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Submitted on December 3, 2004
Accepted on February 11, 2005
The Center for Research in Reproduction and Division of Endocrinology, Department of Internal Medicine; University of Virginia Health System, Charlottesville, Virginia 22908; Division of Reproductive Endocrinology, Department of Reproductive Medicine, University of California- San Diego, La Jolla, California 92093
* To whom correspondence should be addressed. E-mail: skc6u{at}virginia.edu.
Compared with normal women, adults with PCOS require higher progesterone (P) concentrations to inhibit GnRH (LH) pulse frequency, which contributes to persistently rapid GnRH pulses and elevated LH levels in PCOS. To explore the origin of this abnormality, we assessed hypothalamic sensitivity to P feedback in 9 normal controls and 11 hyperandrogenemic (HA) adolescents.
Subjects first underwent frequent blood sampling for 11 h to assess baseline LH pulse frequency. Thereafter, oral estradiol and micronized P were given for 7 days to achieve mean estradiol and P levels of 143 ± 16 pg/ml (524 ± 60 pmol/l) and P 7.8 ± 0.7 ng/ml (24.9 ± 2.3nmol/l), respectively. LH pulse frequency was then reassessed.
On Day 7, the slope of percentage reduction of LH pulses/11 h as a function of Day 7 P concentration was less in the HA group compared with controls (P = 0.02), despite similar P levels. LH pulse frequency was suppressed in all NC (mean 7.0 to 3.4 pulses/11 h), but was unchanged in 6 of the HA girls (mean 8.3 to 7.5 pulses/11 h). In contrast, in the other 5 HA adolescents, P induced similar slowing of LH pulses to that seen in NC (mean 10.0 to 5.0 pulses/11 h). Baseline free T levels were similar in both HA groups; the only observed difference between these HA groups is that the P-suppressible subjects were all of Hispanic descent.
These data suggest that hyperandrogenemia during adolescence is variably associated with decreased sensitivity to P, which may have a partially genetic basis.
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