LAUSR

M. Chen and colleagues recently published a paper entitled ‘Effects of oral contraceptives on ovulation induction in in vitro fertilization patients with premature ovarian insufficiency’. They claim that oral contraceptives, by reducing follicle stimulating hormone (FSH) levels, may be an effective method for inducing ovulation in such patients. I have a different interpretation of their results. In my own experience, it is 17b-estradiol that may be responsible for such facilitation. The lack of follicular response to stimulation in these cases may be due to a lesser bioactive FSH, to fewer granulosa cell receptors for FSH, and to fewer granulosa cells. Estradiol, the physiological trigger for ovulation, has several important actions: (1) it may affect the synthesis of pituitary FSH isoforms into more bioactive ones; (2) it may induce granulosa cell mitosis; (3) it may increase FSH receptors in granulosa cells; and (4) it may have a positive feedback on luteinizing hormone release, which is the ovulatory trigger. We have succeeded in treating three such patients, who were resistant to FSH stimulation. All three women ovulated and one of them carried a full-term pregnancy to a normal delivery of a healthy baby. In conclusion, I think that this favorable effect of oral contraceptives was due to the effect of ethinylestradiol on the ovary and not to the progestational steroid.