M. Schachter et al., HYPOGONADOTROPIC PATIENTS WITH ULTRASONOGRAPHICALLY DETECTED POLYCYSTIC OVARIES - ENDOCRINE RESPONSE TO PULSATILE GONADOTROPIN-RELEASING-HORMONE, Gynecological endocrinology, 10(5), 1996, pp. 327-335
To characterize the endocrine response during induction of ovulation i
n patients with hypogonadotropic hypogonadism and ultra sound findings
of polycystic ovary, we performed a retrospective analysis of 22 trea
tment cycles with pulsatile gonadotropin-releasing hormone (GnRH) in s
uch patients and of 17 treatment cycles in similar patients with ultra
sonographically normal ovaries. Of the 21 patients studies, 11 had art
ultrasound finding of polycystic ovaries and ten had ovaries that app
eared normal. Serum luteinizing hormone (LH), follicle-stimulating hor
mone (FSH) and estradiol levels, number of follicles of diameter > 12
mm (by ultrasound), and ovulation and conception rates were measured.
Patients with hypogonadotropic hypogonadism and ultrasound-diagnosed p
olycystic ovary had pretreatment endocrine status similar to those wit
h normal ovaries, but had much higher baseline ovarian volume. Ovulati
on induction with pulsatile GnRH induced much higher serum LH concentr
ations in the former group despite similar FSH levels. This difference
preceded any charge in estradiol levels. Tile former group consistent
ly recruited significantly more follicles during pulsatile GnRH treatm
ent. However, ovulation and conception rates were (non-significantly)
higher in the latter group. In conclusion, this study characterized a
subgroup of hypogonadotropic patients with ovarian morphology, volume
and response to ovulation induction similar to in patients with polycy
stic ovary syndrome. When treated with pulsatile GI?RH, those with pol
ycystic ovary significantly hypersecreted LH before their estradiol le
vel changed significantly. The primary lesion in polycystic ovary synd
rome seems to be in the ovary, with pituitary hypersecretion of LH sec
ondary to disturbed ovarian feedback signalling.