A 25-year-old woman with PCOS is started on a combined oral contraceptive pill (COCP) for cycle regulation and hyperandrogenism. She asks about the mechanism by which COCPs reduce free androgen levels in PCOS. Which mechanism is MOST important?
- A Progestogen directly inhibits 5-alpha reductase in skin, reducing DHT formation
- B Estrogen component directly inhibits adrenal androgen synthesis via CRH suppression
- C Both estrogen and progestogen compete with androgens at the AR receptor, reducing androgenic effect
- D Estrogen component increases hepatic SHBG synthesis, reducing free androgen levels; progestogen component suppresses LH and ovarian androgen production ✓
Explanation
COCPs reduce free androgen levels in PCOS through two synergistic mechanisms: (1) The ethinylestradiol component stimulates hepatic synthesis of sex hormone-binding globulin (SHBG), which binds testosterone and reduces its free (bioactive) fraction; and (2) the progestogen component suppresses pituitary LH secretion (negative feedback), thus reducing ovarian theca cell androgen synthesis. This dual mechanism effectively lowers both free and total testosterone, improving clinical features of hyperandrogenism. Anti-androgenic progestogens (cyproterone acetate, drospirenone) additionally block androgen receptors and inhibit 5-alpha reductase.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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