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Human Reproduction, Vol. 10, No. 3, pp. 513-519, 1995
© 1995 European Society of Human Reproduction and Embryology


research-article

Endocrinology: Ultrasonographic appearance of polycystic ovaries is associated with exaggerated ovarian androgen and oestradiol responses to gonadotrophin-releasing hormone agonist in women undergoing assisted reproduction treatment

Anne-Maria Suikkari, Vivien MacLachlan, Joseph Montalto2, Ilan Calderon, David L. Healy and Robert I. McLachlan1

1Monash IVF 185-187 Hoddle Street, Richmond, Victoria 3121 2Royal Children's Hospital Parkville, Victoria 3052 Department of Obstetrics and Gynaecology, Monash University Clayton, Victoria, 3168, Australia

Correspondence: 1To whom correspondence should be addressed

While no single biochemical test is diagnostic of polycystic ovary syndrome (PCOS), most patients show a characteristic ovarian ultrasonographic appearance. It has been proposed that a dysfunction of cytochrome P-450c17{alpha} in PCOS leads to an increased 17-hydroxyprogesterone (17-OHP) response to a gonadotrophin-releasing hormone (GnRH) agonist-induced gonadotrophin rise. We postulated that this abnormality of steroid metabolism might influence the ovarian response during assisted reproduction treatment. We investigated 106 patients undergoing a short ’boost‘ stimulation regimen for assisted reproduction treatment, including in-vitro fertilization and gamete intra-Fallopian transfers. The ovarian ultrasound pattern was correlated with serum testosterone, 17-OHP, androstenedione and oestradiol responses, and with the clinical outcome. Polycystic ovaries, defined ultrasonographically as the presence of ≥ 10 follicles between 2 and 10 mm diameter in either ovary, were found in 48% of the whole study population. Dexamethasone was given to suppress adrenal androgen secretion. Functional ovarian hyperandrogenism (FOH) was defined as serum testosterone >0.5 nmol/l after dexamethasone. There was a significantly (P < 0.001) higher prevalence of FOH in patients with polycystic ovaries (23%) compared with normal ovaries (7%). Patients with polycystic ovaries had approximately double the 17-OHP, androstenedione and oestradiol responses to a GnRH agonist as patients with non-polycystic ovaries. Exaggerated 17-OHP and oestradiol responses to GnRH agonist were found in 89% of patients with clinically diagnosed PCOS. The number of oocytes retrieved was positively correlated (r = 0.51, P < 0.001) with the oestradiol responses in all patients. Although there was no difference in the total amount of follicle stimulating hormone (FSH) used between the patients with polycystic and normal ovaries, the median peak oestradiol concentration was 1.6 times and the oocyte yield 2.3 times greater in patients with polycystic ovaries. The overall pregnancy rate per transfer was 32% and did not differ between patients with or without polycystic ovaries and FOH. No pregnancies occurred when the baseline FSH concentration was >10 IU/l. We conclude that the ultrasonographic changes characteristic of polycystic ovaries should be sought in all women undergoing assisted reproduction treatment.

Key words: cytochrome P-450/in-vitro fertilization/ovarian hyperandrogenism


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