Increased progesterone/estradiol ratio in the late follicular phase could be related to low ovarian reserve in in vitro fertilization-embryo transfer cycles with a long gonadotropin-releasing hormone agonist.

OBJECTIVE

To gain insight into the physiologic as well as the clinical significance of premature luteinization in the long gonadotropin-releasing hormone agonist (GnRH-a) cycles and to evaluate whether it may be a manifestation of low ovarian reserve.

DESIGN

Prospective evaluation.

SETTING

A university-affiliated reproductive medicine unit.

PATIENT(S): Seventy-six consecutive infertile women.

INTERVENTION(S): The long GnRH-a protocol was used for IVF-ET treatment.

MAIN OUTCOME MEASURE(S): Women in the study were prospectively evaluated in their first cycle of treatment and were divided into those with (study group) or without premature luteinization (control group). Premature luteinization was defined as P/E2 ratio of more than 1 on the day of hCG administration.

RESULTS(S): Thirty-one (41%) of the women in the study demonstrated premature luteinization. Patients' characteristics were comparable between the two groups. Late follicular P/E2 ratio was significantly and considerably higher in the study as compared to the control group, 2.4 +/- 1.7 and 0.7 +/- 0.2, respectively. Ovarian reserve parameters including day 3 FSH, E2 level on hCG day, total amount of hMG, number of follicles, oocytes, and embryos were significantly inferior in the study as compared to the control group. P levels on hCG day were significantly higher in the study as compared to the control group, 1.9 +/- 0.7 ng/mL and 1.2 +/- 0.6 ng/mL, respectively. However, LH levels on hCG day did not differ between the groups, 1.4 +/- 0.7 mIU/mL and 1.2 +/- 0.7 mIU/mL, respectively. The clinical pregnancy rate was significantly lower in the premature luteinization group as opposed to controls, 13% and 42%, respectively.

CONCLUSION(S): Premature luteinization, defined as late follicular P/E2 >1, in long GnRH-a cycles seems to adversely affect clinical outcome. Our findings in this setting support the notion that premature luteinization could be related to low ovarian reserve and that this manifestation is not necessarily an LH-dependent event.