LUTEAL FUNCTION FOLLOWING OVULATION INDUCTION IN POLYCYSTIC-OVARY-SYNDROME PATIENTS USING EXOGENOUS GONADOTROPINS IN COMBINATION WITH A GONADOTROPIN-RELEASING-HORMONE AGONIST
Pfj. Donderwinkel et al., LUTEAL FUNCTION FOLLOWING OVULATION INDUCTION IN POLYCYSTIC-OVARY-SYNDROME PATIENTS USING EXOGENOUS GONADOTROPINS IN COMBINATION WITH A GONADOTROPIN-RELEASING-HORMONE AGONIST, Human reproduction, 8(12), 1993, pp. 2027-2032
The luteal phase was studied in 12 polycystic ovary syndrome (PCOS) pa
tients following ovulation induction using exogenous gonadotrophins co
mbined with a gonadotrophin-releasing hormone agonist (GnRH-a). Human
menopausal gonadotrophin (HMG) was preceded by 3 weeks of treatment wi
th GnRH-a (buserelin; 1200 mug/day intra-nasally) and administered in
a step-down dose regimen starting with 225 IU/day i.m. GnRH-a was with
held the day before administration of human chorionic gonadotrophin (H
CG; 10 000 IU i.m.). Blood sampling and ultrasound monitoring was perf
ormed every 2-3 days until menses. The luteal phase was significantly
shorter in PCOS patients as compared to eight regularly cycling contro
ls: 8.8 (3.3-11.4) days [median(range)] versus 12.8 (8.9-15.9) days (P
= 0.01). Median peak values for progesterone did not show significant
differences comparing both groups: 52.3 (17.1-510.3) nmol/l versus 43
.0 (31.2-71.1) nmol/l, respectively (P = 0.8). The interval between th
e day of the progesterone peak and return to baseline was significantl
y shorter in the PCOS patients than in controls: 2.5 (0.3-4.9) days ve
rsus 4.2 (3.9-10.5) days (P < 0.005). Luteinizing hormone (LH) concent
rations during the luteal phase as reflected by area under the curve w
ere significantly lower in PCOS as compared to controls: 4.4 (1.6-21.0
) IU/l x days and 49.0 (27.8 - 79.6) IU/l x days, respectively (P < 0.
001). In conclusion, patients with PCOS may suffer from insufficient l
uteal phases after ovulation induction using HmG/HCG in combination wi
th a GnRH-a. The corpus luteum apparently lacks the support of endogen
ous LH and may be stimulated only by the pre-ovulatory injection of HC
G. Potential involvement of adjuvant GnRH-a medication or HCG itself i
n luteal suppression of endogenous gonadotrophin secretion, and the im
portance of luteal function for pregnancy rates following treatment, w
arrant further studies.