(1) The function of the hypothalamus-pituitary-ovarian glandular axis is not yet perfect during puberty, and the positive feedback effect of the hypothalamus and pituitary gland on estrogen is defective, so the ovulatory cycle is mostly anovulatory one to three years after menarche, and as the hypothalamus-pituitary-ovarian glandular axis gradually develops and matures, ovulation is established in late puberty. (2) Increased synthesis of androgens by the adrenal glands and ovaries leads to physiological hyperandrogenemia, acne and pubic and axillary hair growth; (3) Decreased insulin sensitivity of the body tissues during puberty leads to physiological insulin resistance and hyperinsulinemia; (4) Multifollicular ovaries are often seen under ultrasound in normal adolescent girls. (5) The frequency and amplitude of gonadotropin-releasing hormone pulse secretion increases during puberty, LH secretion increases, and the wake-sleep difference disappears, resulting in a change in the LH/FSH ratio from <1 to >1. (2) Differentiation of pubertal PCOS from pubertal physiological changes: Pubertal PCOS needs to be differentiated from congenital adrenocortical hyperplasia, Cushing’s syndrome, androgen-secreting tumors. The difference between adolescent PCOS and the physiological changes of puberty. It is important to note that there are many similarities between the physiological changes of normal puberty and the clinical manifestations of adolescent PCOS, and it is important to distinguish between the two for the early diagnosis and treatment of patients with adolescent PCOS. It has been suggested that early screening for PCOS is necessary for adolescent girls with: (1) hirsutism or acne with irregular menstruation or obesity; (2) severe acne that requires treatment in early adolescence or is not treated with conventional methods; (3) failure to establish a normal menstrual cycle 2 years after menarche; (4) excessive weight gain in adolescence with acanthosis nigricans, and/or metabolic syndrome or family history of type 2 diabetes mellitus. (3) Theories related to the pathogenesis of PCOS during puberty 1, hyperpuberty: PCOS may be a continuation and expansion of puberty, due to abnormal initiation of puberty and hyperpuberty, which can be called “hyperpuberty” or “hyperpuberty” phenomenon. The main reason is that the physiological insulin resistance in adolescence develops into pathological insulin resistance for some reason and/or continues into adulthood and becomes the central link in the pathogenesis of PCOS. Insulin is one of the hormones necessary for growth and development during puberty. The decrease in insulin sensitivity of body tissues during puberty and the emergence of physiological insulin resistance mainly affect the glucose metabolism of peripheral tissues, resulting in a compensatory increase in insulin secretion and causing hyperinsulinemia. Physiological insulin resistance in adolescence is necessary for the normal growth and development of the body. When there is some reason for excessive increase of insulin level in puberty, excessive increase of androgen and IGF I1 level and enhanced ovarian response to gonadotropin cause dysregulation of insulin/IGF-1 system, thus insulin resistance persists and becomes a pathological state, which in addition to affecting glucose metabolism of peripheral tissues, also makes skeletal muscle and adipose tissue less sensitive to insulin, and may induce PCO. 2. Genetic theory The clinical manifestations and symptoms of PCOS are highly heterogeneous and change from time to time; its pathophysiology also shows that PCOS is multifactorial and multi-causal, and the heterogeneity of PCO clinical manifestations may be caused by different genetic mechanisms. 3, the fetal origin theory The late 1980s Dr. Barker proposed. The hypothesis is that the fetus reacts to intrauterine malnutrition by adaptive regulation of its own metabolism and organ architecture, and if malnutrition is not corrected in time, this adaptive regulation will lead to permanent changes in the metabolic patterns of body tissues and organs, including blood vessels, pancreas, liver and lungs, which will evolve into adult-onset diseases. This long “programmed” change can be amplified by many acquired environmental factors that enhance and accelerate the development of adult disease. Intrauterine malnutrition can lead to fetal growth retardation and low birth weight, and affect the fetal metabolic and hormonal environment to ensure survival, and this adaptive change can persist until after birth, when more insulin is secreted to achieve greater weight gain in order to catch up with growth. IV. Clinical features of pubertal PCOS Since there are certain similarities between the physiological changes during puberty and the pathophysiological aspects of pubertal PCOS, understanding the clinical features of pubertal PCOS patients can help distinguish normal pubertal females from pubertal PCOS patients. 