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Results for “PUBERTY, PRECOCIOUS”

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At least 19 recordsLinked to original sources
PubMed1975

Responsivity of pituitary gonadotropes to luteinizing hormone-releasing factor in idiopathic precocious puberty, precocious thelarche, precocious adrenarche, and in patients treated with medroxyprogesterone acetate.

One hundred micrograms synthetic luteinizing hormone-releasing factor (LRF) were administered to 13 girls and 2 boys with idiopathic precocious puberty, 3 girls with precocious thelarche, 2 girls with precocious adrenarche, and 5 children treated with medroxyprogesterone acetate (MPA). Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sex steroid responses were assessed. The mean readily releasable LH rose to a peak of 8.4 plus or minus 1. 8 ng/ml (LER 960) in the children with idiopathic precocious puberty and was significantly greater than in normal prepubertal (1.8 plus or minus 0.14) or pubertal children (4.9 ng/ml) (LER 869) was higher in precocious puberty but not significantly greater than in normal prepubertal (5.3 plus or minus 1.9) or pubertal girls (6.0 plus or minus 1.2). The mean concentration of plasma estradiol rose significantly above resting levels after LRF in the girls with idiopathic precocious puberty. The LH response in girls with precocious the larche was in the prepubertal range. In 4 of 5 children with sexual precocity treated with MPA, the LH release evoked by LRF was diminished.

Child↗
PubMed1998

Gonadotrophin and prolactin secretory dynamics in girls with normal puberty, idiopathic precocious puberty and precocious puberty due to hypothalamic hamartoma.

OBJECTIVE: This study was designed to test the hypothesis that hypothalamic hamartoma causes precocious puberty through a different neuroendocrine mechanism than that of normal puberty or of idiopathic precocious puberty. DESIGN AND PATIENTS: We compared the pattern of gonadotrophin secretion among 4 girls with precocious puberty due to hypothalamic hamartoma, 27 girls with idiopathic precocious puberty, and 14 girls with normal puberty. All subjects were breast stage 3 or 4. Blood samples were obtained every 20 min for 4 h during the day (1.000 hours to 1400 h) and night (22.00 hours to 0200 h). MEASUREMENTS: LH, FSH, and prolactin were measured in each blood sample. Girls also underwent LHRH-stimulation with measurement of LH and FSH before and after stimulation. RESULTS: There were no significant differences in mean LH level, LH peak amplitude, or LH or FSH peak frequency during either the day or the night among the three diagnostic groups. However, the mean +/- SD LHRH-stimulated peak LH levels were greater in girls with hypothalamic hamartoma than in girls with normal puberty or with idiopathic precocious puberty (194 +/- 142 vs 85 +/- 60 or 66 +/- 54 IU/l, respectively, P < 0.05). The LHRH-stimulated peak FSH level in girls with hypothalamic hamartoma exceeded the level for the normal pubertal girls (31 +/- 19 vs 17 +/- 7 IU/l, P < 0.05), but not the level for the girls with idiopathic precocious puberty (25 + 12 IU/l). The peak LH to peak FSH ratio in the girls with hypothalamic hamartoma exceeded the ratio for the girls with idiopathic precocious puberty (7.3 +/- 3.9 vs 2.6 +/- 3.0 IU/l, P < 0.05), but not the ratio for the normal pubertal girls (5.0 + 2.9). There were no significant differences in mean prolactin level, peak amplitude or frequency, or in the ratio of mean night to mean day prolactin, among the 3 diagnostic groups. CONCLUSIONS: We conclude that spontaneous gonadotrophin and prolactin secretion are similar among girls with hypothalamic hamartoma, idiopathic precocious puberty, or normal puberty. However, the increased LHRH-stimulated peak LH in the girls with hypothalamic hamartoma suggests subtle differences in neuroendocrine regulation that may underlie their more rapid pubertal maturation.

Adolescent↗
PubMed1991

Drug treatment in precocious puberty.

