The antiprogestin RU486 delays the midcycle gonadotropin surge and ovulation in gonadotropin-releasing hormone-induced cycles.

Abstract:

OBJECTIVE:To investigate whether the antiprogestin RU486 acts primarily on the hypothalamus to delay the midcycle gonadotropin surge and thus gain insight into the site(s) of action of P in the control of ovulation. DESIGN:Prospective, crossover, single-blinded clinical study. SETTING:Outpatient clinic in an academic research environment. PATIENTS:Women with hypothalamic amenorrhea. INTERVENTIONS:RU486 or a placebo was given orally at a low dose of 1 mg/d for 5 days, starting when the dominant follicle reached 14 to 16 mm, to women with hypothalamic amenorrhea undergoing ovulation induction with GnRH pulses of unvarying frequency and dose. Blood samples and ovarian ultrasounds were obtained daily in the late follicular phase and every 3 to 4 days in the remainder of the cycle. MAIN OUTCOME MEASURES:Follicular diameter and plasma levels of LH, FSH, E2, and P. RESULTS:RU486 consistently delayed the timing of the midcycle gonadotropin surge and ovulation. Gonadotropin and steroid levels were suppressed during RU486 treatment, but follicular growth progressed normally in most patients. CONCLUSIONS:RU486 does not act primarily on the hypothalamus to delay ovulation. Rather, this compound appears to antagonize P at the pituitary level to suppress gonadotropin and steroid hormone secretion. P may thus act on the pituitary, independent of any hypothalamic effects, to regulate the timing of the midcycle gonadotropin surge and ovulation.

journal_name

Fertil Steril

journal_title

Fertility and sterility

authors

Batista MC,Cartledge TP,Zellmer AW,Nieman LK,Loriaux DL,Merriam GR

doi

10.1016/s0015-0282(16)56811-3

subject

Has Abstract

pub_date

1994-07-01 00:00:00

pages

28-34

issue

1

eissn

0015-0282

issn

1556-5653

pii

S0015-0282(16)56811-3

journal_volume

62

pub_type

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