Gonadotropin and Sex Steroid Response to Luteinizing Hormone-Releasing Hormone in Patients with Premature Adrenarche

Lee, Peter A.; Gareis, Frank J.

doi:10.1210/jcem-43-1-195

Cited by 20 publications

(8 citation statements)

References 9 publications

(23 reference statements)

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“…As female puberty is accompanied by a modest rise in ovarian-derived testosterone in girls with normally-timed 33 or precocious puberty, 34 the current model can be extended to determine the effect of premature testosterone exposure on delta power. While we did not measure testosterone levels in the current studies, our data suggest that, at least in girls, testosterone is unlikely to be responsible for the decline in delta power during adolescence.…”

Section: Discussionmentioning

confidence: 99%

“…CPP participants and study controls demonstrated a similar distribution of chronotype scores, with the average score in both groups falling within the "intermediate" category, defined as scores of 24-32 (CPP: 27.5 ± 1.7 ; controls: 25.2 ± 3.1 [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33]). Suppressive therapy with a GnRHa and/or the passage of time had no effect on CPP participants' morningness/ eveningness preference, and chronotype did not correlate with chronologic age or stage of breast development in combined analyses of CPP participants and study controls (r = −0.06, p > .05 for both tests).…”

Section: Chronotype In Cpp Participants and Study Controlsmentioning

confidence: 99%

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The Relationship Between Estrogen and the Decline in Delta Power During Adolescence

McHill

Klerman

Slater

et al. 2017

Sleep

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Study Objectives: During adolescence, there is a precipitous decrease in slow-wave sleep (SWS) and its spectral correlate, delta power, which may reflect cortical reorganization. The temporal association between the decrease in delta power and puberty suggests that sex steroids may initiate these changes. This association has not been previously investigated. Methods: To determine whether estrogen triggers the adolescent decline in delta power, we compared delta power in 14 girls with central precocious puberty (CPP) and 6 age-matched, prepubertal controls. Five CPP participants were re-studied 7-14 months after pubertal suppression to determine if the changes in delta power are reversible after restoring a prepubertal hormonal milieu. The change in delta power was also compared between CPP participants and five historic controls from a longitudinal polysomnographic study. Results: CPP participants (6.7-10.5 years) spent 30% of the night in SWS. Delta power (3.7 × 10 6 ± 2.7 × 10 5 µV 2 ) predominated in the first 2 non-rapid eye movement episodes and decayed exponentially (tau 0.006 minutes). Age-matched controls demonstrated similar sleep staging (24% SWS) and delta dynamics (3.3 × 10 6 ± 5.1 × 10 5 µV 2 , tau 0.004 minutes). Four out of 5 CPP participants had a significant decrease (26%) in delta power after hormone suppression (p < .05), similar to historic controls. Conclusion: Using an innovative model of girls with CPP studied before and after estrogen suppression, the effects of puberty on the decline in delta power were dissociated from those of chronologic age. The current studies suggest that increased estrogen does not cause the adolescent decline in delta power and indicate that neurodevelopmental changes per se or other factors associated with puberty drive these sleep changes.

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Section: Discussionmentioning

confidence: 99%

Section: Chronotype In Cpp Participants and Study Controlsmentioning

confidence: 99%

The Relationship Between Estrogen and the Decline in Delta Power During Adolescence

McHill

Klerman

Slater

et al. 2017

Sleep

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“…The steroids produced at such a specific time of the rat prepubertal period may have a role in prepubertal development. In the human, this idea has been the subject of some dispute since precocious adrenarche may not always be followed by similarly precocoius puberty (Sizonenko & Paunier 1975, Lee & Gareis 1976, and precocious puberty Figure 9 Plasma testosterone levels in male rats during the postnatal period (meanGS.E.M., nR11 throughout). The first point at which clearly elevated testosterone levels were observed was at day 35.…”

Section: Discussionmentioning

confidence: 99%

Adrenarche in the rat

Pignatelli

Xiao

Gouveia

et al. 2006

Journal of Endocrinology

120

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Normal pubertal development in humans involves two distinct processes: maturation of adrenal androgen secretion (adrenarche) and activation of the hypothalamic-pituitary-gonadal axis (gonadarche). One factor thought to contribute to the adrenarche in man is increased adrenal 17-hydroxylase (CYP17) activity. In the rat, there is evidence for adrenal involvement in the initiation of puberty, but the adrenal glands of this species are generally thought to express CYP17 only very poorly at best. To further examine the nature of postnatal adrenal development in rat, plasma samples and adrenal tissues were taken from animals aged 2-90 days, circulating adrenal steroids assayed, and adrenal zones assessed quantitatively. A relative increase in zona reticularis, and peaks of circulating cortisol, androstenedione, and 17-OH-progesterone were observed around postnatal days 16-20, clearly before the development of the gonads, which begins at 30-35 days. Quantitative reverse transcriptase PCR confirmed a peak in mRNA coding for CYP17 in adrenal tissue from rats of similar age. The results suggest that the rat adrenal has the capacity to secrete steroids arising from 17-hydroxylation, and that this may contribute to a process similar to human adrenarche.

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“…In premature isolated development of pubic hair (premature adrenarche), response to the LH-RH test is in the normal prepubertal range, thus suggesting that the hypothalamo-pituitary gonadal maturation is not modified {Lee and Gareis, 1976).…”

Section: Lh-rh Test In Congenital Virilizing Adrenal Hyperplasia and mentioning

confidence: 99%

The Use of Luteinizing Hormone-Releasing Hormone in Pediatric Patients

Job¹,

Chaussain²,

Gamier³

1977

Horm Res

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Luteinizing hormone-releasing hormone (LH-RH), first synthetized in 1971; became soon available for clinical purposes and was immediately used as a diagnostic tool in children and adolescents as well as in adults. The first results of the LH-RH test in pediatrics were reported in 1972 and soon after discussed in meetings allowing comparison of the data from different groups. From this time, a great number of publications has been devoted to the diagnostic usefulness of LH-RH in the study of pubertal development and of pituitary-gonadal disorders in children and adolescents. Until recently, the therapeutic use of LH-RH has been restricted by the lack of availability of sufficient amounts, so that only few preliminary data have been reported in this field. Thus the scope of this review is mainly to present a critical survey of the data concerning LH-RH test in pediatric patients.

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Gonadotropin and Sex Steroid Response to Luteinizing Hormone-Releasing Hormone in Patients with Premature Adrenarche

Cited by 20 publications

References 9 publications

The Relationship Between Estrogen and the Decline in Delta Power During Adolescence

The Relationship Between Estrogen and the Decline in Delta Power During Adolescence

Adrenarche in the rat

The Use of Luteinizing Hormone-Releasing Hormone in Pediatric Patients

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