Coupon Accepted Successfully!


Introduction: Androgen in female

Circulating androgens found in the blood of premenopausal women include dedhydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), androstenedione, and testosterone. Androgens are produced by the adrenal glands the ovary, and from peripheral conversion of estrogen (with the help of enzyme aromatase).


  • Produced in equal amounts by the adrenal glands (50%) and the ovaries (50%)
  • Majority of androstenedione is converted to testosterone
  • Normal serum concentration ranges from 60 to 300 ng/ dL


  • Second most potent androgenic hormone (first being DHT)
  • In women, nearly 25% of testosterone is secreted from the ovaries and 25% is from the adrenal glands. The remaining one-half is produced from peripheral conversion of androstenedione to testosterone in the skin, muscle kidneys, liver, and adipose tissue.
  • Normal circulating concentrations range from 20 to 80 ng/ dL.


  • Androgen precursors, much less potent than testosterone and produced predominantly by the adrenal glands
    (DHEA-S is produced only by adrenal).
  • DHEA is metabolized quickly, thus measurement of its serum concentration does not reflect adrenal gland activity. DHEA-S has a much longer half-life than
  • DHEA, and measurement of its serum level is used to assess adrenal function.

Causes of Hirsutism

Hirsutism is associated with excess androgen production (either from ovaries or adrenals), so any cause which increases androgens causes hirsutism.

  • Most of the testosterone is bound to sex hormone binding globulin (SHBG) and is considered biologically inactive.
  • Testosterone which is not bound to SHBG is considered biologically active, therefore any factor which decreases SHBG; cause increase in free testosterone and therefore causes hirsutism.

Medical Treatment of Hirsutism


Treatment Category

Specific Regimens

Weight loss

Hormonal suppression





Steroidogenic enzyme inhibitors

5a-reductase inhibitors




Insulin sensitizer


Oral contraceptives


Gonadotropin-releasing hormone analogues





Cyproterone acetate




Laser hair removal

Hyperprolactemia and Galactorrhea

  • Galactorrhea is the secretion of a milky fluid which is inappropriate (unrelated to child birth). The secretion contains fat globules when examined under microscope and is confirmatory for milk.
  • Prolactin (PRL) is the most important hormone involved in the pathophysiology of amenorrhea and/or galactorrhea. Prolactin is under tonic hypothalamic inhibitory control of prolactin inhibitory factor (PIF).
  • Prolactin inhibits GnRH pulse secretion. So gonadotropin levels are suppressed. Hyperprolactinemia inhibits ovarian steroidogenesis. Thus it results in hypogonadotropic hypogonadism, oligomenorrhea, amenorrhea, anovulation and many other clinical effects of hypoestrogenism.
  • PRL levels should be estimated in all women with galactorrhea, oligomenorrhea or amenorrhea. TSH level should also be measured to rule out primary hypothyroidism.
  • Prolactinoma is present in about 50 percent of women with hyperprolactinemia. Serum prolactin level when raised on repeat assay beyond 20 ng/ mL, suggests evaluation of sella turcica. Level beyond 100 ng/mL is associated with high incidence of prolactinoma. Most of the prolactinomas are microadenornas. About 33 percent of women with high prolactin levels, have galactorrhea. However, galactorrhea can be seen in women with normal serum prolactin.
    Bromocriptine is the drug used for galactorrhea. Cabergoline is more effective and well tolerated as compared to bromocriptine and has become the DOC for treting hyperprolactinemia.

Note: Pregnancy following bromocriptine has teratogenic effect on the offspring. There is no increased incidence of multiple pregnancy'.


Investigation: to work of a case of infertility following investigations are to be done.

  1. General: CBC / ESR / Blood sugar/ LFT / KFT/ TSH/ Blood group / Urine complete / VDRL / HIV
  2. Male:
    1. HSA
    2. Incase of aspermia – serum FSH / LH / Testosterone
    3. Testicular biopsy
    4. Sex chromatin study
    5. Immunological tests like sperm antibodies.
  3. Female:
    1. Test of ovulation –



1. Menstrual history

2. BBT

3. Cervical mucous study

4. Hormonal estimation:

• D 3 LH FSH ratio–FSH:LH 1:1 (If LH is higher, may be PCOS)

• D 14/15 LH should be more than 40 miu/ml (I-sure Kits)

• Serum LH at the time of ovulation - >40 miu/ml

• Mid luteal progesterone levels on D21 – 3 mg/ml


• Prolactin

5. Endometrial biopsy

6. Sonography (Follicle monitoring)

7. Vaginal cytology


Extra Edge:


Vaginal cytology gives a fair idea about the hormonal status and inturn about ovulation and overian cycle.


Vagina is lined by stratified squamous epithelium which is composed of the following types of cells:


- Parabasal / basal cells: Which are predominant when there is no hormonal dominance.


- Intermediate cells: Which are predominant when there is progesterone predominance i.e. in luteal phase / later half of menstrual cycle.


- Superficial cells: Which are predominant when there is estrogen predominance, i.e. in follicular phase – first half of menstrual cycle.


Maturation Index from birth to menopause

At birth













 0/100/0 or 100/0/0

Test Your Skills Now!
Take a Quiz now
Reviewer Name