摘要
20世纪80年代中期促性腺激素释放激素激动剂（GnRH—a）和促性腺激素（Gn）的联合应用，即垂体降调节后的促排卵，或称控制性卵巢刺激（COS），避免或减少了因促排卵后雌激素水平升高而诱发的早发黄体生成素（LH）峰的出现，减少了取消周期，促进了卵泡的同步发育，对提高体外受精／卵胞浆内单精子注射一胚胎移植（IVF／ICSI—ET）的妊娠率起着重要作用，经过20余年的临床资料分析、总结经验，该方案越来越趋于个体化，如减少GnRH—a及Gn的剂量，进周期前口服避孕药（OCP，oralcon—traceptive pills）或黄体期雌激素的应用，以及重组卵泡刺激素（rFSH）、重组黄体生成素（rLH）的应用等，
The conventional ovarian stimulation protocols for IVF/ICSI-ET, controlled ovarian stimulation under pituitary down regulation by GnRH-a （gonadotropin releasing hormone agonist） have been practiced successfully more than 20 years, and improved timely. However, such regimens are associated with the risk of complications such as OHSS （ovarian hyperstimulation syndrome）, and burden patients with much time, financial and emotional stresses. In 1996, mild ovarian stimulation protocols were advocated by Edwards et al. The aim of mild stimulation is to develop safer and more patient-friendly protocol in which the risks of treatment are minimized. And with the deeper understanding to the physiology of follicle development, ovarian stimulation regimens without making much disturbance to the physiological process are reassessed and improved by the recent ten years. Without pituitary down regulation, the ovaries were stimulated by CC （ clomiphene citrate）, LE （letrozole）, or low dose GN （gonadotropin）, or CC and LE combined with low dose GN separately. And the final maturations of follicles were induced by HCG or GnRH-a. The results of IVF/ICSI-ET after the mild stimulations are acceptable, though the cycle cancellation rate is around 20% due to the premature LH rises. The premature LH rises could be inhibited by the addition of GnRH-ant （gonadotropin releasing hormone antagonist） during the process. However, it is still a challenge to clinicians how a suitable LH range is kept during the ovarian stimulation process. It means how to decide the time, the duration, and the dosage of GnRH-ant and GN. It needs hard and long time work to develop optimal ovarian stimulation protocols.
出处
《生殖医学杂志》
CAS
2009年第A01期8-14,共7页
Journal of Reproductive Medicine
基金
山东省自然科学基金2002~2005
17β雌二醇非基因型作用机理研究(Z2002C05)
