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At least 541 records · Page 30Linked to original sources
PubMed1999

Treatment with a gonadotropin-releasing-hormone analog and attainment of full height potential in a male monozygotic twin with gonadotropin-releasing hormone-dependent precocious puberty.

UNLABELLED: We report on a pair of male monozygotic twins, one unaffected and the other affected with gonadotropin-releasing hormone (GnRH)-dependent precocious puberty, and discuss the role of treatment with a GnRH analog in the attainment of full height potential in GnRH-dependent precocious puberty. At 1.6 years of age, the affected twin was studied for tall stature (+3.8 SD), and was diagnosed as having GnRH-dependent precocious puberty due to a hypothalamic hamartoma of the tuber cinereum. He was treated with oral cyproterone acetate (110-170 mg/m(2) daily) from 1.8 through 5. 0 years of age, with oral cyproterone acetate and intranasal buserelin acetate (700-900 microg/m(2) daily) from 5.0 through 7.5 years, and with intranasal buserelin acetate alone (1100- 1400 microg/m(2) daily) from 7.5 through 12.6 years. He attained a final height of 171.0 cm at 14.9 years of age (+0.10 SD) and his twin 170. 0 cm at 15.3 years of age (-0.10 SD), with their target height being 174.5 +/- 9.0 cm. CONCLUSION: This study indicates that GnRH analog treatment may preserve near full height potential in some patients with GnRH-dependent precocious puberty.

Administration, Inhalation↗
PubMed2000

Growth, puberty and hypothalamic-pituitary function in children with suprasellar arachnoid cyst.

UNLABELLED: A suprasellar arachnoid cyst may cause disorders of growth, puberty and hypothalamic-pituitary function, due to the proximity of the cyst to the hypothalamic-pituitary area. A total of 30 patients (17 boys) with cyst diagnosed at 4.3 +/- 1 years were routinely evaluated at 5.4 +/- 1 years; 24 of them had one or multiple cyst derivations. Some 23 cases had an abnormal height, weight or puberty: short (< -2SD, 5 cases) or tall ( > 2SD, 10 cases) stature, overweight (body mass index, BMI, > 2SD, 6 cases), central precocious puberty (10 cases) and/or no progression of pubertal development (3 cases). The growth hormone (GH) peaks after pharmacological stimulation test were low (< 10 MICROg/L) in 16 patients, confirmed by a second evaluation in 8/11 of them. The plasma free thyroxine was low in five patients, prolactin was high in two and the cortisol and concomitant plasma and urinary osmolalities were normal. BMI was correlated negatively with the GH peaks (r = -0.37, P < 0.01) and positively with the plasma leptin concentrations (r = 0.55, P < 0.01). The plasma fasting insulin concentrations were also correlated negatively with the GH peaks (r = -0.55, P < 0.02) and positively with the plasma insulin-like growth factor I concentrations (r = 0.64, P < 0.002). The adult height (12 cases) was at 4SD in 1 and < -2SD in 4 patients, two of whom had precocious puberty untreated with gonadotropin releasing hormone (GnRH) analogue, and two had untreated GH deficiency. The adult height of those treated was normal. One girl had primary amenorrhoea and two boys had low plasma testosterone, despite a normal gonadotropin response to a GnRH test. CONCLUSION: Suprasellar arachnoid cysts may cause deficiencies of growth hormone and thyrotropin, stimulation of the hypothalamic-pituitary-gonadal axis, tall stature and/or overweight. These last two disorders may be due to hyperinsulinism, itself due to suprasellar arachnoid cyst.

Adolescent↗
PubMed2006

GPR54 and KiSS-1: role in the regulation of puberty and reproduction.

