Clinical manifestations of polycystic ovary syndrome in adolescence: PCOS is a heterogenous disease in which each patient may have the basic phenomena of anovulation, menstrual disorders, hyperandrogenism and polycystic ovaries, infertility, and insulin resistance, but each has its own characteristics. Peripubertal primary PCOS is characterized clinically by hyperandrogenemia, menstrual disorders, and obesity with hyperinsulinemia. Hyperandrogenemia is most common with hirsutism and acne, or with signs of masculinity. In 1935, Stein-Leventhal syndrome listed obesity as one of the symptoms, and in 1980, Burghan proposed that hyperinsulinemia/insulin resistance was closely related to the obesity phenomenon of PCOS. is closely related. Obesity in PCOS is a manifestation of complex factors, mainly by high androgens prompting a marked increase in anabolism, with energy production far exceeding consumption and accumulating as triacylglycerols stored in adipose tissue, especially in the upper abdomen and abdominal cavity. This can be interspersed with the effects of genetic factors of obesity, metabolic syndrome and insulin resistance (or) changes in living and working conditions. The average length of obese cells is 67-98 μm. In severe obesity adipocytes are not only hypertrophic but also have a 3-fold increase in cell number. The occurrence of both hypertrophy and hyperplasia of adipocytes in infancy and early childhood is a critical moment in the development of obesity, so it is not recommended that fetuses or children under 3 years of age be overweight. Peripubertal PCOS is often accompanied by obesity, and obesity begins at school age and is aggravated by puberty, and rapid weight gain is often demonstrated before the onset of PCOS symptoms after menarche. The direct effect of obesity on sex hormone abnormalities in PCOS: CYP19 (aromatase) is expressed in obese tissues. In normal weight and menstruating women, 1.5% of androstenedione is converted to estrone and 0.15% of testosterone is converted to estradiol in the peri-sexual conversion of sex hormones. In obese PCOS patients, adipose tissue becomes a sustained base for the synthesis of higher amounts of estrone, which can have abnormal effects on the regulation of the endometrium, ovaries and gonadal axis. It has been proposed that Agouti protein, originally found on hair follicles, in the hypothalamus, can inhibit the signaling of melanocortin-4 receptors and stimulate appetite and obesity; the stimuli found in the late 20th century mainly from the gastrointestinal tract such as PPY3~36 and ghrelin secreted by growth hormone inhibit and stimulate appetite through the center, respectively; due to the increase in obese people, women with high androgens among them are prone to develop In PCOS, patients with PCOS will eat more if they have mental stress, and if they do not pay attention to energy consumption, they are more likely to have fat accumulation, which is one of the reasons why adolescent PCOS is prone to obesity. Acanthosis nigricans (AN) (velvety, warty, hyperpigmented skin often found on the neck, armpits, under the breasts, and in the vulva, groin, and other body folds) is a nonspecific skin marker associated with insulin resistance. The production of acanthosis nigricans may be associated with growth factors including insulin, IGF-1, epidermal growth factor, and testosterone. Hyperandrogenism (HA), insulin resistance and acanthosis nigricans together are known as HAIR-AN syndrome. black echinoderma in PCOS is notable for its distribution in the neck, axillae and groin areas, with an early light brown velvety sensation, due to localized skin keratinization and hyperpigmentation. Obesity and acanthosis nigricans are often considered clinical signs of insulin resistance, and the phenomenon of acanthosis nigricans can also be reduced with the improvement of obesity and insulin resistance. In PCOS, hyperandrogenism refers to an increase in sexual hair, mainly on the upper lip or under the chin, around the areola and in the midline of the lower abdomen, with coarse, long, black and hard hairs. Androgen-stimulated hair areas (periareolar, midline, perilabial, cheek, trunk and extremities) appear as terminal hair follicles and produce terminal hairs. It is characterized by long, dark, stiff hairs that are distinct from excessive body hair. Hirsutism is a more homogeneous, generalized increase in fine hair, not caused by excess androgens or abnormal androgen metabolism, but associated with legacy specific drugs, physical stimuli or malignancy. Hirsutism in PCOS accounts for 60-70% of cases. The increased secretion of androgens stimulates the hyperplasia of sebaceous glandular sacs to increase the production of sebum to appear as acne, mostly around the time of menarche. The distribution of acne is mostly on the face, forehead, cheekbones, nose, and even on the neck and back of the chest. Patients with PCOS have different acne from general adolescent acne, often with rough skin and enlarged pores, and are characterized by heavy symptoms, long duration, persistence and poor response to treatment. The degree of clinical manifestations of hirsutism and acne may not be consistent with the concentration of androgens. In addition, the distribution and severity of hirsutism and acne on the body surface are independent, and patients may have only one or both. Other signs of masculinity associated with hyperandrogenism may include poorly developed breasts, muscularity, enlarged clitoris, low voice, and the appearance of laryngeal nodes. In adolescents with PCOS, the menstrual pattern is mainly sporadic (menstrual cycle of 35 days to 6 months), secondary amenorrhea (menopause of ≥ 6 months) or primary amenorrhea (absence of menstruation at age 16), irregular uterine bleeding (irregular menstrual cycle or period or volume of menstruation). Adolescents with PCOS usually have normal age at menarche and occasionally have delayed menarche with hirsutism or masculinity. Most patients with PCOS have irregular periods since menarche and may present with amenorrhea, scanty periods, irregular periods with no ovulation, or severe menstrual disorders. Several studies have reported that adolescent girls with sporadic menstruation are characterized by clinical and biochemical hyperandrogenism, and 45% to 57% of them have PCOS; a survey of 2705 girls aged 14-16 years showed that 57% of those with sporadic menstruation and amenorrhea had luteinizing hormone (LH) and testosterone (T) levels in the 95% quadrant of regular menstruation. This suggests that adolescent menorrhagia is not an excessive stage of maturation of the hypothalamic-pituitary-ovarian axis during puberty, but an early sign of PCOS. Bilateral cystic ovarian enlargement The ovaries in PCOS vary in morphology from normal looking ovaries to enlarged ovaries with a thickened and shiny envelope (“oyster shell”), numerous small peripheral cysts, increased stroma, or follicular membrane cell proliferation disorder. In PCOS, the number of developing and atretic follicles increases exponentially, ranging from 20 to 100 follicles, and in most cases the ovaries are enlarged, with numerous small cysts (≥10 follicular cysts 2 to 8 mm in diameter) along the periphery below the ovarian cortex, giving a “string of pearls”-like appearance; in PCOS Strong echogenicity and increased cross-sectional area of the ovarian stroma are common. In adolescents with anovulation around puberty and menarche, the ovaries may have multiple cysts or multifollicular ovaries with small cysts distributed throughout the ovary and no increase in stroma. It is important to note that “PCO-like” ovaries can occur in patients with other sources of androgen excess (congenital adrenocortical hyperplasia, adrenal adenoma, hyperprolactinemia, hypothyroidism, Cushing’s disease, etc.) and are not unique to PCOS. Atiomo and colleagues found that the most sensitive features were follicles ≥10 and distributed in the periphery; stromal shining (increased stroma relative to total area) was considered the most specific. Normal adolescent girls with follicular ovaries are also distinguished from polycystic ovaries in that the former have 6-10 follicles, 4-10 mm in diameter, normal echogenicity of the ovarian stroma, and a smaller total volume. In adolescent patients with PCOS, multiple follicles with enhanced interstitial echogenicity and increased volume (>10 ml) are seen on ultrasound in the ovary.