BES2002 Poster Presentations Reproduction (28 abstracts)
1Department of Endocrinology, Christie Hospital NHS Trust, Manchester, UK; 2Department of Oncology, Christie Hospital NHS Trust, Manchester, UK; 3MRC Human Reproductive Sciences Unit, Centre for Reproductive Biology, Edinburgh, UK.
Cytotoxic chemotherapy is a well recognised cause of premature ovarian failure (POF). A proportion of women with biochemical evidence of POF following treatment recover ovarian function with a return of normal menses and fertility, but there are no indicators that allow the identification of this subgroup of patients. In addition, we have previously reported only minor reductions in BMD in a cohort of women with POF following cytotoxic chemotherapy and had postulated that this may relate to residual ovarian function. We therefore compared ovarian function in 12 women with chemotherapy-induced POF, a cohort of women with POF from other causes and normal pre- and post-menopausal women. Estradiol, inhibin A and B and androgens were measured before and after ovarian stimulation with a GnRH analogue. Women with chemotherapy-induced POF were then followed for at least 2 years to determine whether there was any evidence of a return of ovarian function. There was no difference in mean basal or GnRH-stimulated estradiol, inhibin A and B or androgens between the 3 groups with ovarian failure (basal estradiol 15.9 vs. 14.6 vs. 21.1 pmol/l; peak estradiol 24.1 vs. 32.8 vs. 28.5 pmol/l). One women with chemotherapy-induced POF had a return of ovarian function and pregnancy during follow-up. It was not possible to distinguish her from the other 11 on the basis of hormonal parameters (basal and peak estradiol 4.1 and 5.8 pmol/l; inhibin A and B undetectable throughout). We conclude that women with POF following chemotherapy do not have significantly different residual ovarian hormone production compared with women with non-chemotherapy-induced POF or normal menopause. Furthermore, women who have the potential to recover ovarian function cannot be identified on the basis of basal or GnRH-stimulated estradiol, inhibin or androgen levels.