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PubMed1977

Hypothalamic hamartoma: a source of luteinizing-hormone-releasing factor in precocious puberty.

The presence of a hypothalamic hamartoma and precocious puberty in a 19-month-old boy provided an opportunity to study their relation. Excised tissue had the ultrastructural characteristics of an independent neuroendocrine unit -- i.e., neurons containing neurosecretory granules and blood vessels with fenestrated endothelium and double basement membranes. Immunofluorescence studies using specific antibody to luteinizing-hormone-releasing factor showed antigenicity to the factor in the hamartoma. The testicular-hypothalamic-pituitary axis was tested. Clomiphene unresponsiveness suggested a lack of maturation of central-nervous-system events characteristic of normal puberty. The negative feedback system between gonad and brain was intact but partially resistant to steroid suppression. These studies suggest that hypothalamic hamartomas may cause precocious puberty by autonomous production and release of luteinizing-hormone-releasing factor into vessels that communicate with the pituitary portal blood system.

Brain Neoplasms↗
PubMed1983

Long-term treatment of central precocious puberty with a long-acting analogue of luteinizing hormone-releasing hormone. Effects on somatic growth and skeletal maturation.

The gonadotropin-releasing hormone-like agonist D-Trp6-Pro9-NEt-LHRH (LHRHa) has been shown to induce a reversible short-term suppression of gonadotropins and gonadal steroids in patients with central precocious puberty. Since accelerated statural growth and bone maturation are clinical features of precocity not well controlled by conventional therapies, we examined the effects of prolonged LHRHa therapy for 18 consecutive months on growth and skeletal maturation in nine girls with neurogenic or idiopathic precocious puberty. Suppression of gonadotropin pulsations and gonadal steroids was maintained in all subjects. Growth velocity fell from a mean rate (+/- S.E.M.) of 9.35 +/- 0.64 cm per year during the 19 months before treatment to 4.58 +/- 0.60 cm per year during treatment (P less than 0.001). Bone age advanced a mean of 9.4 +/- 2.3 months during treatment. These changes resulted in a mean increase of 3.3 cm in predicted height (P less than 0.01). Complete suppression of the pituitary-gonadal axis can be maintained by LHRHa therapy, resulting in slowing of excessively rapid growth and skeletal maturation and in increased predicted adult height in girls with precocious puberty.

Age Determination by Skeleton↗
PubMed1986

Treatment of precocious puberty in the McCune-Albright syndrome with the aromatase inhibitor testolactone.

The McCune-Albright syndrome is characterized by café au lait spots, fibrous dysplasia of bones, and sexual precocity. Girls with precocious puberty due to this syndrome have episodic increases in serum estrogen levels together with the formation of large ovarian cysts. The serum gonadotropin levels are typically suppressed, and the precocious puberty has not responded to treatment with long-acting analogues of luteinizing hormone-releasing hormone (LHRH). Encouraged by our initial success in a pilot study of one patient, we have now treated five girls with the McCune-Albright syndrome with the aromatase inhibitor testolactone, which blocks the synthesis of estrogens. Testolactone decreased the levels of circulating estradiol (P less than 0.05) and the ovarian volume (P less than 0.05), and there was a return to pretreatment levels after testolactone was stopped. During treatment, the peak responses of luteinizing hormone and follicle-stimulating hormone to stimulation by LHRH rose above suppressed pretreatment levels--significantly above pretreatment levels for follicle-stimulating hormone (P less than 0.02)--and then returned to pretreatment levels after testolactone was discontinued. Growth rates fell in three patients during treatment but could not be assessed in the other two because of bone deformities. The mean rate of bone maturation decreased and menses stopped in three of the four girls who were menstruating regularly. We conclude that testolactone is an effective treatment of precocious puberty in the McCune-Albright syndrome.

Aromatase Inhibitors↗
PubMed1989

Normal or early development of puberty despite gonadal damage in children treated for acute lymphoblastic leukemia.

