Overall, neither growth hormone nor aromatase inhibitors are recommended for constitutional delay to increase growth.Girls can be started on estrogen with the same goals as their male counterparts.Overall, studies have shown no significant difference in final adult height between adolescents treated with sex steroids and those who were only observed with no treatment. Malnutrition or chronic disease
If the delay is due to systemic disease or malnutrition, the therapeutic intervention is likely to focus direction on those conditions. In patients with coeliac disease, an early diagnosis and the establishment of a gluten-free diet prevents long-term complications and allows restoration of normal maturation. Thyroid hormone therapy will be necessary in the case of hypothyroidism. Primary failure of the ovaries or testes (hypergonadotropic hypogonadism)
Whereas children with constitutional delay will have normal levels of sex hormones post-puberty, gonadotropin deficiency or hypogonadism may require lifelong sex steroid replacement.In girls with primary ovarian failure, estrogen should be started when puberty is supposed to start. Progestins are usually added after there is acceptable breast development, about 12 to 24 months after starting estrogen, as starting treatment with progestin too early can negatively affect breast growth. After acceptable breast growth, administering estrogen and progestin in a cyclical manner can help establish regular menses once puberty is started. The goal is to complete sexual maturation over 2 to 3 years. Once sexual maturation has been achieved, a trial period with no hormonal therapy can determine whether or not the child will require life-long treatment.
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.