The finding of inactivating mutations in GPR54 in IHH patients and the lack of reproductive maturation of the GPR54 null mouse have uncovered a previously unrecognized role for GPR54 and KiSS-1 in the physiologic regulation of puberty and reproduction. This newly identified function for GPR54 and its cognate ligand, kisspeptin, has led to additional studies that have localized GPR54 and KiSS-1 mRNA in the hypothalamus, colocalized GPR54 in GnRH neurons, demonstrated GnRH-dependent activation of LH and FSH release by kisspeptin, and shown increased hypothalamic KiSS-1 and GPR54 mRNA levels at the time of puberty. Taken together, these findings establish the role of the kisspeptin-GPR54 system in the stimulation of GnRH neurons during puberty. The mechanisms by which kisspeptin activates GnRH release, as well as the trigger for this pathway at the onset of puberty, are yet to be elucidated. In the future, modulators of GPR54 activity, including kisspeptin, may prove valuable in clinical applications in the fields of both cancer therapy and reproductive medicine.

Gonadotropins↗
PubMed2006

Hypomelanosis of Ito associated with precocious puberty.

Hypomelanosis of Ito has been associated with precocious puberty in two cases. This study reports a third case involving a female with hypomelanosis of Ito including severe mental retardation and seizure disorder with autonomic symptoms (gastroesophageal reflux and asthma). At age 5 she developed vaginal discharge, thelarche, and adrenarche. Soon after, she died of pneumonia stemming from her neurologic deficits. A postmortem examination revealed normal gonads and endocrine organs. The breasts and vulva were prematurely developed. Central nervous system findings included megalencephaly, neuronal eosinophilic inclusions, leptomeningeal neuroglial heterotopias, and cortical dysplasia. Both previously reported cases of hypomelanosis of Ito associated with precocious puberty had abnormal gonads and responded to cyproterone acetate therapy, indicating a peripheral mechanism of precocious puberty (gonadotrophin-independent). The current case, which was autopsied, lacks significant gonadal pathology, and has extensive neurologic involvement that suggests that a central mechanism of precocious puberty (gonadotrophin-dependent) can also be associated with hypomelanosis of Ito.

Brain↗
PubMed2005

IGF-1 administration to prepubertal female rats can overcome delayed puberty caused by maternal Pb exposure.

Because prepubertal female rats maternally exposed to lead (Pb) exhibit suppressed serum levels of insulin-like growth factor-1 (IGF-1) and delayed puberty, we investigated the ability of centrally administered IGF-1 to stimulate luteinizing hormone (LH) release in vivo and LH-releasing hormone (LHRH) release in vitro from maternally Pb-exposed prepubertal female rats. Additionally, we assessed whether IGF-1 replacement could affect the timing of female puberty. Results demonstrated that IGF-1 stimulated significantly LH release in both control and Pb-exposed animals. When median eminences from control and Pb-exposed females were incubated with rat IGF-1 in vitro, they responded similarly with significant peptide-induced LHRH release. Lastly, we showed IGF-1 replacement reversed the delay in puberty caused by Pb. These results indicate the central LHRH response to IGF-1 is intact and that Pb-induced delayed puberty is due, at least in part, to suppressed circulating IGF-1 available to the hypothalamus.

Animals↗
PubMed2005

Evolution, development and timing of puberty.

The age of menarche has fallen as child health has improved. Although there is ample evidence of delayed puberty being associated with poorer childhood nutrition, menarche is also influenced by prenatal factors. In particular, early onset of puberty is reported in children who have migrated from developing to developed countries. Evolutionary perspectives suggest that these effects can be explained by adaptive mechanisms. They also provide an explanation for the human pubertal growth spurt. In the past few decades, as puberty has advanced, biological maturation has come to precede psychosocial maturation significantly for the first time in our evolutionary history Although this developmental mismatch has considerable societal implications, care has to be taken not to medicalize contemporary early puberty inappropriately.

Adolescent↗
PubMed1993

Predictors of axial and peripheral bone mineral density in healthy children and adolescents, with special attention to the role of puberty.

