Specific, time-dependent actions of low-dose ethinyl estradiol administration on the episodic release of growth hormone, follicle- stimulating hormone, and luteinizing hormone in prepubertal girls with Turner's syndrome

N. Mauras, A. D. Rogol, Johannes D Veldhuis

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Abstract

To investigate the actions of acute and chronic low doses of ethinyl estradiol (EE) on the pulsatile characteristics of GH and gonadotropin release we studied seven girls with Turner's syndrome [mean age, 7.5 ± 0.75 (± SE) yr] on 3 separate study days. At baseline (study I), blood was drawn every 20 min from 2000-0800 h for GH, LH, and FSH determinations. One month after study I the patients were started on 100 ng/kg EE, orally, daily, and an identical study was repeated 1 week (study II) and 5 weeks (study III) from the initiation of low dose EE therapy. A pulse detection algorithm, Cluster, was used to objectively analyze pulsatility profiles. There were consistent and significant increases in all seven patients after 5 weeks of low dose EE therapy in mean GH concentrations (study I, 7.0 ± 1.1 μg/L; study III, 13.4 ± 1.7; P = 0.008), mean area under the GH pulse (study I, 602 ± 52 μg/L · min; study III, 1350 ± 261; P = 0.026), and mean GH pulse amplitude (study I, 14.0 ± 2.2 μg/L; study III, 32.8 ± 6.0; P = 0.018); with no detectable changes in GH pulse frequently (study I, 5.3 ± 0.6 pulses/12 h; study III, 5.3 ± 0.4) These findings were not accompanied by any significant changes in plasma somatomedin-C or serum estradiol concentrations or urinary cytological maturation indexes. Conversely, the amount of radioimmunoassayable FSH activity was suppressed after low dose EE therapy, with a decrease in mean FSH concentrations (study I, 23.5 ± 6.6 IU/L; study III, 5.9 ± 1.2; P = 0.035) and mean pulse amplitude (study I, 28.6 ± 8.6 IU/L; study III, 8.2 ± 1.8; P = 0.038), with no detectable changes in FSH pulse frequency (study I, 7.6 ± 0.6 pulses /12 h; study III, 7.3 ± 0.6). Similar qualitative changes in LH pulsatility were observed after low dose estradiol administration. In conclusion, our results demonstrate that low dose EE therapy results in a significant augmentation of pulsatile GH activity, with reciprocal decreases in gonadotropin concentrations in girls with Turner's syndrome. Such observations indicate an exquisite sensitivity of gonadotrope and somatotrope function to low dose estrogen action in this prepubertal hypogonadal model.

Original languageEnglish (US)
Pages (from-to)1053-1058
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume69
Issue number5
StatePublished - 1989
Externally publishedYes

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Turner Syndrome
Ethinyl Estradiol
Follicle Stimulating Hormone
Luteinizing Hormone
Growth Hormone
Gonadotropins
Estradiol
Therapeutics
Insulin-Like Growth Factor I
Estrogens
Blood
Plasmas
Serum

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

@article{b10a0d2a04c64aba929471f5e7e39556,
title = "Specific, time-dependent actions of low-dose ethinyl estradiol administration on the episodic release of growth hormone, follicle- stimulating hormone, and luteinizing hormone in prepubertal girls with Turner's syndrome",
abstract = "To investigate the actions of acute and chronic low doses of ethinyl estradiol (EE) on the pulsatile characteristics of GH and gonadotropin release we studied seven girls with Turner's syndrome [mean age, 7.5 ± 0.75 (± SE) yr] on 3 separate study days. At baseline (study I), blood was drawn every 20 min from 2000-0800 h for GH, LH, and FSH determinations. One month after study I the patients were started on 100 ng/kg EE, orally, daily, and an identical study was repeated 1 week (study II) and 5 weeks (study III) from the initiation of low dose EE therapy. A pulse detection algorithm, Cluster, was used to objectively analyze pulsatility profiles. There were consistent and significant increases in all seven patients after 5 weeks of low dose EE therapy in mean GH concentrations (study I, 7.0 ± 1.1 μg/L; study III, 13.4 ± 1.7; P = 0.008), mean area under the GH pulse (study I, 602 ± 52 μg/L · min; study III, 1350 ± 261; P = 0.026), and mean GH pulse amplitude (study I, 14.0 ± 2.2 μg/L; study III, 32.8 ± 6.0; P = 0.018); with no detectable changes in GH pulse frequently (study I, 5.3 ± 0.6 pulses/12 h; study III, 5.3 ± 0.4) These findings were not accompanied by any significant changes in plasma somatomedin-C or serum estradiol concentrations or urinary cytological maturation indexes. Conversely, the amount of radioimmunoassayable FSH activity was suppressed after low dose EE therapy, with a decrease in mean FSH concentrations (study I, 23.5 ± 6.6 IU/L; study III, 5.9 ± 1.2; P = 0.035) and mean pulse amplitude (study I, 28.6 ± 8.6 IU/L; study III, 8.2 ± 1.8; P = 0.038), with no detectable changes in FSH pulse frequency (study I, 7.6 ± 0.6 pulses /12 h; study III, 7.3 ± 0.6). Similar qualitative changes in LH pulsatility were observed after low dose estradiol administration. In conclusion, our results demonstrate that low dose EE therapy results in a significant augmentation of pulsatile GH activity, with reciprocal decreases in gonadotropin concentrations in girls with Turner's syndrome. Such observations indicate an exquisite sensitivity of gonadotrope and somatotrope function to low dose estrogen action in this prepubertal hypogonadal model.",
author = "N. Mauras and Rogol, {A. D.} and Veldhuis, {Johannes D}",
year = "1989",
language = "English (US)",
volume = "69",
pages = "1053--1058",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "5",

}

TY - JOUR

T1 - Specific, time-dependent actions of low-dose ethinyl estradiol administration on the episodic release of growth hormone, follicle- stimulating hormone, and luteinizing hormone in prepubertal girls with Turner's syndrome

AU - Mauras, N.

