The reduction of the potency of luteinizing hormone (LH) by estrogen was investigated. The bioactive and immunoreactive forms of LH from basal and luteotropin-releasing-hormone-stimulated serum samples from 6 teen-age girls with gonadal dysgenesis before and during induction of secondary sex changes with estrogen were assayed. The 6 girls, 13-15 years of age, were feminized daily with doses of 10 or 20 mcg of oral ethinyl estradiol (EE). The girls showed satisfactory secondary sexual development, including breast development and menses, within the 1st 6 months of estrogen therapy. Both forms of LH declined with increasing dose and time of therapy. However, the ratio of the bioactive to the immunoreactive form of the hormone was significantly higher (p .001) before treatment than after 3 months of treatment with 10 mcg of EE and after 3 additional months of treatment with EE during which time the daily dose was increased to 20 mcg. 2 younger girls, ages 9 and 11, with gonadal dysgenesis showed no elevation of the immunoreactive form of the hormone, a weak response to luteotropin-releasing hormone, and a low ratio of bioactive to immunoreactive LH. These data indicate that estrogen produces qualitative and quantitative changes in serum LH in girls with gonadal dysgenesis.
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Lucky et al. (1979) studied this question.
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