Impact of Cyproterone Acetate and Ethinylestradiol on Clomiphene-Resistant PCOS Patients with High Serum AMH Levels

A female with PCOS and androgenetic alopecia is starting treatment with oral Minoxidil, topical Minoxidil 5% with finasteride, and plans to add mesotherapy. She previously tried anti-androgenic contraceptive pills but couldn't tolerate them and is using Myo Inositol for weight management.

The conversation discusses using cyproterone acetate at 12.5 mg to manage hair loss, with concerns about its effects on testosterone and potential health issues. Other treatments mentioned include finasteride, dutasteride, minoxidil, and RU58841, with varying experiences and outcomes.

Some users have experienced good hair regrowth with estradiol, cyproterone acetate, spironolactone, and bicalutamide, but these treatments may cause feminization and other side effects. It's advised to consult a doctor before using these treatments, as they can lower testosterone and have significant risks.

A 30-year-old female with PCOS and male pattern baldness is frustrated with her endocrinologist's recommendation of only Spironolactone and minoxidil, feeling that dutasteride, finasteride, and progesterone would be more effective. Other users suggest various online sources for treatments, warn against self-medicating due to potential risks, and recommend seeking a specialized endocrinologist or considering additional treatments like Inositol, Berberine, and dermaneedling.

The conversation discusses using estradiol mesotherapy to replicate hormone replacement therapy results while minimizing systemic exposure. It also covers the use of Spironolactone cream, which reportedly has no systemic side effects, and the potential risks of using bicalutamide and Spironolactone in men.

The user has been using oral minoxidil and dutasteride for hair loss without success and is considering adding topical 17α-estradiol, Pyrilutamide, Clascoterone, or cetirizine. They have confirmed low serum DHT levels and are exploring additional treatments due to genetic sensitivity to DHT and prostaglandin D2.