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Short stature and delayed sexual development are cardinal features of the syndrome described by Henry Turner in 1938 (1). On average, adult stature of women with Turner syndrome is 20 cm less than the population mean for normal adult women, and at least some degree of short stature is almost universally present (2). Because of extremely short stature, this condition has long been considered a natural target for growth-promoting therapies. Early attempts at growth promotion using androgens generally yielded disappointing effects on adult stature.

Sex steroids are known to affect growth and growth hormone (GH) secretion throughout mammalian life. Early studies on the imprinting effects of testosterone (T) on growth and GH secretion in rats (1) showed that neonatal gonadectomy (GX) caused significant disruption of GH secretion in adult male rats. Treatment of neonatally GX male rats with T during neonatal and adult life restored a significant component of the GH pulsatile pattern. The presence of the ovary prevented the imprinting effect of T that would occur if female rats had otherwise undergone neonatal GX (2). These imprinting effects most likely involve the brain as the primary target.