Plasma glycoprotein hormone α-subunit in the syndrome of gonadal dysgenesis: The effect of estrogen replacement in hypergonadotropic hypogonadism

Dennis M Styne, F. A. Conte, M. M. Grumbach, S. L. Kaplan

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Abstract

Elevated plasma LH and FSH levels in hypergonadotropic hypogonadism can be reduced by estrogen therapy, but the change in readily releasable glycoprotein hormone α-subunit with therapy is undefined. We administered 100 μg LRF iv to seven patients (11-19 yr old) with the syndrome of gonadal dysgenesis before and during 9 months of therapy with oral conjugated estrogens at a dose of 0.3 mg/day. The control group was seven normal girls, aged 12-16 yr. Mean basal glycoprotein hormone levels for the untreated and treated gonadal dysgenesis groups and the control group were, respectively; α-subunit, 4.2, 1.3, and 0.8 ng/ml; LH, 9.3, 3.3, and 1.4 ng/ml; and FSH, 46.7, 17.8, and 1.6 ng/ml. Mean peak LRF-stimulated values for the untreated and treated gonadal dysgenesis groups and the control group were, respectively: α-subunit, 18.9, 5.1, and 3.7 ng/ml; LH, 43.4, 11.8, and 6.4 ng/ml; and FSH, 78.0, 23.3, and 3.6 ng/ml. Mean basal and peak plasma α-subunit, LH, and FSH concentrations in untreated patients with gonadal dysgenesis were higher (P < 0.005) than those in controls and treated patients (P < 0.05). The mean basal and peak plasma α-subunit and LH concentrations in treated patients were not significantly different than those in control patients. Mean basal and peak FSH concentrations in treated patients with gonadal dysgenesis were significantly higher (P < 0.05) than those in the control group. We concluded that 1) basal and peak LRF-stimulated plasma α-subunit values are significantly higher in untreated patients with gonadal dysgenesis than in normal girls and low dose estrogen therapy decreases α-subunit concentrations to normal; 2) estrogen therapy lowers basal and LRF-stimulated plasma LH concentrations to the normal range and lowers basal and LRF-stimulated FSH concentrations to a lesser degree; and 3) the release of the α-subunit in patients without primary thyroid disease is stimulated by hypothalamic LRF, as are the gonadotropins, but the secretion of α-subunit is more closely associated with the secretion of human LH than with that of human FSH.

Original languageEnglish (US)
Pages (from-to)1049-1052
Number of pages4
JournalJournal of Clinical Endocrinology and Metabolism
Volume50
Issue number6
StatePublished - 1980

Fingerprint

Gonadal Dysgenesis
Estrogen Replacement Therapy
Hypogonadism
Glycoproteins
Estrogens
Hormones
Plasmas
Control Groups
Human Follicle Stimulating Hormone
Conjugated (USP) Estrogens
Gonadotropins
Therapeutics
Thyroid Diseases
Reference Values

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Plasma glycoprotein hormone α-subunit in the syndrome of gonadal dysgenesis : The effect of estrogen replacement in hypergonadotropic hypogonadism. / Styne, Dennis M; Conte, F. A.; Grumbach, M. M.; Kaplan, S. L.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 50, No. 6, 1980, p. 1049-1052.

Research output: Contribution to journalArticle

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title = "Plasma glycoprotein hormone α-subunit in the syndrome of gonadal dysgenesis: The effect of estrogen replacement in hypergonadotropic hypogonadism",
abstract = "Elevated plasma LH and FSH levels in hypergonadotropic hypogonadism can be reduced by estrogen therapy, but the change in readily releasable glycoprotein hormone α-subunit with therapy is undefined. We administered 100 μg LRF iv to seven patients (11-19 yr old) with the syndrome of gonadal dysgenesis before and during 9 months of therapy with oral conjugated estrogens at a dose of 0.3 mg/day. The control group was seven normal girls, aged 12-16 yr. Mean basal glycoprotein hormone levels for the untreated and treated gonadal dysgenesis groups and the control group were, respectively; α-subunit, 4.2, 1.3, and 0.8 ng/ml; LH, 9.3, 3.3, and 1.4 ng/ml; and FSH, 46.7, 17.8, and 1.6 ng/ml. Mean peak LRF-stimulated values for the untreated and treated gonadal dysgenesis groups and the control group were, respectively: α-subunit, 18.9, 5.1, and 3.7 ng/ml; LH, 43.4, 11.8, and 6.4 ng/ml; and FSH, 78.0, 23.3, and 3.6 ng/ml. Mean basal and peak plasma α-subunit, LH, and FSH concentrations in untreated patients with gonadal dysgenesis were higher (P < 0.005) than those in controls and treated patients (P < 0.05). The mean basal and peak plasma α-subunit and LH concentrations in treated patients were not significantly different than those in control patients. Mean basal and peak FSH concentrations in treated patients with gonadal dysgenesis were significantly higher (P < 0.05) than those in the control group. We concluded that 1) basal and peak LRF-stimulated plasma α-subunit values are significantly higher in untreated patients with gonadal dysgenesis than in normal girls and low dose estrogen therapy decreases α-subunit concentrations to normal; 2) estrogen therapy lowers basal and LRF-stimulated plasma LH concentrations to the normal range and lowers basal and LRF-stimulated FSH concentrations to a lesser degree; and 3) the release of the α-subunit in patients without primary thyroid disease is stimulated by hypothalamic LRF, as are the gonadotropins, but the secretion of α-subunit is more closely associated with the secretion of human LH than with that of human FSH.",
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T1 - Plasma glycoprotein hormone α-subunit in the syndrome of gonadal dysgenesis

T2 - The effect of estrogen replacement in hypergonadotropic hypogonadism

AU - Styne, Dennis M

AU - Conte, F. A.