The role of various physical and lifestyle factors in determining axial bone mineral density (BMD) at the lumbar segment of the spine, as measured by dual-photon absorptiometry, and peripheral BMD at the distal third of the radius, as measured by single-photon absorptiometry, was assessed in 299 healthy white children of both sexes, aged 6 to 18 years. The BMD measurements were correlated with age, height, weight, body mass index, and pubertal status. Peripheral and axial BMD were highly correlated with age, height, weight, and pubertal stage, and more weakly with body mass index. Approximately 76% of the observed changes in peripheral BMD were accounted for by age, height, weight, and pubertal stage, with weight being the single strongest predictor. Up to 80% of the variation in axial BMD was explained by weight and pubertal stage, with pubertal stage being the strongest single predictor. After adjustment for weight, the effect of puberty on axial BMD in both sexes was greatest between middle and late puberty. These data indicate that a large amount of the observed changes on BMD is accounted for by standard measures of growth and development, which are largely genetically determined. Peripheral BMD rose steadily with age. Axial BMD increased steadily before puberty, followed by accelerated increases during puberty, beginning at 10 years of age in girls and 13 years of age in boys. A significant positive effect of dietary calcium intake on peripheral BMD and of physical activity on axial BMD indicated a potentially important impact of physical activity and calcium intake on peak bone mass.

Adolescent↗
PubMed1977

Postpubertal evaluation of gonadal function following cyclophosphamide therapy before and during puberty.

Evaluation of pituitary gonadotropins, gonadal steroids, spermatogenesis, and menstrual function was undertaken in 32 patients (19 males and 13 females) treated with cyclophosphamide because of nephrotic syndrome. Patients were treated before, during, or after puberty. Evaluations took place after or in very late puberty. Spermatogenic dysfunction occurred in six of 15 boys who received the entire course before and during puberty and was probably dose related. Menstrual dysfunction did not occur following treatment of six prepubertal or pubertal girls, though only low total doses were used. Therapy after puberty was associated with spermatogenic dysfunction in all four boys, but did not cause menstrual dysfunction in any of seven women. Tentative guidelines are suggested that many minimize gonadal toxicity when cyclophosphamide is used in children with nephrotic syndrome. Factors of particular importance in the interpretation of gonadotropin determinations and of sperm counts in young cyclophosphamide-treated patients are discussed.

Cyclophosphamide↗
PubMed1980

LH bioactivity increases more than immunoreactivity during puberty.

We have measured bioactive LH in the plasma of 60 normal boys and 45 normal girls throughout puberty because the rise in immunoreactive LH has seemed too small to account for the profound changes in sexual maturation during adolescence. Bioactive LH was determined using an in vitro bioassay (rat interstitial cell testosterone production); I-LH was measured by radioimmunoassay using the same LH standard, LER 907. Bioactive LH was measurable in all 270 plasma samples; I-LH in 218. In both boys and girls, B-LH rose more than I-LH when compared to chronological age, bone age, and pubertal stage. In boys, B-LH increased 8.2-fold (P < 0.001) from prepuberty to late puberty, whereas I-LH rose 3.0-fold (P < 0.001). Similarly, in girls B-LH increased 23.1-fold (P < 0.001) while I-LH increased 4.9-fold (P < 0.001). Between pubertal stages there was less overlap of individual values of B-LH, in comparison to those of I-LH. We conclude that B-LH increases more than I-LH during normal puberty and is a more discriminating measure of maturation. One implication of these findings is that a qualitative change in gonadotropin secretion may occur during puberty.

Adolescent↗
PubMed1995

Predictive factors in the determination of final height in boys with constitutional delay of growth and puberty.