To determine the timing of pubertal development and the frequency of gonadal dysfunction in children who survive acute lymphoblastic leukemia, we assessed pubertal status and the plasma levels of sex steroids, gonadotropin, and inhibin in 45 children (20 girls and 25 boys) who had received combination chemotherapy along with 24 Gy of irradiation to the cranium (modified LSA2L2 protocol). We also reexamined testicular biopsy specimens, obtained at the time of the cessation of chemotherapy, for the presence of germ cells. Germ-cell damage, indicated by marked elevations in the plasma level of follicle-stimulating hormone (P less than 0.001 for the comparison with normal children), was evident in both sexes and was confirmed in the boys by the absence of germ cells in the testicular biopsy specimens and by the small size of the testes for pubic-hair stage. Only 44 percent of the pubertal girls had measurable plasma inhibin levels, as compared with more than 93 percent of normal pubertal girls. Although plasma sex-steroid levels were normal, the secretion of luteinizing hormone in response to stimulation with gonadotropin-releasing hormone was elevated in the pubertal children (P less than 0.01 for the comparison with normal controls)--a finding that suggests compensation for decreased gonadal function. Despite clear evidence of gonadal damage, girls had early menarche at a mean age (+/- SD) of 11.95 +/- 0.91 years, as compared with the Australian standard of 12.98 +/- 1.11 years (P less than 0.01). Thus, in girls, puberty was early despite primary gonadal damage. Thirteen of 23 boys reached puberty at a mean age of 12.36 +/- 0.73 years. We conclude that treatment for acute lymphoblastic leukemia may lead to primary gonadal damage in both sexes, regardless of the age at treatment, but that the secondary characteristics of puberty develop at a normal age or, in girls, relatively early.

Adolescent↗
PubMed1991

Changes in vertebral bone density in black girls and white girls during childhood and puberty.

BACKGROUND: The prevalence of osteoporosis and the incidence of vertebral fractures are lower in black women than in white women, findings generally attributed to racial differences in adult bone mass. Little is known, however, about the factors that contribute to racial variations in bone mass or the time of life when such differences become manifest. This study was done to characterize the changes in vertebral bone density at various stages of sexual development in black and white females. METHODS: We measured cancellous vertebral bone density by quantitative computed tomography in 75 black female subjects between 2 and 20 years old and 75 whites matched for age and stage of sexual development. RESULTS: The vertebral bone density did not differ between black girls and white girls before puberty. Bone density increased during puberty in each racial group, but the magnitude of the increase from prepubertal values was substantially greater in black than in white subjects (34 percent vs. 11 percent). CONCLUSIONS: The marked difference between black and white females in cancellous vertebral bone density occurs during a relatively brief period late in puberty. Metabolic and hormonal events related to the achievement of sexual maturity during adolescence may be important determinants of racial differences in bone mass in women.

Adolescent↗
PubMed2003

The GPR54 gene as a regulator of puberty.

BACKGROUND: Puberty, a complex biologic process involving sexual development, accelerated linear growth, and adrenal maturation, is initiated when gonadotropin-releasing hormone begins to be secreted by the hypothalamus. We conducted studies in humans and mice to identify the genetic factors that determine the onset of puberty. METHODS: We used complementary genetic approaches in humans and in mice. A consanguineous family with members who lacked pubertal development (idiopathic hypogonadotropic hypogonadism) was examined for mutations in a candidate gene, GPR54, which encodes a G protein-coupled receptor. Functional differences between wild-type and mutant GPR54 were examined in vitro. In parallel, a Gpr54-deficient mouse model was created and phenotyped. Responsiveness to exogenous gonadotropin-releasing hormone was assessed in both the humans and the mice. RESULTS: Affected patients in the index pedigree were homozygous for an L148S mutation in GPR54, and an unrelated proband with idiopathic hypogonadotropic hypogonadism was determined to have two separate mutations, R331X and X399R. The in vitro transfection of COS-7 cells with mutant constructs demonstrated a significantly decreased accumulation of inositol phosphate. The patient carrying the compound heterozygous mutations (R331X and X399R) had attenuated secretion of endogenous gonadotropin-releasing hormone and a left-shifted dose-response curve for gonadotropin-releasing hormone as compared with six patients who had idiopathic hypogonadotropic hypogonadism without GPR54 mutations. The Gpr54-deficient mice had isolated hypogonadotropic hypogonadism (small testes in male mice and a delay in vaginal opening and an absence of follicular maturation in female mice), but they showed responsiveness to both exogenous gonadotropins and gonadotropin-releasing hormone and had normal levels of gonadotropin-releasing hormone in the hypothalamus. CONCLUSIONS: Mutations in GPR54, a G protein-coupled receptor gene, cause autosomal recessive idiopathic hypogonadotropic hypogonadism in humans and mice, suggesting that this receptor is essential for normal gonadotropin-releasing hormone physiology and for puberty.