1, menstrual pattern: normal adolescent girls will have regular ovulatory menstruation 2 years after menarche, 12% of girls will have sporadic menstruation at age 18, 5l% of sporadic menstruation can not be reversed thus leading to PCOS, the persistence of this menstrual abnormality is mainly related to excessive weight gain, LH and androgen elevation, etc. Domestic study found that only 23.1% of normal pubertal controls had menstrual abnormalities, and all were sporadic, while the incidence of menstrual abnormalities in 58 cases of pubertal PCOS patients increased significantly to 87.9%, in addition to 55.2% for sporadic menstruation, there were 20.7% amenorrhea and 12.1% menstrual disorders, from the age grouping of pubertal PCOS, menstrual abnormalities in the middle and late pubertal groups 2, hairy, acne: normal adolescent women show signs of hairy, acne, etc., only 3.8%, not as obvious as PCOS patients, and with the transition to adulthood, its signs gradually reduced, acne is mainly scattered in the face, hair is mainly distributed in the pubic hair, axillary hair and other parts. The hyperandrogenemia in adolescent PCOS patients does not disappear with the transition from puberty to adulthood. We should pay high attention to adolescent girls with hairiness and menstrual disorders at the same time, and if necessary, conduct a detailed and comprehensive examination to exclude adolescent PCOS. 3. Obesity: It is also a common clinical manifestation of PCOS, and is often obese in men (waist circumference/hip >10.85). the incidence of obesity in patients with PCOS is about 50%, mostly in adolescence. And obese PCOS patients are more serious androgen excess and insulin resistance. The difference between follicular ovaries and polycystic ovaries in normal adolescent girls is that the former have 6-10 follicles, 4-10 mm in diameter, normal ovarian stromal echogenicity, and a smaller total volume. In adolescent PCOS patients, multiple ovarian follicles (more than 10 follicles unilaterally) with enhanced interstitial echogenicity and increased volume (>10m1) are seen on ultrasound. This indicates that the increase in ovarian volume as a feature of adolescent PCOS can be well differentiated between adolescent PCOS and normal ovaries. The specificity and sensitivity of the diagnosis of pubertal PCOS by the number of follicles ≥11 in a single ovary was >85%. The combination of ovarian volume and follicle number to diagnose pubertal PCOS had a higher specificity (96.2%), but its sensitivity was lower (77.3%). 5, insulin resistance and abnormal glucose tolerance: adolescent PCOS patients not only have insulin resistance, most also have abnormal glucose tolerance, Lu Xiang et al. reported that the incidence of low glucose tolerance in adolescent PCOS was 24.1%, and the insulin resistance group was as high as 40%. The prevalence of insulin resistance in adolescent PCOS was 33.5% in the endocrine outpatients of the Obstetrics and Gynecology Hospital of Fudan University, and the degree of IR was aggravated by obesity. In the second hospital of Sun Yat-sen University, the incidence of insulin resistance in PCOS patients with adolescent onset was 25.5%, and the incidence of insulin resistance in obese people (BMI ≥ 24 kg/m) was higher than in those who were not obese, and there was a significant difference between the two. 6, biochemical indicators: compared with normal controls there are also significant changes, such as luteinizing hormone (LH) levels, LH/FSH ratio. Our study showed that LH was negatively correlated with body weight, obesity may inhibit hypothalamic GnRH pulse frequency or pituitary LH responsiveness, and the negative correlation between LH and BMI may be related to the distribution and volume of adipose tissue. Moreover, IH levels, LH/FSH were higher in obese PCOS patients than in controls, suggesting that these two indicators may be independent factors associated with PCOS in Chinese PCOS patients. LH levels, LH/FSH were significantly higher in patients with lean body type than in overweight patients, and LH levels were elevated in 76.27% of PCOS patients.