A new contraceptive pill containing 17ß-estradiol and nomegestrol acetate.

Most combined oral contraceptive pills contain ethinyl estradiol (EE) with progestins. In order to minimize the pill's cardiovascular risks, the concept of using 17ß-estradiol (E2), the endogenous estradiol, arose in the 1970s. Many attempts to develop a pill containing 17ß-E2 have failed as cycle control was low. The first pill containing 17ß-E2 was launched in 2011. This monophasic pill contains 24 pills with 1.5 mg 17ß-E2 and 2.5 mg nomegestrol acetate, and four placebo pills. Studies conducted in Europe and the USA demonstrate that its Pearl index is 0.38 and 1.13, respectively. It has less influence on hemostasis, fibrinolysis markers, lipids and carbohydrate metabolism than the combined oral contraceptive levonorgestrel/EE (150 g/30 g and 100 µg/20 µg). Withdrawal bleedings are shorter and lighter as compared with women using drospirenone/EE (3 mg/ 30 µg). The number of women without withdrawal bleeding is approximately 30% after 12 months. Even though its contraindications are identical to other combined oral contraceptives, this nomegestrol acetate/E2 pill should be considered to be of interest for many women.

[Premature ovarian failures]. / Insuffisances ovariennes prématurées.

Premature ovarian failure (POF) is clinically suspected by amenorrhea and confirmed by an elevated FSH serum level above 40 mUI/L (even 20 mUI/L) twice, in a woman before the age of 40. Prevalence of POF is between 1 to 2% in women. In 90% of cases, no aetiology is identified. Obvious causes are chemotherapy, pelvic radiotherapy, ovarian surgery and diethylstilbestrol exposure in utero. A karyotype should be performed as Turner Syndrome is the most frequent genetic cause of POF. Some X abnormalities such as X deletion or X autosome translocation can be found. FMR1 pre-mutation (fragile X syndrome) should be searched for, even though no cases of mental retardation are known, in the family. Other genetic abnormalities can be suggested by associated symptoms (i.e.: FOXL2, SF1 mutations). Auto-immune aetiology can be suspected if other auto-immune features are present, however, there are no reliable auto-antibodies to confirm auto-immunity in POF. Treatment of POF is based on hormonal replacement therapy in order to avoid estrogen deficiency, suppress vasomotor symptoms and avoid bone loss as well as cardiovascular risk. Estrogens should be associated with progesterone or a progestin, at least up to the age of 51. Patients with POF should be informed that spontaneous pregnancies may occur (in 5% of cases). In case of desire of pregnancy, the patient should be oriented to a specialized unit for in vitro fertilization with oocyte donation. Psychological support is essential and should be part of the treatment. POF is associated with an increased risk of emotional distress and depression. No preventive treatment of POF is available so far.

Impact of endogenous luteinizing hormone serum levels on progesterone elevation on the day of human chorionic gonadotropin administration.

OBJECTIVE: To assess the relationship between endogenous LH serum levels after GnRH analogue administration and serum P elevation on the day of hCG administration (P hCG). DESIGN: Retrospective study. SETTING: Reproductive medicine center in a university hospital. PATIENT(S): A total of 708 patients undergoing a GnRH agonist or antagonist protocol for IVF intracytoplasmic sperm injection. INTERVENTION(S): Controlled ovarian stimulation. MAIN OUTCOME MEASURE(S): Serum P values according to GnRH analogue; correlation between serum LH measurements and P hCG values. RESULT(S): Serum P hCG values were significantly lower following the GnRH antagonist than agonist protocol. A positive correlation between serum P hCG and LH area under the curve or day 6 LH values was found in the GnRH agonist group and between P hCG and LH hCG levels in both GnRH analogue regimens. With multivariate analysis, P hCG values were positively correlated with serum E(2) levels on hCG administration day and with the total FSH dose in both GnRH analogue-treated groups. Additionally, the correlation between serum P hCG and LH hCG values was positive in patients treated with the GnRH agonist protocol. CONCLUSION(S): The lower serum P levels on hCG administration day following the GnRH antagonist protocol are mainly explained by lower granulosa cell steroidogenic activity. The correlation with serum LH hCG values was positive in the GnRH agonist-treated group.