Animals↗
PubMed2001

Nodular Leydig cell hyperplasia in a boy with familial male-limited precocious puberty.

In boys with familial male-limited precocious puberty, an activating mutation of the luteinizing hormone receptor causes Leydig cell hyperplasia, resulting in excess testosterone production. There are no reports of Leydig cell masses in boys with familial male-limited precocious puberty. We describe a 10-year-old boy with familial male-limited precocious puberty who developed Leydig cell nodules.

Child↗
PubMed2005

Increased hypothalamic GPR54 signaling: a potential mechanism for initiation of puberty in primates.

To further study the role of GPR54 signaling in the onset of primate puberty, we used the monkey to examine the ability of kisspeptin-10 to elicit the release of gonadotropin-releasing hormone (GnRH) precociously, and we describe the expression of GPR54 and KiSS-1 in the hypothalamus during the peripubertal period. Agonadal juvenile male monkeys were implanted with a lateral cerebroventricular cannula and a jugular vein catheter. The responsiveness of the juvenile pituitary to endogenous GnRH release was heightened with a chronic pulsatile i.v. infusion of synthetic GnRH before kisspeptin-10 (112-121) injection. Intracerebroventricular (30 microg or 100 microg) or i.v. (100 microg) bolus injections of kisspeptin-10 elicited a robust GnRH discharge, as reflected by luteinizing hormone secretion, which was abolished by pretreatment with a GnRH-receptor antagonist. RNA was isolated from the hypothalamus of agonadal males before (juvenile) and after (pubertal) the pubertal resurgence of pulsatile GnRH release and from juvenile, early pubertal, and midpubertal ovary-intact females. KiSS-1 mRNA levels detected by real-time PCR increased with puberty in both male and female monkeys. In intact females, but not in agonadal males, GPR54 mRNA levels in the hypothalamus increased approximately 3-fold from the juvenile to midpubertal stage. Hybridization histochemistry indicated robust KiSS-1 and GPR54 mRNA expression in the region of the arcuate nucleus. These findings are consistent with the hypothesis that GPR54 signaling by its cognate ligand in the primate hypothalamus may be activated at the end of the juvenile phase of development and may contribute to the pubertal resurgence of pulsatile GnRH release, the central drive for puberty.

Animals↗
PubMedDate not supplied

Estimating puberty in a prehistoric skeletal collection.

A method was introduced to estimate the age of puberty in prehistoric skeletal collections using stages of fusion of the epiphyses of the distal humerus, proximal radius and proximal ulna, as well as fusion of the ilium, ischium and pubis. Fusion of these bones is associated with the hormonal release coincident with the onset of puberty. Dental age-at-death and stage of fusion of these bones were compared in 22 sub-adult individuals from the Moundville (1TU500) site in Alabama, USA. The age for the onset of puberty in this skeletal sample from Moundville, including both males and females, was estimated to be 14.95 +/- 2.53 years. These results represent an initial application of this methodology to a small data set. The application of this method on a larger scale may provide a better understanding of reproductive lifespans in earlier populations, as well as insight into possible effects of nutritional or socio-economic differences on the sexual development of children within those populations.

Age Determination by Skeleton↗
PubMedDate not supplied

Intra-pair similarity in physical growth of opposite-sex twin pairs during puberty.

