the changes of endometrial tissues after the insertion of levonorgestrel intrauterine system (LNG-IUS).Methods The endometrial tissues were harvested from 21 cases after endometrial polyps resection by hysteroscopy.And the patients received a 1-year follow-up.The immunohistochemical stains for estrogen receptor ( ER),progesterone receptor ( PR),Ki-67,bcl-2 and bax were used for semi-quantitative analyses.The changes of endometrial thickness were monitored and uterine weight was observed with a 3-year follow-up.Results The endometrial thickness and uterine weight declined continuously after the insertion of LNG-IUS.The endometrial thickness decreased from the preoperative level of (9.8 ±1.2) mm to (3.5 ± 1.0) mm while the uterine weight dropped from the preoperative level of (98.8 ±8.6) g to (66.6 ±9.8) g.The expressions of ER,PR and Ki-67 were significantly lower than those of the para-polyps endometrial tissue ( P ＜ 0.05 ).The expressions of bcl-2 and bax were significantly higher than those of the para-polyps endometrial tissue ( P ＜ 0.05 ).Conclusion LNG-IUS may prevent the recurrence of uterine endometrial polyps through its inhibited expressions of ER,PR and Ki-67 and induced endometrial apoptosis.