Congenital ovarian insufficiency, also known as Turner’s syndrome, is a congenital chromosomal abnormality. It was confirmed in 1959 to be due to a sex chromosome abnormality and is also known as Turner’s syndrome because it was first reported by Turnet in 1938. Due to the sex chromosome abnormality, the ovaries are unable to grow and develop, so they are fibrous and have no primordial follicles and no eggs. Therefore, there is a lack of female hormones. The syndrome is the only survivable monosomy in humans, resulting in non-development of secondary sex characteristics and primary amenorrhea. The abnormal karyotype includes: ①45,XO. is the most common type, 95% of spontaneous abortion elimination, only a few survived birth, with typical clinical manifestations; ②45,XO/46,XX, i.e. chimeric type. It accounts for about 25% of this sign; ③46, Xdel (Xp) or 46, Xdel (Xq), i.e., deletion of the short arm of one X chromosome with long arm; ④46, Xi (Xq): i.e., deletion of the short arm of one X chromosome to form an isobaric chromosome. [Signs and symptoms] Typical Turter syndrome presents at birth with lagging height and weight, marked swelling of the dorsum of the hands and feet, and flaccid skin on the side of the neck. The main clinical features are: female phenotype, low posterior hairline, 50% of the children have cervical webbing, shield-shaped chest, widened nipple spacing, elbow ectropion and multiple moles. About 35% of children have cardiac anomalies. Aortic constriction is the most common. In addition. In addition, renal malformations (such as horseshoe kidney, ectopic kidney, hydronephrosis, etc.), hypoplastic finger (toe) nails, short 4th and 5th metacarpal bones and multiple nevi can be seen. The external genitalia of the child remain infantile. The labia minora were hypoplastic and the uterus was not palpable. Most children have normal intelligence. They are often seen for growth retardation, absence of pubertal development, and primary amenorrhea. Serum FSH and LH are increased in infancy, but estradiol levels are very low. [The diagnosis of Turner’s syndrome can be made if the normal female chromosome is 46,XX, and the karyotype is 45,XO, i.e., one sex chromosome X is missing, or 46,XXP or 46,XXq or their chimerism. In addition to clinical manifestations and karyotype analysis, X chromatin of oral mucosal epithelial cells or amniotic fluid cells, etc. can be examined to aid in the diagnosis. In normal females, one x chromosome is inactivated in the interphase cells and concentrated in the x chromatin. After smearing and staining the packet, the detection rate can be about 30%, while in males, it is less than 10%. [Since most of the children with this syndrome have normal intellectual development, improving their eventual adult height and sex development is an important measure to ensure their mental health. Once the diagnosis is clear, the child can be treated with recombinant human growth hormone, which can be injected subcutaneously at 0.15U/kg per day to make the child grow significantly. Thyroid function and bone age development should be tested regularly during the drug administration. Oral low-dose estrogen therapy can be given when the child reaches 12 years of age or older to promote breast and vulva development, such as premarin, starting at 310 μg per day and gradually increasing the dose according to clinical results; or ethinylestradiol (10-20 μg/d); or hexestrol (0.1-0.5 mg/d). A very small number of chimeric patients may be fertile, but their spontaneous abortion and stillbirth rates are extremely high, and 30% of live births have chromosomal aberrations, with 45,X/46,XX and 47,XX (or XY), +21 being the most common. No treatment can promote ovarian development or restore fertility to the patient. The aim of treatment is to promote height and stimulate breast and reproductive organ development.