OBJECTIVE: To investigate the etiology and treatment countermeasures of delayed puberty in males. METHODS: We retrospectively analyzed the clinical data of 43 patients with delayed pubertal development in males treated in the past 4 years. 43 cases were all from outpatient clinics. All 43 cases were from the outpatient clinic. Their ages ranged from 13 to 29 years old, with an average of 15.7 years old. All of them presented to the clinic with gonadal dysgenesis, including no or sparse pubic hair, short external genitalia, small testicles, or breast development; 6 cases presented to the clinic for infertility. 7 cases were accompanied by olfactory dysfunction, and 1 case was combined with acromegaly. ultrasound measured the volume of testicles at 2-6 ml (2.0*1.2cm-2.9*1.8cm), with an average of 3.4 ml. the length of the penis ranged from 3 to 6.5 cm. chromosome examination in 28 cases was 46XY, 14 cases 47XXY, 1 case 46XX. serum testosterone (T) were significantly reduced: 0.17~1.75ng/ml, average 0.76ng/ml. plasma luteinizing hormone (LH): 23 cases were below normal concentration, 20 cases were elevated. fsh was significantly elevated in 20 cases, significantly reduced in 13 cases, and normal in 10 cases. RESULTS: Based on gonadal hormone levels (FSH/LH/T), 20 cases of hypergonadotropic hypogonadism were diagnosed, including 16 cases of KS sign (Klinefelter ), 1 case of 46xx male, 1 case of congenital absence of testes, and 2 cases of acquired hypergonadotropic androgenic hypogonadism (due to mumps). There were 23 cases of hypogonadotropic type, including 7 cases of anosmia-sexual naivety syndrome (Kallmann’s syndrome), 2 cases of idiopathic hypogonadotropic type, 10 cases of simple LH deficiency, 1 case of hypogonadotropic hypogonadism caused by postoperative pituitary tumors, 1 case of sexual naiveté-pigmentary retinitis-multiple digits (toes) deformity syndrome (Laurence-Moon-Biedl’s syndrome).2 cases were diagnosed as Somatic delayed puberty. Except for two cases of somatic delayed puberty androgen experimental treatment was discontinued after 1-2 months; the rest of the cases were treated with androgen replacement therapy according to the etiology and hormone level characteristics: the high-gonadotropin type was given Anterol 40-80mg orally twice a day. For the hypogonadotropic type, chorionic gonadotropin (HCG) 2000 IU was given by intramuscular injection 2-3 times a week, or Antel orally. Follow-up ranged from three months to four years, with varying degrees of improvement in male signs, increased pubic hair, penile growth, and a significant increase in testicular volume measured in 20 patients. Sexual function, mood and body mass index of the married patients also improved accordingly. DISCUSSION: The peak of male pubertal development in China is at the age of 10-14 years. Congenital and acquired factors can affect the testis itself, or the hypothalamus and pituitary gland, resulting in reduced testosterone production or receptor disorders, affecting the development of secondary sex characteristics and testicular development. It is not uncommon in clinical practice and deserves attention. Delayed pubertal development in males is categorized into 3 types according to its pathogenesis: (1) Somatic delayed pubertal development, which is temporary, related to genetic factors, often with a family history, and capable of initiating development on its own. (2) Functional hypogonadotropic hypogonadism, often due to chronic systemic diseases such as diabetes? Asthma, etc. or malnutrition caused by hypothalamic-pituitary dysfunction. Pubertal development can be restored after removal of systemic diseases. (3) Male hypogonadotropic hypogonadism, including hypogonadotropic hypogonadotropic hypogonadism caused by congenital developmental abnormality of the hypothalamus-pituitary function or acquired diseases, and hypogonadotropic hypogonadotropic hypogonadism caused by testicular tissue pathology. The former is also known as secondary hypogonadotropic hypogonadism and the latter as primary hypogonadotropic hypogonadism. Both are permanent delays in male puberty and require lifelong sex hormone replacement. Both are permanent delays in male puberty and require lifelong sex hormone replacement therapy. The principle of treatment for male hypogonadotropic hypogonadism is to mimic normal pubertal development and to provide lifelong replacement therapy. Hypergonadotropic hypogonadism can only be treated with androgen supplementation and does not address fertility. Hypogonadotropic hypogonadism can be treated with both androgens and FSH & LH, the latter of which can promote testicular growth and spermatogenesis and may resolve fertility. Hormone therapy should be followed closely.