Seventy-eight patients who had constitutional delay of growth and puberty were included in a retrospective study to determine whether, at the time of first evaluation, any predictive features could suggest final height outcome. Mean chronologic age was 14.3 years (range, 12 to 18 years), and all were either prepubertal or in an early stage of pubertal maturation (4 ml testicular volume). Initial mean (+/- SD) height standard deviation score was -2.74 (+/- 0.71); 85% had a relatively short spine compared with subischial leg length. Mean (+/- SD) growth rate was 4.8 (+/- 1.6) cm/year, and epiphyseal maturation was delayed by 2.4 (+/- 1) years. Sixteen boys were treated with a sustained-action preparation of testosterone (50 mg monthly for 3 to 4 months), six with oxandrolone (1.25 mg daily for a mean of 4 months), and one with both drugs in sequence. At final height attainment, 58% of the boys failed to achieve their full genetic potential; among the remaining 42%, only 0.7% attained a final height above corrected mid-parental height. The relative disproportion between the segments had no significant change at final height attainment. Regression analysis showed that final height impairment (the difference between mid-parental height and final height) was negatively influenced by standing height and growth velocity when initially evaluated and positively by the degree of segmental body proportion; that is, patients who were taller, were growing at a faster rate, and who had a major degree of segmental body disproportion with a short spine and long leg length attained a final height closer to their mid-parental height, irrespective of the degree of delayed epiphyseal maturation. Neither testosterone nor oxandrolone administered during early puberty modified final height attainment or segmental proportion. We conclude that a late onset in the timing of puberty seems to be deleterious to spinal growth and consequently to final height attainment. An alternative diagnosis should be sought among patients with features of constitutional delay of growth and puberty who do not have a significant degree of body disproportion. In these patients, as well as in those who are extremely short, who have a poor growth rate, or who have an unfavorable genetic potential, an alternative therapeutic approach may be required.

Adolescent↗
PubMed1998

Central precocious puberty in girls: internal genitalia before, during, and after treatment with long-acting gonadotropin-releasing hormone analogues.

Pelvic ultrasonography was systematically performed on 33 girls with idiopathic central precocious puberty to investigate the impact of treatment with gonadotropin-releasing hormone analogues on female internal genitalia. All girls were treated with a long-acting gonadotropin-releasing hormone analogue (Decapeptyl Depot; Ferring Co., Copenhagen, Denmark) 75 micrograms/kg every 4 weeks. Before, during, and after treatment, pelvic ultrasonography was performed and ovarian and uterine volumes were calculated. The size of follicles > 5 mm were accurately measured. The results were related to a normative study of healthy Danish schoolgirls. Our data demonstrated that ovaries and uterus are enlarged in a significant number of girls (50%) with the diagnosis of central precocious puberty at the time of diagnosis. Median ovarian volume at time of diagnosis was 1.1 standard deviation scores (range -0.6 to 3.2 SD), median uterine volume was 1.8 standard deviation scores (range 0.0 to 3.5 SD). Within 3 months of treatment, both ovarian and uterine volumes decreased significantly (p < 0.01) to normal values appropriate for age. Median ovarian volume after 3 months of treatment was 0.0 SD (range -2.4 to 1.5 SD); median uterine volume was 0.7 SD (range -0.6 to 4.1 SD). Ovarian and uterine volume remained within normal range (< 2 standard deviation scores) after discontinuation of treatment. Follicles and macrocysts regressed during treatment. None of the girls' ovaries had a polycystic appearance during or after treatment with the gonadotropin-releasing hormone analogue. Our results confirmed pelvic ultrasonography as a reliable tool for investigation of internal genitalia in girls with precocious puberty and as a valid method for evaluation of the efficacy of treatment with gonadotropin-releasing hormone analogues. We suggest that repeated investigations be performed when evaluating treatment because the morphologic changes, including follicular maturation or regression, reflect ovarian stimulation or suppression. We found no evidence that girls with precocious puberty treated with long-acting gonadotropin-releasing hormone analogues have enlarged polycystic ovaries develop.

Adnexa Uteri↗
PubMed2002

Cognitive efficiency on a match to sample task decreases at the onset of puberty in children.

