Management of puberty in growth hormone deficient children

At puberty there occur marked increases in gonadotropin, gonadal steroid and GH secretion. An important physiological synergism exists between the gonadal and somatotropic axes to permit the growth spurt and adolescent development; however, epiphyseal maturation is also accelerated leading to cessation of long-bone growth. GH deficiency may be absolute, but often is not and the diagnosis may be complicated by a constellation of physical and hormonal findings that are along a spectrum from low normal GH sufficiency to absent GH secretion. Growth hormone therapy not only accelerates the growth velocity, but also promotes the redistribution of adipose tissue stores to more peripheral sites. Given the remarkable physiological alterations in the activities of the GH and gonadotropin gonadal axes during adolescence in normal children, how should the therapeutic plan for the treatment of prepubertal GH deficiency be altered at puberty? Evidence for efficacy has been reported for each of the following for the treatment of GH deficiency at adolescence: 1) GH alone at the usual dosage (approximately 0.3 mg.kg-1.day-1); 2) Double or triple the amount of GH to mimic the finding of increased GH release at puberty. 3) GH at the usual or moderately increased dose and gonadotropin releasing hormone agonist analog to halt pubertal development. The latter two plans are at present hypotheses that must withstand the rigor of proper controlled trials. The end point is more than merely adult height, because of the significant psychological and skeletal system dysregulation that accompany decrements in the gonadal steroid hormones during adolescence.