Clinical and experimental obstetrics & gynecology · 2009
Failure to have menses following progesterone withdrawal in a normal estrogenic woman with polycystic ovarian syndrome who menstruates with oral contraceptives.
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Check J H, Mitchell-Williams J
Аннотация
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.
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.