Ap. Cheung et al., PULSATILE GONADOTROPIN-SECRETION IN WOMEN WITH POLYCYSTIC-OVARY-SYNDROME AFTER GONADOTROPIN-RELEASING-HORMONE AGONIST TREATMENT, Human reproduction, 12(6), 1997, pp. 1156-1164
In polycystic ovary syndrome (PCOS), increased luteinizing hormone (LH
) pulse frequency has been attributed to either the hypothalamic gonad
otrophin-releasing hormone (GnRH) pulse generator or ovarian oestrogen
feedback, To address this issue, a detailed examination of pulsatile
LH secretion was undertaken during recovery from GnRH agonist (GnRHa)
suppression, Each of six women with PCOS and six normal ovulatory wome
n received daily GnRHa treatment for 14 weeks, Frequent blood samples
were collected and assayed for gonadotrophins, androgens and oestrogen
s before, during and up to 4 weeks after treatment, Women with PCOS ha
d higher basal LH pulse frequency and amplitude and increased serum co
ncentrations of LH, androstenedione, testosterone and oestrone than co
ntrols, After 3 months of GnRHa treatment, all these parameters were s
uppressed with no differences observed between the two groups, One wee
k after cessation of GnRHa, LH pulse frequency promptly returned to pr
etreatment range with no between-group differences noted, whereas LH p
ulse amplitude, serum gonadotrophins and ovarian steroids remained max
imally suppressed and equivalent in the two groups, Subsequent LH puls
e frequency remained constant while LH pulse amplitude and circulating
concentrations gradually increased in parallel with a return of serum
oestrogen to pre-treatment values, Despite comparable resumption of L
H secretion in the two groups, corresponding androgen concentrations i
n women with PCOS were greater than those of normal ovulatory women, T
hus, the immediate restoration of LH pulse frequency after discontinui
ng GnRHa treatment is largely independent of ovarian oestrogen product
ion and reflects primacy of the GnRH pulse generator in determining ba
sal LH pulse frequency, Equivalent LH pulse frequency rates in the two
groups during the recovery period do not suggest an intrinsic hypotha
lamic-pituitary hyperactivity in PCOS.