AU - Rogol, A. D.

AU - Veldhuis, Johannes D

PY - 1989

Y1 - 1989

N2 - To investigate the actions of acute and chronic low doses of ethinyl estradiol (EE) on the pulsatile characteristics of GH and gonadotropin release we studied seven girls with Turner's syndrome [mean age, 7.5 ± 0.75 (± SE) yr] on 3 separate study days. At baseline (study I), blood was drawn every 20 min from 2000-0800 h for GH, LH, and FSH determinations. One month after study I the patients were started on 100 ng/kg EE, orally, daily, and an identical study was repeated 1 week (study II) and 5 weeks (study III) from the initiation of low dose EE therapy. A pulse detection algorithm, Cluster, was used to objectively analyze pulsatility profiles. There were consistent and significant increases in all seven patients after 5 weeks of low dose EE therapy in mean GH concentrations (study I, 7.0 ± 1.1 μg/L; study III, 13.4 ± 1.7; P = 0.008), mean area under the GH pulse (study I, 602 ± 52 μg/L · min; study III, 1350 ± 261; P = 0.026), and mean GH pulse amplitude (study I, 14.0 ± 2.2 μg/L; study III, 32.8 ± 6.0; P = 0.018); with no detectable changes in GH pulse frequently (study I, 5.3 ± 0.6 pulses/12 h; study III, 5.3 ± 0.4) These findings were not accompanied by any significant changes in plasma somatomedin-C or serum estradiol concentrations or urinary cytological maturation indexes. Conversely, the amount of radioimmunoassayable FSH activity was suppressed after low dose EE therapy, with a decrease in mean FSH concentrations (study I, 23.5 ± 6.6 IU/L; study III, 5.9 ± 1.2; P = 0.035) and mean pulse amplitude (study I, 28.6 ± 8.6 IU/L; study III, 8.2 ± 1.8; P = 0.038), with no detectable changes in FSH pulse frequency (study I, 7.6 ± 0.6 pulses /12 h; study III, 7.3 ± 0.6). Similar qualitative changes in LH pulsatility were observed after low dose estradiol administration. In conclusion, our results demonstrate that low dose EE therapy results in a significant augmentation of pulsatile GH activity, with reciprocal decreases in gonadotropin concentrations in girls with Turner's syndrome. Such observations indicate an exquisite sensitivity of gonadotrope and somatotrope function to low dose estrogen action in this prepubertal hypogonadal model.

AB - To investigate the actions of acute and chronic low doses of ethinyl estradiol (EE) on the pulsatile characteristics of GH and gonadotropin release we studied seven girls with Turner's syndrome [mean age, 7.5 ± 0.75 (± SE) yr] on 3 separate study days. At baseline (study I), blood was drawn every 20 min from 2000-0800 h for GH, LH, and FSH determinations. One month after study I the patients were started on 100 ng/kg EE, orally, daily, and an identical study was repeated 1 week (study II) and 5 weeks (study III) from the initiation of low dose EE therapy. A pulse detection algorithm, Cluster, was used to objectively analyze pulsatility profiles. There were consistent and significant increases in all seven patients after 5 weeks of low dose EE therapy in mean GH concentrations (study I, 7.0 ± 1.1 μg/L; study III, 13.4 ± 1.7; P = 0.008), mean area under the GH pulse (study I, 602 ± 52 μg/L · min; study III, 1350 ± 261; P = 0.026), and mean GH pulse amplitude (study I, 14.0 ± 2.2 μg/L; study III, 32.8 ± 6.0; P = 0.018); with no detectable changes in GH pulse frequently (study I, 5.3 ± 0.6 pulses/12 h; study III, 5.3 ± 0.4) These findings were not accompanied by any significant changes in plasma somatomedin-C or serum estradiol concentrations or urinary cytological maturation indexes. Conversely, the amount of radioimmunoassayable FSH activity was suppressed after low dose EE therapy, with a decrease in mean FSH concentrations (study I, 23.5 ± 6.6 IU/L; study III, 5.9 ± 1.2; P = 0.035) and mean pulse amplitude (study I, 28.6 ± 8.6 IU/L; study III, 8.2 ± 1.8; P = 0.038), with no detectable changes in FSH pulse frequency (study I, 7.6 ± 0.6 pulses /12 h; study III, 7.3 ± 0.6). Similar qualitative changes in LH pulsatility were observed after low dose estradiol administration. In conclusion, our results demonstrate that low dose EE therapy results in a significant augmentation of pulsatile GH activity, with reciprocal decreases in gonadotropin concentrations in girls with Turner's syndrome. Such observations indicate an exquisite sensitivity of gonadotrope and somatotrope function to low dose estrogen action in this prepubertal hypogonadal model.

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