Pubertal Growth: Physiology and Pathophysiology

Abstract

Publisher Summary This chapter provides an overview of pubertal growth. The current hypothesis is that pubertal growth in girls is driven by low levels of estrogen, on the order of about 4 μg/day, whereas pubertal growth in boys is driven both by low levels of estrogen and by high, that is, late pubertal levels of androgen. Earlier investigators have established that growth hormone and thyroxin play a permissive role in pubertal growth. The contribution of increased growth hormone and somatomedin C secretion at puberty to the pubertal growth spurt, however, is uncertain. Normal pubertal growth rates can be achieved without increased circulating growth hormone or somatomedin C in growth hormone-replaced, sex steroid-treated hypo pituitary children. Clinical evidence suggests that the adrenal androgens contribute little if anything to pubertal growth. In girls with Turner syndrome, who normally lack a pubertal growth spurt, low dose estrogen increases growth rate and improves predicted height. In the children with central precocious puberty, long-term LHRH analog treatment decreases growth rate and bone maturation and improves predicted height. In boys with familial male precocious puberty, control of pubertal growth appears to require removal of the effects of both androgens and estrogens. The potential to enhance height by delay of normal puberty is likely to be modest.