POLYCYSTIC OVARIAN DISEASE

Clinical Presentation average age 15-30 years anovulation hirsutism  infertility  obesity  virilization ...

Clinical Presentation

1. average age 15-30 years
2. anovulation
3. hirsutism 
4. infertility 
5. obesity 
6. virilization

• most common pathologic finding: white, smooth, sclerotic ovary with a thick capsule, multiple follicular cysts in various stages of
  atresia, hyperplastic theca and stroma

• but ovarian pathology varies and none is pathognomonic so  diagnosis is biochemical
• fundamental defect = bad signals to hypothalamo pituitary axis:

high androgens + obesity = increased formation of estrone (acyclic estrogen) ---->acyclic positive feedback on LH + negative feedback on FSH ---->high LH with plasma LH/FSH > 2 -----> hyperplasia of ovarian stroma and theca cells ----> increased androgen production ----->more substrate for peripheral aromatization ---> chronic anovulation

• increased incidence of endometrial cancer due to unopposed estrogen

Treatment

1. interrupt the self-perpetuating cycle by:
   
   • decreasing ovarian androgen secretion: BCP (wedge resections used in past)
   • decreasing peripheral estrone formation: weight reduction
   • enhancing FSH secretion: clomiphene, hMG (Pergonal),LHRH, purified FSH
2. to prevent endometrial hyperplasia: progesterone (Provera), BCP
3. for pregnancy
   
   • medical induction of ovulation
   • clomiphene citrate (Clomid)
   • human menopausal gonadotropin (Pergonal)