A comparison has been made of within-pair similarity in physical growth for opposite-sex twin pairs and pairs of unrelated controls attending the same classes as the twins. Height and weight measurements were originally collected for 97 pairs of twins and controls from 10 to 16 years of age for the girls and from 10 to 18 years for the boys. The twins showed significantly smaller within-pair differences than the controls for both height and weight during the whole investigation period. Within-pair correlations for height and weight were negative for the controls and moderately positive for the opposite-sex twins. The weight correlations for the twins were lower than for height from 11 to 14 years of age. At age 15 the height and weight correlations tended to be of the same magnitude due to a drop in within-pair similarity for height at this age. Profile similarity in physical growth has been studied both for each pair individually (D-values) and for the whole group of twins and controls (analysis of variance). Both comparisons showed both the twins and the controls to be very dissimilar in growth profiles during puberty. Onset of puberty was estimated by age at peak height velocity (PHV) and peak weight velocity (PWV). The average within-pair difference for the controls was shown to be a little more than two years and for the twins a little less. The small and non-significant differences between the groups lead to the main conclusion that sex differentiation at puberty exerts a very powerful influence overshadowing the hereditary and environmental similarities existing for the twins.

Adolescent↗
PubMed1999

Growth hormone treatment during suppression of early puberty in adopted girls. Swedish Growth Hormone Advisory Group.

Girls adopted from developing countries often have early or precocious puberty, requiring treatment with gonadotropin-releasing hormone (GnRH) analogues. During such treatment decreased growth velocity is frequent. The aim of this investigation was to study whether the addition of growth hormone (GH) to GnRH analogue treatment improves height velocity and final height in girls with early or precocious puberty. Forty-six girls with early or precocious puberty adopted from developing countries were randomized for treatment with GnRH analogue or a combination of GH and GnRH analogue. After 2 y of treatment the mean growth in the GH/GnRH analogue group was significantly higher, 14.6 cm, compared to 10.9 cm in the control group. The increase in bone age did not differ, while the difference in predicted adult height increased by 2.7 cm in favour of the combination group. Although data on final height are not yet available, combined GH/GnRH analogue treatment for 2 y resulted in a higher growth velocity and predicted final height compared to GnRH analogue treatment alone.

Adoption↗
PubMed1999

The Adolescence Scale (AS-ICSM): a tool for the retrospective assessment of puberty milestones.

Neurodevelopmental theories of psychosis, and schizophrenia in particular, have led to renewed interest in the relationships between brain maturation, adult personality and timing of puberty. Here we present a brief Adolescence Scale (AS-ICSM) for the retrospective assessment of puberty milestones. The recommended version comprises one item for females, three for males and one common to both. An original version of five items was administered to 318 young adults. We found good internal consistencies of Cronbach's alpha = 0.87 for females and 0.83 for males, having excluded an item assessing timing of growth spurt. These findings show that the AS-ICSM is a reliable and economic tool for research into the concomitants of early and late puberty.

Adolescent↗
PubMed2004

Is neuropeptide Y responsible for constitutional delay of puberty in girls? A preliminary report.

Constitutional delay of puberty (CDP). in otherwise healthy girls is defined as failure to develop secondary sexual features past the age of 13 years (two standard deviations above the mean age at which secondary sexual features appear in the population of girls). The inhibitory action of neuropeptide Y (NPY) on the gonadotropic and somatotropic systems in experimental animals and stimulation by NPY of the hypothalamic-pituitary-adrenal axis have been reported, prompting us to study the levels of NPY, insulin-like growth factor-I (IGF-I) and cortisol in eight girls with CDP and normal weight (body mass index (BMI) 21.7+/-4.5 kg/mn2). The results were compared with those from a group of 40 girls (BMI = 20.0+/-3.1 kg/m2) who demonstrated a normal course of puberty (NP). All girls were studied at menarche (mean age at menarche, study vs. control: 16.4+/-0. 7 vs. 12.6+/-0.9 years). To measure NPY and IGF-1 we used a radioimmunoassay method, whereas cortisol was measured with an enzyme immunoassay. Blood was collected between 08.00 and 09.00 following an overnight fast. NPY was higher in girls with CDP (181.6+/-106.4 pg/ml) than in girls with NP (55.5+/-26.3 pg/ ml; p < 0.001). In the former group, cortisol was higher (397.3+/-241.6 nmol/l) than in NP girls (142.7+/-98.0 nmol/l; p < 0.01). Levels of IGF-I in CDP girls were lower than in NP girls (558.0+/-122.6 vs. 756.5+/- 226.8 ng/ml; p < 0.01). The results corroborate the involvement of NPY in sexual maturation and its role in delayed puberty.

