Abstract
In 31 patients with G.D. adult castrate levels of urinary gonadotropins (mean±SEM = 3637±426 mIU/hr for FSH, and 2621±508 mIU/hr for LH) were obtained by a chronologic age of 11 and a bone age of 10. Oral, conjugated estrogen (CE) treatment in 18 individuals, ages 12-17, caused gonadotropin suppression to the prepubertal range (FSH <160, LH <90 mIU/hr) with 0.6 or 0.3 mg of CE daily, but not with 0.15 mg. According to published data in the acutely castrate woman, more than 2.5 mg of CE daily is needed to suppress LH and FSH into the normal adult range. All of 9 girls on continuous treatment with 0.6 or 0.3 mg of CE escaped from gonadotropin suppression with FSH (2700±527 mIU/hr) and LH (1460±265 mIU/hr) levels returning to the castrate range over a 9-30 mo period. In 5 agonadal girls, ages 12-15, who had previously been exposed to endogenous or exogenous estrogen, gonadotropins were not suppressed to prepubertal levels with 0.6 or 0.3 mg of CE. In contrast, in a 34-yr old woman with G.D. and no previous estrogen treatment, 0.3 mg of CE was sufficient to suppress FSH and LH excretion to the prepubertal range. Conclusions: 1) The gonadostat remains highly sensitive to estrogen in the absence of exposure to female sex steroids. 2) Escape from gonadotropin suppression during CE treatment suggests that further maturational changes occur with estrogen exposure. 3) Sex steroids themselves may modify the gonadostat.
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Kulin, H., Maruca, J. & Santner, S. Changes in sensitivity of the gonadotropin-gonadal negative feedback axis (Gonadostat) in patients with gonadal dysgenesis (G.D.). Pediatr Res 15, 1564 (1981). https://doi.org/10.1203/00006450-198112000-00176
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DOI: https://doi.org/10.1203/00006450-198112000-00176