Serious growth delay in pubescent children poses a serious treatment problem. The unrelenting pace of bone age acceleration brought on by sex steroids, which reduces the amount of time available for development, dramatically reduces the impact of administering growth hormone in cases of GH deficiency and in those with idiopathic short height (short stature without known diseases).
Both girls and boys' epiphyseal fusion is primarily controlled by oestrogen. Puberty causes GH production rates and growth velocities to more than double. High doses of GH have been demonstrated to promote linear growth in a dose-dependent manner, but they can also elevate insulin-like growth factor I concentrations over a physiological threshold and increasing treatment costs. Gonadotropin-releasing hormone analogues prevent normal puberty and, when combined with GH, can significantly improve both male and female height potential while momentarily making adolescents hypogonadal at a crucial developmental stage. While permitting normal virilization in males and increasing longitudinal bone growth via actions on the androgen receptor on the growth plate, aromatase inhibitors prevent testosterone to oestrogen conversion, reducing growth plate fusion. Here, we go through pubertal growth physiology, the effects of oestrogen and androgen on the epiphyses, and the therapeutic effects of GH, both by itself and in conjunction with GnRHa and AIs. It also reviews key studies on the effectiveness and safety of powerful oral AIs in children. In particular when paired with GH, the time-restricted use of AIs is an effective option to enhance development in pubertal males. Individualised treatment plans should be used when using targeted growth-promoting medications in adolescence to account for the effect of sex hormones on growth plate fusion.
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