Abstract
Purpose: To evaluate a case of a normal estrogenic woman with amenorrhea and polycystic ovarian syndrome who fails to get menses after progesterone withdrawal but who menstruates with oral contraceptives. Methods: The following sera assays were obtained: total testosterone (T), free T, weakly bound T, dehydroepiandrosterone sulfate, 17 hydroxyprogesterone, estradiol, free thyroxin, thyroid stimulating hormone, prolactin, evening Cortisol, LH and FSH. Results: The total testosterone was markedly elevated but the free testosterone was normal and the free and weakly bound testosterone was the high end of normal. The LH/FSH ratio was markedly increased consistent with the ultrasound findings of polycystic ovarian syndrome. Vaginal cytology showed a mixed high estrogen/high androgen effect and the endometrial thickness was only 5 mm. Twice she failed to have menses following progesterone withdrawal. Conclusions: One hypothesized mechanism is that the high testosterone levels even though mostly in the bound form inhibited estrogen from causing adequate endometrial development.
Original language | English (US) |
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Pages (from-to) | 141-142 |
Number of pages | 2 |
Journal | Clinical and Experimental Obstetrics and Gynecology |
Volume | 36 |
Issue number | 3 |
State | Published - Oct 12 2009 |
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All Science Journal Classification (ASJC) codes
- Reproductive Medicine
- Obstetrics and Gynecology
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Failure to have menses following progesterone withdrawal in a normal estrogenic woman with polycystic ovarian syndrome who menstruates with oral contraceptives. / Check, J. H.; Mitchell-Williams, Jocelyn.
In: Clinical and Experimental Obstetrics and Gynecology, Vol. 36, No. 3, 12.10.2009, p. 141-142.Research output: Contribution to journal › Article
TY - JOUR
T1 - Failure to have menses following progesterone withdrawal in a normal estrogenic woman with polycystic ovarian syndrome who menstruates with oral contraceptives
AU - Check, J. H.
AU - Mitchell-Williams, Jocelyn
PY - 2009/10/12
Y1 - 2009/10/12
N2 - Purpose: To evaluate a case of a normal estrogenic woman with amenorrhea and polycystic ovarian syndrome who fails to get menses after progesterone withdrawal but who menstruates with oral contraceptives. Methods: The following sera assays were obtained: total testosterone (T), free T, weakly bound T, dehydroepiandrosterone sulfate, 17 hydroxyprogesterone, estradiol, free thyroxin, thyroid stimulating hormone, prolactin, evening Cortisol, LH and FSH. Results: The total testosterone was markedly elevated but the free testosterone was normal and the free and weakly bound testosterone was the high end of normal. The LH/FSH ratio was markedly increased consistent with the ultrasound findings of polycystic ovarian syndrome. Vaginal cytology showed a mixed high estrogen/high androgen effect and the endometrial thickness was only 5 mm. Twice she failed to have menses following progesterone withdrawal. Conclusions: One hypothesized mechanism is that the high testosterone levels even though mostly in the bound form inhibited estrogen from causing adequate endometrial development.
AB - Purpose: To evaluate a case of a normal estrogenic woman with amenorrhea and polycystic ovarian syndrome who fails to get menses after progesterone withdrawal but who menstruates with oral contraceptives. Methods: The following sera assays were obtained: total testosterone (T), free T, weakly bound T, dehydroepiandrosterone sulfate, 17 hydroxyprogesterone, estradiol, free thyroxin, thyroid stimulating hormone, prolactin, evening Cortisol, LH and FSH. Results: The total testosterone was markedly elevated but the free testosterone was normal and the free and weakly bound testosterone was the high end of normal. The LH/FSH ratio was markedly increased consistent with the ultrasound findings of polycystic ovarian syndrome. Vaginal cytology showed a mixed high estrogen/high androgen effect and the endometrial thickness was only 5 mm. Twice she failed to have menses following progesterone withdrawal. Conclusions: One hypothesized mechanism is that the high testosterone levels even though mostly in the bound form inhibited estrogen from causing adequate endometrial development.
UR - http://www.scopus.com/inward/record.url?scp=70349660094&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70349660094&partnerID=8YFLogxK
M3 - Article
C2 - 19860350
AN - SCOPUS:70349660094
VL - 36
SP - 141
EP - 142
JO - Clinical and Experimental Obstetrics and Gynecology
JF - Clinical and Experimental Obstetrics and Gynecology
SN - 0390-6663
IS - 3
ER -