 Determining the estrogen replacement regimen which is optimal with GH therapy is an important issue in the management of Turner syndrome today. The estrogen effect on growth is biphasic, stimulatory at low doses but inhibitory at higher doses 1. In addition, the form, route, and timing of estrogen seem to be important determinants of estrogen effects on growth 2. Pubertal estrogen replacement treatment is customarily delayed until about 15 years of age in the USA to give GH treatment more time to act because standard estrogen treatment inhibits growth 3, in part by direct effects on epiphyseal senescence and fusion 4, 5 and in part by acting as a GH antagonist 6. 