Pubertal sexual development is not an independent event of the reproductive system; it is characterized by systemic changes and is influenced by general health conditions, such as malnutrition, excessive weight loss and obesity. Delayed pubertal development is defined as an actual age that is more than two standard deviations above the mean of normal sexual developmental age before the development of sexual characteristics. In clinical practice, the age limit for pubertal delay is generally set at 14 years for boys and 13 years for girls. The causes of pubertal delay may be organic lesions of the hypothalamic-pituitary gonadal axis, including lesions of hypothalamic gonadotropin-releasing hormone (GnRH) cells or pulse generators, the anterior pituitary gland, or the gonads; hypothalamic-pituitary lesions causing sexual maturation disorders are also known as hypogonadotropic hypogonadotropic hypogonadism, and those caused by congenital or acquired gonadal lesions are known as hypogonadotropic hypogonadotropic hypogonadism. Hypogonadotropic hypogonadism is also known as hypergonadotropic hypogonadism. In addition, there is a special type called idiopathic or somatic pubertal delay, in which children do not have organic lesions of the hypothalamic-pituitary gonadal axis system, but only a later than normal initiation of natural puberty, a condition that can be attributed to a functional abnormality of the hypothalamic pulse generator. 1 Etiology The etiology of idiopathic pubertal delay is unknown. Most children are associated with growth retardation, basal secretion of growth hormone (GH) and mildly diminished secretory response of GH to excitatory factors such as growth hormone-releasing hormone (GHRH) or excitatory tests such as insulin hypoglycemic excitatory test. However, after administration of exogenous androgens or estrogens, there is a significant increase in the amplitude of the GH secretion peak and the secretory response to GHRH excitation, suggesting that there is a temporary GH secretion deficit in idiopathic pubertal growth retardation. In a few children, there is no reduction in physical growth rate and height is normal, and the parents or brothers of the children often have a history of delayed puberty, so the possibility of genetic factors as the cause of the disease cannot be ruled out. 2 Clinical manifestations Idiopathic pubertal delay is more common in boys. The length and weight of the child at birth are in the normal range, and no abnormality is found in early childhood. The linear growth rate of the body slows down from school age, and the annual height growth is about 3-4 cm, which is basically in line with the 3rd percentile of the height growth curve. Bone age lags behind actual age, and the body’s growth rate is normal or only mildly reduced compared to bone age. The child is normal except for being shorter than children of the same age and asexual development. A detailed family history often reveals a tendency for delayed puberty in family members, such as a father or some members of close family elders who initiated puberty at 14-18 years of age, or a mother with delayed menarche. Laboratory tests reveal mildly diminished basal secretion of GH and secretory response of GH to GHRH excitation. Basal secretion of plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) is at a low level, usually less than 2.0 U/L, and no secretory pulses appear on pulse analysis either at night or during the day.There is no elevation or only a slight elevation in plasma LH and FSH levels in the GnRH excitability test (100ug IV push) (no or low response). Basal levels of plasma testosterone or estradiol (E2) and the secretory response of testosterone to human chorionic gonadotropin (hCG) excitatory testing were similar to those of prepubertal children. In conclusion, the functional status of the hypothalamic-pituitary-gonadal axis system in children with idiopathic pubertal developmental delay is lower than the actual age of the child, consistent with the bone age of the child. Thyroid and adrenal function were normal. In addition, these children have a delayed onset of adrenocortical function. The absence of signs of pubertal onset at age 13 years in girls or 14 years in boys warrants a complete workup to identify idiopathic pubertal delay.