Precocious puberty, as defined by the onset of pubertal development before the age of 8 years in girls or 9 years in boys, can be classified into central and peripheral aetiologies. Central precocious puberty (CPP) results from early activation of the hypothalamic-pituitary-gonadal axis and has similar physical and hormonal characteristics to normal puberty. Extrapituitary gonadotrophin secretion or independent sex steroid secretion results in peripheral precocious puberty (PPP). Precocious puberty is characterised by rapid growth and advancement of skeletal age. The skeletal advancement is greater than the growth increase, so that final adult height is compromised. Long-acting gonadotrophin releasing hormone (GnRH) agonists are the current therapy of choice for central precocious puberty, having demonstrated effectiveness in halting the precocious development associated with this condition with minimal side effects. GnRH agonists are not effective as therapy for peripheral precocious puberty, but a number of other agents have been used with some success. These include androgen antagonists, testolactone, ketoconazole, and medroxyprogesterone acetate. The use of GnRH agonists has been associated with an increase in predictions of final height; however, continuing studies in treated cohorts are necessary to determine the true benefit of any of these agents on increasing ultimate height.

Adolescent↗
PubMed2000

The radiological approach to precocious puberty.

Precocious puberty is caused by a heterogeneous group of disorders, which range from idiopathic to malignant tumours. The radiologist's role is to help: (1) differentiate precocious puberty from pubertal variants; (2) identify the underlying cause of precocity if present; and (3) assess for effectiveness of treatment. This pictorial review discusses the types of precocious puberty and their underlying aetiologies, differentiates precocious puberty from pubertal variants and illustrates the appropriate imaging evaluation for the patient diagnosed with precocious puberty.

Algorithms↗
PubMed2006

[Precocious puberty].

Precocious puberty is usually defined as the appearance of secondary sexual development before the age of 8 years in girls and 9 years in boys. Precocious puberty is a heterogenous condition generally divided into central and peripheral forms driven respectively by hypothalamic-pituitary axis or by excessive production of sex steroids. Taking into account the risk associated with the underlying disorder as well as the impact of precocious puberty on stature growth and development of reproductive and mental functions, this condition has important consequences for affected children and their families. In this paper, the pathophysiology, clinical presentation, laboratory and radiological features, and treatment of the disorders leading to precocious puberty are reviewed. Particular attention is devoted to the results of the recently published studies.

Child↗
PubMed2000

A brief review of the effects of chronic hydrocephalus on the gonadotropin releasing hormone system: implications for amenorrhea and precocious puberty.

Precocious puberty and amenorrhea have been associated with hydrocephalus, but the pathogenesis has not been determined. Approximately 22 cases of amenorrhea, and a few cases of precocious puberty, have been reported in hydrocephalic patients. Shunt treatment leads to initiation and maintenance of normal reproductive cycles in most cases. An underlying mechanism responsible for reproductive dysfunction may involve the role of gonadotrophin releasing hormone (GnRH). The exact pathway by which hydrocephalus disrupts the hypothalamic GnRH system is unknown. However, compressive forces, ischemia, and impairment of neurotransmitter feedback loops are likely candidates.

Amenorrhea↗
PubMed1986

[Central precocious puberty].

Precocious puberty is a stressful event for patient and environment. The diagnostic evaluation will be discussed. LHRH analogs will give a new approach in the treatment of central precocious puberty.

Age Determination by Skeleton↗
PubMed1979

The child with precocious puberty.

Precocious puberty can be very confusing and frightening to an affected child and his or her family. The following presentation includes the pertinent physiology, psychology, etiology, diagnosis, and treatment of precocious pubertal development. Radioimmunoassays for gonadotropins and several key hormones are now available which enable the clinician to evaluate and follow the patient's condition with confidence and expertise. Three drugs have been proven effective and the most recent one, cyproterone acetate, has produced exciting clinical remissions with virtually no known side effects.

Adolescent↗
PubMed1986

Is heterozygosity for the steroid 21-hydroxylase deficiency responsible for hirsutism, premature pubarche, early puberty, and precocious puberty in children?

