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,
MARCO FILICORI
and
WILLIAM F. CROWLEY, JR.
Reproductive Endocrine Unit, Departments of Medicine and Gynecology, Vincent Research Laboratories, Massachusetts General Hospital Boston, Massachusetts 02114
Address requests for reprints to: Dr. William F. Crowley Jr., Reproductive Endocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114.
To examine gonadotropin secretory frequency as a component of the disordered neuroendocrine regulation of gonadotropin secretion in women with polycystic ovarian disease (PCOD), we measured serum gonadotropin concentrations in 12 women with PCOD at 10-min intervals for periods of 12-24 h. The patterns of LH and FSH release in these patients were compared to the findings of 24 studies in 21 age-matched normal women during the early, mid- and late follicular phases (EFP, MFP and LFP) of their cycles. Serum sex steroid levels during the 12-24 h of study in the women with PCOD were compared to those in normal women studied during the follicular phase.
The mean serum estradiol (E2) level in the women with PCOD was similar to that in normal women studied in the EFP, but lower than those in normal women in the MFP (P < 0.05) and LFP (P < 0.01). Mean serum estrone, however, was significantly higher in women with PCOD than in women in the EFP and MFP (P < 0.05 and P < 0.02, respectively), but lower than that in women in the LFP (P < 0.02). Total and unbound testosterone (T) levels were significantly elevated in women with PCOD compared to those in normal women at all stages of the follicular phase (P < 0.001).
The mean serum LH concentration and LH pulse amplitude were markedly elevated in the women with PCOD compared to normal women at all three stages of the follicular phase (P < 0.05 or less). In addition, LH pulse frequency was faster in women with PCOD [24.8 ± 0.9 (±SE) pulses/24 h] than that in women in the EFP (15.6 ± 0.7; P < 0.01), MFP (22.2 ± 1.1; P < 0.05) and LFP (20.8 ± 1.2; P < 0.01). This increased LH pulse frequency in women with PCOD correlated with ambient serum E2 levels on the day of study (r = 0.84; P < 0.001), but not with serum estrone, T, or unbound T. Repeat studies in four women with PCOD demonstrated a similarly abnormal gonadotropin secretory pattern in each.
We conclude that 1) women with PCOD have an increase in both the amplitude and frequency of LH secretion compared to those in normally cycling women throughout the follicular phase; 2) the defect in women with PCOD is reproducible; 3) this evidence of increased neuroendocrine secretion of LH as well as the relative suppression of FSH characteristic of this disorder suggest that partial pituitary desensitization secondary to increased frequency of GnRH secretion may exist in women with PCOD; and 4) the relationship between circulating E2 levels and LH pulse frequency suggests an etiological role for this steroid in increasing the frequency of GnRH release.
* This work supported by NICCHD Grants HD-15080 and RR-1066 and the Vincent Research Fund.
Recipient of a Research Fellowship from the Medical Research Council of Canada.
Current address: Department of Reproductive Medicine, University of Bologna, via Massarenti 13, Bologna, Italy.
Received April 13, 1987.
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