Does gonadotropin suppression result in follicular development in premature ovarian failure?

It was hypothesized that premature ovarian failure is a self-perpetuating problem and that suppression of the endogenously raised gonadotropin levels may allow synchronization of follicular growth, so that when the suppression is removed, follicular development may be stimulated by the rapid rise in follicle stimulating hormone (FSH) levels. Microgynon (ethinylestradiol, 30 micrograms and levonorgestrel, 150 micrograms) was administered to eight women with premature ovarian failure for 12 weeks. Serum samples were collected weekly for radioimmunoassay of FSH, luteinizing hormone (LH), estradiol, progesterone and inhibin. On stopping Microgynon, ovarian ultrasonography was carried out, in addition to blood sampling, to monitor any follicular growth. Both FSH and LH levels declined to the normal follicular-phase range after 5 weeks of Microgynon treatment (mean +/- SD: FSH, 6.5 +/- 1.2 IU/l; LH, 8.9 +/- 1.6 IU/l). Both hormone levels rose rapidly after stopping treatment and were above the normal follicular-phase range by the 1st week. FSH reached pretreatment levels by 3 weeks, but LH did not reach the previously high levels until 7 weeks after stopping Microgynon administration. Estradiol and immunoreactive inhibin levels in serum were undetectable throughout the study. No follicular growth was seen on ultrasound scanning. Therefore, gonadotropin suppression in premature ovarian failure does not result in a resumption of follicular activity.