How many cases of true precocious puberty in girls are idiopathic?

Cacciari, E; Frejaville, E; Cicognani, Alessandro; Pirazzoli, Piero; Frank, Giorgio; Balsamo, Antonio; Tassinari, Davide; Zappulla, F; Bergamaschi, R.; Cristi, Gianfranco

doi:10.1016/s0022-3476(83)80648-9

Cited by 76 publications

(35 citation statements)

References 9 publications

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“…The four patients in whom treatment was stopped prematurely showed no rapid deterioration in height prognosis. We could find no difference in the pattern of growth potential between patients who had normal neuroradiology and those who had hypothalamic hamartomata, despite a report that the endocrinology may differ in these two groups [5]. Although the mean dose of cyproterone acetate in the majority of our patients was below that usually recom- Mean dose of cyproterone acetate mg/m z/day Fig.…”

Section: Resultscontrasting

confidence: 62%

The effect of cyproterone acetate on the growth of children with central precocious puberty

et al. 1987

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We have examined the growth and skeletal maturation of 19 children (6 male, 13 female) with central precocious puberty. The aetiology in nine patients (5 male, 4 female) was secondary to a hypothalamic hamartoma. Six children (2 male, 4 female) received no treatment whereas 13 children (4 male, 9 female) were treated with cyproterone acetate in a mean dose of 68 mg/m2 per day (range, 34-260) for a mean duration of 4.5 years (range, 0.8-7.9). There was no significant difference between height SDS for bone age at the beginning and end of observation in either treated or untreated groups. No significant relationship between the mean dose of cyproterone acetate used and change in height SDS for bone age could be determined. We conclude that cyproterone acetate has no beneficial effect on the growth prognosis of children with central precocious puberty.

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Section: Resultscontrasting

confidence: 62%

The effect of cyproterone acetate on the growth of children with central precocious puberty

et al. 1987

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“…Other series have reported no change in follow-ups of up to 1 1 years [25][26][27]. Downloaded from www.ajronline.org by 54.191.190 …”

Section: Hypothalamic Hamartomamentioning

confidence: 93%

CT of cerebral abnormalities in precocious puberty

Kg¹,

Comite²,

Aj³

et al. 1987

American Journal of Roentgenology

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“…1). Although most cases of precocious puberty of cerebral origin occur in girls and are diagnosed as idiopathic (2), computed axial tomography has revealed that an increasing number of these cases are associated with discrete hypothalamic pathology (2,3). Experimentally, female sexual precocity can be induced in both primates and rodents by lesions of the hypothalamus (4,5).…”

mentioning

confidence: 99%

Transforming growth factor alpha contributes to the mechanism by which hypothalamic injury induces precocious puberty.

Junier

Jin

Costa

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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It has long been known that lesions of the hypothalamus lead to female sexual precocity. While an increased production of luteinizing hormone-releasing hormone (LHRH), the neurohormone that controls sexual development, appears to mediate the advancement of puberty induced by these lesions, little is known about the mechanism(s) by which hypothalamic injury activates LHRH secretion. Since brain lesions result in accumulation of neurotrophic/mitogenic activities in the injured area, we tested the hypothesis that transforming growth factor a (TGF-a), a mitogenic polypeptide recently shown to stimulate LHRH release, is produced in response to hypothalamic injury and mediates the effect of the lesion on puberty. Radiofrequency lesions of the preoptic area-anterior hypothalamic area (POA-AHA) of 22-day-old female rats resulted in precocious puberty within 7 days after the operation. RNA blot hybridization revealed that lesioninduced puberty was preceded by an increase in TGF-a mRNA levels in the POA-AHA. Epidermal growth factor (EGF) mRNA was undetectable in both intact and lesioned hypothalami. TGF-a mRNA levels, quantitated by RNase protection assays, were 3.5-fold greater in lesioned animals approaching puberty than in age-matched controls. Immunohistochemical studies, utilizing single-and double-staining procedures, demonstrated the presence of TGF-a precursor-like immunoreactivity in reactive astrocytes surrounding the lesion site. Hybridization histochemistry showed increased TGF-a mRNA expression in cells of the same area, further implicating reactive astrocytes as a site of TGF-a synthesis. The onset of mammalian puberty depends on the activation of neurons that are located in the diencephalon and secrete the neurohormone luteinizing hormone-releasing hormone (LHRH) (for review, see ref. 1). Although most cases of precocious puberty of cerebral origin occur in girls and are diagnosed as idiopathic (2), computed axial tomography has revealed that an increasing number of these cases are associated with discrete hypothalamic pathology (2, 3). Experimentally, female sexual precocity can be induced in both primates and rodents by lesions of the hypothalamus (4, 5).Lesions of the anterior hypothalamus in rodents (5) result in true sexual precocity, as animals bearing these lesions mate and rear litters normally (6). The mechanisms underlying this phenomenon are unknown, but the notion that lesions accelerate sexual development by eliminating a site(s) for steroid inhibitory control (5) has gained acceptance. To date, an involvement of neurotrophic/mitogenic activities produced locally in response to brain injury (7) has not been considered in lesion-induced precocious puberty. We have taken advantage of this unique model (5, 6) to test the hypothesis that neurotrophic/mitogenic factors, thought to be involved in the reorganization of the brain that follows injury (7), are responsible for the advancement ofpuberty caused by hypothalamic lesions. We focused our attention on transforming growth factor a (TGF-a)...

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How many cases of true precocious puberty in girls are idiopathic?

Cited by 76 publications

References 9 publications

The effect of cyproterone acetate on the growth of children with central precocious puberty

The effect of cyproterone acetate on the growth of children with central precocious puberty

CT of cerebral abnormalities in precocious puberty

Transforming growth factor alpha contributes to the mechanism by which hypothalamic injury induces precocious puberty.

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