1. The mechanism of occurrence and diagnosis of AGA in women Androgenetic alopecia (AGA) is hair loss caused by androgens in genetically susceptible males or females, which generally starts to appear between the ages of 12 and 40, with no significant difference in the incidence between men and women. The mechanism of AGA is that on sensitive hair follicles, dihydrotestosterone binds to androgen receptors and activates downstream target genes, which gradually transforms the original large terminal hair follicles into miniaturized hair follicles, resulting in the conversion of terminal hairs into fine hairs, manifesting as thinning and eventual loss of hairs in the lesioned area. The pathology is characterized by a shortening of the follicular growth phase in the early stages and an increase in the proportion of resting follicles; in the later stages, the follicles become smaller and the terminal hairs are replaced by fine hairs, and finally the fine hairs disappear. Clinically, AGA in women is different from that in men. In women, the distribution of fine hairs is more scattered, and although it is most prominent on the forehead and top scalp, it usually does not fall out completely, and the forehead hairline usually does not move back, but retains a complete hairline on the forehead (Figure 1). Female AGA conditions are often classified into three levels according to the Ludwig method (Figure 2). Most female patients with AGA have normal menstruation, are able to have normal pregnancies, and have normal sex hormone tests. Therefore, unless the patient has signs and symptoms of hyperandrogenism such as hirsutism, severe folliculitis or masculine features, a full hormone test is generally not necessary. If necessary, androgen excess can be determined by measuring serum levels of total or free testosterone, dehydroepiandrosterone sulfate and prolactin. AGA in women needs to be differentiated from other causes of diffuse hair loss, such as postpartum, anemia, endocrine changes or other systemic disorders. Measurement of serum thyroxine, iron and ferritin levels can help distinguish between these causes of hair loss. 2. Treatment options for female AGA (1) Minoxidil: Originally a drug for hypertension, it was later found to promote hair follicle growth and was used to treat hair loss. The mechanism of minoxidil in the treatment of hair loss is not completely clear, it is believed that it may be related to opening potassium channels, reducing intracellular calcium ion concentration, stimulating the differentiation and proliferation of hair follicle epithelial cells, prolonging the anagen phase, and also dilating blood vessels and reducing lymphocyte infiltration around the hair follicle and other effects. Dermatology is mainly used for the treatment of AGA (both men and women) and heavy baldness. It is mainly used topically, and two concentrations of 2% and 5% (Mandy) are available. It should be applied directly to the dry scalp, once a day in the morning and once a day in the evening at the beginning, and then gradually reduced to once a night and maintained after the effect and stabilization. Before use, it is advisable to gently massage the scalp until it is hot to increase absorption. Generally, it is effective for 4-6 months, but after 1 month of discontinuation, hair loss can be resumed, so continuous treatment is needed. There are generally no significant side effects, but individual patients may experience facial hirsutism (Figure 3), eye and face and ankle swelling. It should not be used in pregnant women. (2) Cyproterone acetate (CPA): It is an androgen receptor competition inhibitor, which exerts anti-androgenic effects by competing with androgen receptors. CPA is used to treat acne, seborrhea, hirsutism and female-type AGA caused by hyperandrogenemia in women. The most commonly used diane-35 is CPA 2mg and ethinyl estradiol 35μg, which is taken from the first day of menstruation, 1 capsule per day for 21 days, and then stopped for 1 week. Improvement is usually expected after 6-8 months. Adverse reactions include loss of libido, depression, weight gain, headache and stomach discomfort in rare cases, and chloasma and liver function impairment in long-term users. Pregnancy, lactation and a history of vascular embolism are contraindicated. (3) spironolactone: Similar in structure to aldosterone, spironolactone is an aldosterone competition inhibitor, originally used for the treatment of edematous diseases, hypertension and primary aldosteronism, etc. Since it can inhibit testicular and adrenal microsomal cytochrome p450 enzymes, thus inhibiting gonadal production of androgens, and can compete in the skin to block DHT receptors, exerting anti-androgenic effects. It is mainly used in dermatology for the treatment of AGA, acne vulgaris and hirsutism in women. Generally 60-100mg/d orally in 2-3 doses, which can be increased to 150-200mg/d after 1-3 months. 6 months is a course of treatment. Adverse effects are mainly menstrual disorders and electrolyte disorders. Renal insufficiency and pregnant women are prohibited. (4) Cimetidine: It is an H2 receptor antagonist, which can block the binding of DHT and hair follicle receptors to exert anti-androgenic effects. The recommended use is 300mg, 5 times/day for 5 months, or in decreasing doses, i.e. 600mg 3 times a day for 10 days, then 400mg 3 times a day for 4 weeks, then 200mg 3 times a day for 3 months. This drug is a second-line drug for the treatment of AGA in women and should be used depending on the treatment. It is contraindicated in pregnant and lactating women. In addition, this drug may have a transient decrease in WBC, ALT, facial flushing, light diarrhea, etc., but can generally return to normal after discontinuation of the drug. (5) Vitamin A acid: Vitamin A acid can affect cell membrane fluidity and lipid composition, regulate hair follicle and epidermal cell differentiation, and promote hair follicle growth. However, the clinical effect alone is not good, but mostly used in combination with minoxidil and other topical, in order to increase the absorption of the latter and improve the efficacy, but because there are contraindications, it is appropriate to separate the external rubbing, should not be used at the same time. In addition, 5α-reductase inhibitors, including finasteride (flnasteride) (trade name Bofax), dutasteride, etc., are generally not suitable for use in female patients because they have only weak clinical effects but more adverse effects on female patients.