Electrocortical evidence indicates that a wave of synaptic proliferation occurs in the frontal lobes around the age of puberty onset. To study its potential influence on cognition, we examined 246 children (10-17 years) and 49 young adults (18-22 years) using a match-to-sample type of task to measure reaction times to assess emotionally related information. Based upon the instruction set, subjects made a yes/no decision about the emotion expressed in a face, a word, or a face/word combination presented tachistoscopically for 100 ms. The faces were images of a single individual with a happy, angry, sad or neutral expression. The words were 'happy,' 'angry,' 'sad,' or 'neutral,' In the combined stimulus condition, subjects were asked to decide if the face and word matched for the same emotion. Results showed that compared to the previous year, reaction times were significantly slower for making a correct decision at 11 and 12 years of age in girls and boys, the approximate ages of puberty onset. The peripubertal rise in reaction time declined slowly over the following 2-3 years and stabilized by 15 years of age. Analyses of the performance of 15-17 year olds revealed significantly longer reaction times in females to process both faces and words compared to males. However, this sex difference in late puberty appeared to be transient since it was not present in 18-22 year olds. Given the match-to-sample nature of the task employed, the puberty related increases in reaction time may reflect a relative inefficiency in frontal circuitry prior to the pruning of excess synaptic contacts.

Adolescent↗
PubMed1997

Does puberty interfere with asthma?

This study reviews whether, to date, scientific evidence exists that puberty interferes with the occurrence of asthma. This question was triggered by three points: (a) clinical experience with asthma as a relatively benign disease that children often 'grow out of'; (b) observations implying that asthma can change during fluctuations of sexual steroid hormones; and (c) knowledge that puberty is an age of deep hormonal changes. No scientific evidence was found that pubertal changes interfere with the occurrence of asthma. Nevertheless, there is a general agreement about the influence of age and sex on its outcome. The overall occurrence of the disease, which is highest in childhood, declines with age. In the wane phenomena, puberty does not seem to be more important than previous ages. Furthermore, the pattern of occurrence is different in the two sexes. Boys have more asthma before 10 years of age or the mid-teens. Girls then overtake boys and have more asthma up to the years of sexual maturity. During the fifth or sixth decade, asthma again seems to become slightly more prevalent in men than women, or at least the difference between the sexes disappears. It is concluded that the risk of asthma is not influenced by puberty. Age and sex seem to be more important factors, although the reason for this is unknown.

Adolescent↗
PubMedDate not supplied

Role of growth hormone in ovarian physiology and onset of puberty.

OBJECTIVE: To review the role of growth hormone (GH) in the timing of puberty and to summarize the interactions between the somatotrophic and reproductive axes. The use of recombinant GH in patients with GH deficiency is outlined. METHODS: A MEDLINE search was performed of English language manuscripts dealing with the role or use of GH in puberty and reproduction. RESULTS: Growth hormone appears to augment the rate of sexual maturation once a pubertal pattern of gonadotropin secretion is established. Growth hormone may modulate gonadal steroid production by increasing hepatic insulin-like growth factor-I production or by acting directly on GH receptors, localized recently in the granulosa cells and corpus luteum in the human ovary. Patients with isolated GH deficiency exhibit short stature, truncal adiposity, and delayed puberty. However, patients with isolated GH deficiency ultimately undergo spontaneous puberty, and women with GH receptor defects are fertile, suggesting that GH most likely acts as a co-gonadotropin to augment the actions of FSH and LH on estradiol and progesterone production. CONCLUSIONS: Growth hormone appears to increase the rate of sexual maturation once a pubertal pattern of pituitary gonadotropin secretion is established. The ovary is a site of GH reception and action, where it can potentiate steroidogenesis and gametogenesis either directly or through endocrine actions. Continued basic and clinical research is needed to characterize further the role of GH in reproductive physiology.

Animals↗
PubMed1996

An association between precocious puberty and fragile X syndrome?