AU - Grumbach, M. M.

AU - Kaplan, S. L.

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N2 - Elevated plasma LH and FSH levels in hypergonadotropic hypogonadism can be reduced by estrogen therapy, but the change in readily releasable glycoprotein hormone α-subunit with therapy is undefined. We administered 100 μg LRF iv to seven patients (11-19 yr old) with the syndrome of gonadal dysgenesis before and during 9 months of therapy with oral conjugated estrogens at a dose of 0.3 mg/day. The control group was seven normal girls, aged 12-16 yr. Mean basal glycoprotein hormone levels for the untreated and treated gonadal dysgenesis groups and the control group were, respectively; α-subunit, 4.2, 1.3, and 0.8 ng/ml; LH, 9.3, 3.3, and 1.4 ng/ml; and FSH, 46.7, 17.8, and 1.6 ng/ml. Mean peak LRF-stimulated values for the untreated and treated gonadal dysgenesis groups and the control group were, respectively: α-subunit, 18.9, 5.1, and 3.7 ng/ml; LH, 43.4, 11.8, and 6.4 ng/ml; and FSH, 78.0, 23.3, and 3.6 ng/ml. Mean basal and peak plasma α-subunit, LH, and FSH concentrations in untreated patients with gonadal dysgenesis were higher (P < 0.005) than those in controls and treated patients (P < 0.05). The mean basal and peak plasma α-subunit and LH concentrations in treated patients were not significantly different than those in control patients. Mean basal and peak FSH concentrations in treated patients with gonadal dysgenesis were significantly higher (P < 0.05) than those in the control group. We concluded that 1) basal and peak LRF-stimulated plasma α-subunit values are significantly higher in untreated patients with gonadal dysgenesis than in normal girls and low dose estrogen therapy decreases α-subunit concentrations to normal; 2) estrogen therapy lowers basal and LRF-stimulated plasma LH concentrations to the normal range and lowers basal and LRF-stimulated FSH concentrations to a lesser degree; and 3) the release of the α-subunit in patients without primary thyroid disease is stimulated by hypothalamic LRF, as are the gonadotropins, but the secretion of α-subunit is more closely associated with the secretion of human LH than with that of human FSH.

AB - Elevated plasma LH and FSH levels in hypergonadotropic hypogonadism can be reduced by estrogen therapy, but the change in readily releasable glycoprotein hormone α-subunit with therapy is undefined. We administered 100 μg LRF iv to seven patients (11-19 yr old) with the syndrome of gonadal dysgenesis before and during 9 months of therapy with oral conjugated estrogens at a dose of 0.3 mg/day. The control group was seven normal girls, aged 12-16 yr. Mean basal glycoprotein hormone levels for the untreated and treated gonadal dysgenesis groups and the control group were, respectively; α-subunit, 4.2, 1.3, and 0.8 ng/ml; LH, 9.3, 3.3, and 1.4 ng/ml; and FSH, 46.7, 17.8, and 1.6 ng/ml. Mean peak LRF-stimulated values for the untreated and treated gonadal dysgenesis groups and the control group were, respectively: α-subunit, 18.9, 5.1, and 3.7 ng/ml; LH, 43.4, 11.8, and 6.4 ng/ml; and FSH, 78.0, 23.3, and 3.6 ng/ml. Mean basal and peak plasma α-subunit, LH, and FSH concentrations in untreated patients with gonadal dysgenesis were higher (P < 0.005) than those in controls and treated patients (P < 0.05). The mean basal and peak plasma α-subunit and LH concentrations in treated patients were not significantly different than those in control patients. Mean basal and peak FSH concentrations in treated patients with gonadal dysgenesis were significantly higher (P < 0.05) than those in the control group. We concluded that 1) basal and peak LRF-stimulated plasma α-subunit values are significantly higher in untreated patients with gonadal dysgenesis than in normal girls and low dose estrogen therapy decreases α-subunit concentrations to normal; 2) estrogen therapy lowers basal and LRF-stimulated plasma LH concentrations to the normal range and lowers basal and LRF-stimulated FSH concentrations to a lesser degree; and 3) the release of the α-subunit in patients without primary thyroid disease is stimulated by hypothalamic LRF, as are the gonadotropins, but the secretion of α-subunit is more closely associated with the secretion of human LH than with that of human FSH.

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