We applied the ACTH-stimulation test developed in our laboratory for the detection of heterozygous carriers of the 21-hydroxylase deficiency gene to patients suffering from hirsutism (n = 89), premature pubarche (n = 75), early puberty (n = 37), and precocious puberty (n = 22). While, in the general population, this test is positive in less than 2%, we found in 33% of hirsute patients, in 41% of patients with premature pubarche, and in 33% of patients with early puberty a hormonal response similar to the one seen in heterozygous carriers for the 21-hydroxylase defect. In contrast, only 18% of patients with precocious puberty responded abnormally. Thus we speculate that, at least in some patients with hirsutism, premature pubarche, and early puberty, heterozygosity for the 21-hydroxylase defect plays a major role in the pathogenesis of these disorders.

17-alpha-Hydroxyprogesterone↗
PubMed1976

Clinical use of the LH-RH in assessing gonadotropic reserve in children with idiopathic precocious puberty, premature thelarche and premature adrenarche.

Serum LH and FSH were assayed in 31 girls with normal pre puberty, precocious puberty, premature thelarche, and premature adrenarche, aged 2 to 9 years. The effect of synthetic luteinizing hormone-releasing hormone (LH-RH) on serum gonadotropins was evaluated in eleven of them. In all girls with precocious puberty, serum LH was increased up to high levels. The mean releasable LH in two girls with idiopathic precocious puberty was significantly greater than in normal prepubertal or pubertal children. Basal FSH in children with precocious puberty was within the limits of normal prepuberal children, and FSH secretion in response to LH-RH was not significantly greater than in the group of normal prepubertal and pubertal girls. In children with premature thelarche and premature adrenarche, basal levels of LH and FSH, as well as gonadotropin response to LH-RH were in the prepubertal range. These preliminary results show that the LH-RH test might be of clinical value in differenitating abnormal puberal development.

Age Factors↗
PubMed1991

Long-term results with a slow-release gonadotrophin-releasing hormone agonist in central precocious puberty. Dutch-German Precocious Puberty Study Group.

As part of an ongoing international multicentre study, 19 children (14 girls, 5 boys) with central precocious puberty (CPP) were treated with a slow-release gonadotrophin-releasing hormone (GnRH) agonist, triptorelin, for 4 years. After 3 years of treatment, height velocity stabilized at 4.0 cm/year. Predicted adult height (mean +/- SD) increased from 158.9 +/- 6.8 to 164.9 +/- 6.6 cm in girls (n = 14, p less than 0.01), and from 174.4 +/- 18.5 to 184.3 +/- 17.1 cm in boys (n = 4, p less than 0.05). In 12 additional girls who had started the multicentre study but discontinued triptorelin treatment after 2.2 +/- 0.5 years, menses started 9.8 +/- 3.7 months after cessation of treatment in all but one patient. Height velocity increased over the first 6 months after discontinuation of treatment, from 3.6 +/- 0.1 to 5.4 +/- 2.5 cm/year, and remained higher than pretreatment values in the second 6 months, but decreased subsequently. Bone maturation increased, and no significant improvement in predicted adult height was observed. For auxological reasons, therefore, it may be advisable to continue triptorelin treatment for as long as possible. Concomitant growth hormone (GH) therapy was initiated in three girls with CPP with height velocities of 3.2-3.6 cm/year after 3 years of treatment with triptorelin and predicted adult heights of less than the third centile for Dutch girls. Prior to the administration of GH, all patients had subnormal 24-hour GH profiles and GH responses to arginine provocation. GH treatment increased height velocity markedly in all girls, and improved predicted adult height.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1979

[Hormonal regulation and hormone therapy in childhood and adolescence. Part 2: Therapeutic problems (tall stature, amenorrhea, delayed puberty, oligomenorrhea, precocious puberty, anorexia nervosa, anisomastia, hypermastia, acne etc)].

The most important therapeutic problems of female puberty and adolescence are discussed, including high stature, amenorrhoea, oligomenorrhea, pubertas tarda, anovulation, anorexia, anisomastia, hypermastia. Indications for treatment are given and the possibilities for a prophylactic medicine in this age group are stressed.

Acne Vulgaris↗