STUDY OBJECTIVE: To determine the FMR1 gene status in a 10-year, 10-month-old girl with a history of precocious puberty and a family history of fragile X syndrome. DESIGN: Case report. SETTING: The outpatient facility of the Division of Adolescent Medicine and the Division of Genetic and Metabolic Disorders at Children's Hospital of Michigan and the Medical Genetics and Birth Defects Center of Henry Ford Hospital, Detroit, Michigan. PARTICIPANT: A 10-year, 10-month-old girl with a history of precocious puberty. INTERVENTION: Evaluation for menorraghia, DNA extraction, and fragile X gene analysis of blood samples from the patient and her mother. MAIN OUTCOME MEASURES: Identification of a full mutation in the FMR1 gene. RESULTS: Southern blot analysis of the FMR1 gene identified a full mutation in the daughter with approximately 750 repeats of the CGG sequence. Methylation studies showed that the full mutation was completely methylated. FMR1 DNA studies on her mother identified a premutation of approximately 100 repeats. CONCLUSIONS: This report identifies a young girl with a history of precocious puberty and fragile X syndrome. It is also the first report of molecular genetic FMR1 studies in a female with precocious puberty. A possible association between the two conditions is suggested and warrants further investigation.

Blotting, Southern↗
PubMed2003

Sex steroid replacement during and after the induction of puberty.

The main aim of sex steroid replacement during induction of puberty is to obtain a balance between healthy psychological and somatic development and optimal final height and peak bone mass (PBM). At present, the age at which it is considered appropriate to begin inducing puberty is younger than it was in the past. This trend aims for optimisation of prepubertal and pubertal growth through earlier onset of growth hormone (GH) therapy and administration of higher doses during puberty as necessary. Adequate initiation of puberty should ensure not only optimal final height and psychological balance, but also normal body proportions, appropriate bone formation and preservation of fertility for children with GH and gonadotropin deficiencies.

Adolescent↗
PubMedDate not supplied

Leptin and puberty: a review.

Over the last few years, many studies have focused on leptin, the product of the LEP (ob) gene, searching for a possible link between energy balance and reproduction. The involvement of this peptide in the regulation of the hypothalamo-pituitary-adrenal, gonadal, thyroid and somatotroph axes suggests that leptin might play a pivotal role in coordinating the activity of these axes and their relationship with the body's energy balance. The effects of leptin on hypothalamic, pituitary and peripheral hormone levels, as well as the presence of the leptin receptor in a variety of tissues, suggest both an endocrine and a paracrine mode of action. Particular attention was paid to the effect of leptin on the gonadal axis as infertility, a characteristic feature of both the leptin deficient ob/ob mice and the leptin receptor mutant db/db mice, could be corrected in ob/ob mice by leptin administration. Considerable leptin level changes were observed during puberty both in animal and human studies. A matter of controversy is the precise role of leptin in the onset of puberty: is leptin the signal that initiates puberty and the accompanying hormonal changes, or has leptin only a permissive but key role for the onset of puberty, as likely seems to be the case for the maintenance of a functional gonadotroph axis? On current evidence, a mainly permissive role seems most probable.

Animals↗
PubMed2002

Age of puberty and sexual orientation in a national probability sample.

The relations between sexual orientation and age of puberty in both men and women were examined in a national probability sample of the United States. The sample was the National Health and Social Life Survey (E. O. Laumann, J. H. Gagnon, R. T. Michael, & S. Michaels, 1994), which contains 3432 cases. Gay/bisexual men reported an earlier age of puberty (e.g., age of first pubic hair) relative to heterosexual men, but lesbian/bisexual women did not report a different age of puberty (i.e., age of menarche) than heterosexual women. These results confirm findings from prior research examining age of puberty using nonrepresentative samples and add to a body of literature suggesting that gay/bisexual men may score, on average, in the female-typical direction on certain sex-dimorphic physical and developmental characteristics.

Adolescent↗