Premature thelarche (PT) refers to isolated breast development in girls before the age of 8 years without other signs of secondary sexual maturation and was first described by Wilkins. The age of onset of the disease is from birth to 2 years of age. It is characterized by breast enlargement without nipple or areola enlargement or hyperpigmentation, and is not accompanied by the development of other sexual characteristics or accelerated growth. The disease is a variant of precocious puberty and is mostly benign and self-limiting; only rarely does it progress to CPP; Fan et al. investigated Italian children aged 1 week and found that breast tissue was palpable in about 5% of children. PT occurs for several reasons: (1) Transient incomplete HPGA activity. Some evidence now suggests that HPGA is active in childhood and that LH and FSH are detectable in blood and urine by bioassay and immunoassay. patients with PT show a dominant FSH response after GnRH provocation test and are significantly higher than controls, while both basal and post-GnRH provocation test LH levels are not significantly different from normal controls. In contrast, CPP patients showed a predominant LH response after GnRH stimulation test, and it was significantly higher than that of the control group and PT patients. (2) Repeated stimulation by certain levels of estrogen. After repeated administration of estrogen, the breasts can increase in size, bringing them to the size of early puberty, and when estrogen disappears, the breast shape does not deteriorate rapidly with it. (3) Transient secretion of small amounts of estrogen from ovarian follicle cells. Increased follicular microcyst formation in response to gonadotropin stimulation during childhood has led to increased estrogen secretion, as measured by tissue and ultrasound. It has also been reported that the increase in estrogen comes from dehydroisandrosterone (DHEA), a metabolic process by which DHEA can be converted into potentially active sex steroids that may occur in many cells containing estrogen or androgen receptors, such as adipose tissue, bone, muscle, breast, prostate, skin, brain, and especially the liver, where these active DHEA metabolites can be partially released into the school cycle and reach target organs. (4) Abnormal secretion of adrenergic hormones. Studies of some typical PT girls suggest the presence of increased release of LH secretion during sleep, similar to normal adolescent girls, due to the accompanying rapid, yet transient, increase in estrogen levels inhibiting the GnRH response, and presumably the possible presence of transient autonomously active ovarian cells. (5) Increased serum sex hormone-binding globulin (SHBG). Belgoro-sky et al. studied 17 girls with PT and found significantly higher serum SHBG than normal controls, while serum total testosterone, mean serum non-SHBG-bound testosterone and free testosterone were all significantly lower than in normal controls. It was also found that serum SHBG decreased significantly with age in normal controls, while none of the PT patients showed similar changes. It is thus hypothesized that PT may be due to a decrease in biologically active, unbound, free testosterone due to a rise in serum SHBG, which alters the estrogen/androgen ratio in breast tissue and thus contributes to breast development. (6) Exogenous estrogens can also cause PT through ingestion, skin absorption, or other exposure. there was an epidemic of PT in Italy that may have been caused by high estrogen levels in meat. The liver of animals can concentrate estrogen, and long-term consumption of large amounts can also cause the disease. It has also been reported that breast milk contains gonadotropin-releasing hormone, which can occasionally cause the disease. Clinical manifestations in children with PT: PT is more common in low birth weight children and small-footed children (SFD) than in normal children, with most breast development starting between 6 months and 2 years of age. Breast development is mostly bilateral and symmetrical, but can also be bilateral and asymmetrical or unilateral. Breast size varies from 1 cm to 6.5 cm, and most breast development is above stage B2 according to the Tanner Breast Classification. Most breast development is associated with breast tenderness at the onset. There is no sexual development or sexual dysfunction up to the age of 7 years in cases of simple premature breast development. In most girls, breast tissue degenerates between 6 months and 6 years after the diagnosis of PT, and in approximately 10% of patients, breast development continues until puberty. No special treatment is required.