Surges of luteinizing hormone (LH) that result in luteinization but occur prematurely with respect to the diameter of the leading follicle, prevent attempts to induce multiple follicular maturation for in-vitro fertilization (IVF) in a significant number of women. We examined the possibility of blocking premature LH surges by the administration of Cetrorelix, a potent antagonist of gonadotrophin-releasing hormone (GnRH), in a study including 20 patients, some of whom had previously shown premature LH surges. All patients were treated with human menopausal gonadotrophins (HMG) starting on day 2. From day 7 until the induction of ovulation by human chorionic gonadotrophin (HCG) the GnRH antagonist Cetrorelix was given daily. HCG was injected when the dominant follicle had reached a diameter of > or = 18 mm and oestradiol concentration was > 300 pg/ml for each follicle having a diameter of > 15 mm. Oocyte collection was performed 36 h later by transvaginal ultrasound puncture, followed by IVF and embryo transfer. The hormone profiles of these patients and the results of IVF and embryo transfer are comparable to those treated with GnRH agonists and HMG. However, less time and especially less HMG is needed in comparison to patients stimulated with a long agonist protocol. Hence, treatment with Cetrorelix proved to be much more comfortable for the patient. In this study we showed that combined treatment with gonadotrophins and the GnRH antagonist Cetrorelix is a promising method for ovarian stimulation in patients who frequently exhibit premature LH surges and therefore fail to complete treatment.

No abstract

Cetrolix, 0.5 mg/day, administered during the midcycle phase of controlled ovarian hyperstimulation with hMG is enough to prevent completely the premature LH surge. Perhaps even lower dosages would be sufficient. Regarding fertilization rates and use of hMG, the lower dosage seems to be the most favorable.

This technique, used in conjunction with the ICSI procedure, improves pregnancy and fertility rates in cases of severe oligoasthenoteratozoospermia.

Supernumerary pronucleated stage oocytes (PN) are usually cryopreserved. PN are transferred in spontaneous, stimulated or artificial cycles. In this study, an artificial cycle with a transdermal therapeutic system was used for oestradiol release (Estraderm TTS 100) in combination with a targeted drug delivery system for vaginal progesterone release (Crinone 8%). Patients started transdermal 17beta-oestradiol treatment on cycle day 1. Only one clinical monitoring was necessary on day 14 for confirmation of satisfactory endometrial development and exclusion of ovulation by transvaginal ultrasound and endocrine determinations (oestradiol, progesterone and luteinizing hormone). Embryo transfer was performed on the third day of progesterone treatment (day 17). The first 25 cycles were recently completed in a prospective study; no cycles were cancelled due to ovulation or unsatisfactory endometrial development. In comparison with the previous protocol of embryo transfer in stimulated cycles in our clinic which required extensive ultrasound and endocrine monitoring, the pregnancy rate in these oestrogen- and progesterone-supplemented cycles was nearly twice as high (34.8%). Two pregnancies were even achieved with zygotes after micro-injection of frozen-thawed late spermatids extracted from testicular tissue (cryo-TESE). In these cycles, the Estraderm TTS 100/Crinone 8% protocol seems to be superior to stimulation protocols and even to other protocols reported so far for artificial cycles with exogenous oestradiol and progesterone treatment.