Preliminary results suggesting exaggerated ovarian androgen production early in the course of polycystic ovary syndrome

J Adolesc Health Care. 1990 Nov;11(6):480-4. doi: 10.1016/0197-0070(90)90106-c.


Excess ovarian androgen production might be a cause of the polycystic ovary syndrome (PCO). Previous studies have evaluated adult women with long-standing abnormality of the hypothalamic-pituitary gonadal axis. Abnormal ovarian function in such patients could be a primary or even a secondary finding. For that reason, this study was designed to evaluate ovarian androgen production in symptomatic adolescent females. Simultaneous adrenal suppression, by using dexamethasone, and ovarian stimulation, by using gonadotropin-releasing hormone (GnRH), were achieved in 12 patients. Following stimulation, blood was serially obtained over 8 hr to measure gonadotropin, estrogen, and androgen responses. Based on the androgen response, patients could be divided into two groups. Group A (five) had a significant increase (p less than 0.01) in free testosterone, whereas group B (seven) had no increase in any androgen, including free testosterone (significantly different from group A, p = 0.01). All patients in group A had enlarged or cystic ovaries, whereas only one-quarter patients in group B had enlarged ovaries (significantly different from group A, p less than 0.03). The pituitary and estrogenic response was similar in both groups. These preliminary data suggest that some patients with PCO (group A) have a primary abnormality in ovarian androgen production early in the course of their disease.

MeSH terms

  • Adolescent
  • Adult
  • Androgens / biosynthesis*
  • Dexamethasone
  • Female
  • Gonadotropin-Releasing Hormone
  • Humans
  • Hypothalamo-Hypophyseal System / metabolism
  • Ovary / metabolism*
  • Polycystic Ovary Syndrome / diagnosis
  • Polycystic Ovary Syndrome / metabolism*


  • Androgens
  • Gonadotropin-Releasing Hormone
  • Dexamethasone