Others
Growth hormone is another option that has been described, however it should only be used in proven growth hormone deficiency such as idiopathic short stature. Children with a constitutional delay have not been shown to benefit from growth hormone therapy. Although serum growth hormone levels are low in constitutional delay of puberty, they increase after treatment with sex hormones and in those cases, growth hormone is not suggested to accelerate growth.Subnormal vitamin A intake is one of the etiological factors in delayed pubertal maturation. Supplementation of both vitamin A and iron to normal constitutionally delayed children with subnormal vitamin A intake is as efficacious as hormonal therapy in the induction of growth and puberty.More therapies are being developed to target the more discreet modulators of the HPG axis including kisspeptin and neurokinin B.In cases of severe delayed puberty secondary to hypogonadism, evaluation by a psychologist or psychiatrist, as well as counseling and a supportive environment are an important supplemental therapy for the child. Transition from pediatric to adult care is also vital as many children are lost during transition of care. Outlook
Constitutional delay of growth and puberty is a variation of normal development with no long-term health consequences, however it can have lasting psychological effects. Adolescent boys with delayed puberty have a higher level of anxiety and depression relative to their peers.
In this scenario, the brain sends a lot of hormonal signals (high gonadotropin), but the gonads are unable to respond to said signals causing hypergonadotropic hypogonadism. Hypergonadotropic hypogonadism can be caused by congenital defects or acquired defects. Congenital disorders
Congenital diseases include untreated cryptorchidism where the testicles fail to descend from the abdomen. Other congenital disorders are genetic in nature. In males, there can be deformities in the seminiferous tubule as in Klinefelter syndrome (most common cause in males), defects in the production of testicular steroids, receptor mutations preventing testicular hormones from working, chromosomal abnormalities such as Noonan syndrome, or problems with the cells making up the testes. Females can also have chromosomal abnormalities such as Turner syndrome (most common cause in girls), XX gonadal dysgenesis, and XY gonadal dysgenesis, problems in the ovarian hormone synthesis pathway such as aromatase deficiency or congenital anatomical deformities such as Müllerian agenesis. Acquired disorders
Acquired diseases include mumps orchitis, Coxsackievirus B infection, irradiation, chemotherapy, or trauma; all problems causing the gonads to fail. Genetic or acquired defect of the hormonal pathway of puberty (hypogonadotropic hypogonadism)
The hypothalamic–pituitary–gonadal axis can also be affected at the level of the brain. The brain does not send its hormonal signals to the gonads (low gonadotropins) causing the gonads to never be activated in the first-place resulting in hypogonadotropic hypogonadism. The HPG axis can be altered in two places, at the hypothalamic or at the pituitary level. CNS disorders such as childhood brain tumors (e.g.