Adolescent↗
PubMed2006

Primary hypothyroidism presenting as ovarian tumor and precocious puberty in a prepubertal girl.

We report a case of a prepubertal girl with juvenile primary hypothyroidism presenting as ovarian cysts and precocious puberty. The 7-year-old female was referred to our clinic because of a pelvic/abdominal mass and vaginal bleeding. Besides these findings, on physical examination we noticed the thyroid gland globally increased and the presence of secondary sexual characteristics. Based upon the clinical profile and investigations, the patient was diagnosed with juvenile primary hypothyroidism due to autoimmune thyroiditis. The cysts and precocious puberty resolved spontaneously after the simple replacement of thyroid hormone. It is important to bear in mind hypothyroidism in cases of girls presenting ovarian cysts and precocious puberty in order to avoid unnecessary surgery on the ovaries.

Child↗
PubMed1999

Variations and determinants of energy expenditure as measured by whole-body indirect calorimetry during puberty and adolescence.

BACKGROUND: Adolescence is characterized by rapid anatomic, physiologic, and behavioral alterations expected to induce changes in metabolic rate. OBJECTIVE: The aim of the present study was to investigate variations in daily energy expenditure (DEE) and its main components during adolescence and to quantify their significant determinants. DESIGN: Eighty-three children and adolescents (44 boys and 39 girls aged 10-16 y) participated in this cross-sectional study. Tanner stages ranged from 1 to 5. Body composition was assessed by both the skinfold-thickness method and bioimpedance analysis. Energy expenditure (EE) was determined continuously over 24 h by using 2 whole-body calorimeters. The subjects followed a standardized activity program that included four 15-min periods of exercise on a cycle ergometer. RESULTS: Body composition, DEE, sleeping EE (SEE), resting EE, and EE during meals, miscellaneous activities, and physical exercise varied significantly with sex and stage of puberty. The DEE of boys and girls averaged 8.22 and 7.60 MJ in prepubertal children, 11.35 and 9.10 MJ in pubertal children, and 11.73 and 9.68 MJ in postpubertal adolescents, respectively. The significant determinants of DEE and SEE, respectively, were fat-free mass (r2 = 0.842 and 0.826), sex (r2 = 0.017 and 0.022), and season (r2 = 0.021 and 0.011). Stage of puberty and fat mass were not significant factors. DEE and SEE adjusted for fat-free mass were on average 5% higher in boys than in girls and 6% higher in spring than in autumn. CONCLUSIONS: The DEE of adolescents measured under standardized conditions varied with sex, body composition, and season, but not with stage of puberty. These variables could be predicted accurately from fat-free mass, sex, and season.

Adolescent↗
PubMed1997

Morphological changes of the TMJ condyles of 100 patients treated with the Herbst appliance in the period of puberty to adulthood: a long-term radiographic study.

One hundred consecutive patients were treated with the Herbst appliance in the period of puberty to adulthood. The orthopaedic effects on the morphology of the condyles were described from orthopantomographic and transpharyngeal radiographs. The orthopaedic treatment effect was, in most cases, visible as a change in morphology of the condyle, a double contour in the distocranial part of the condyle and sometimes also at the distal surface of the ramus. In patients at the peak of puberty, the double contour was distinct for a short time. In patients in late puberty, the double contour could be seen several months after treatment. At adulthood, males showed, in most cases, double contours, while females showed in most cases nearly unchanged condyles. When double contours were seen, these persisted for a few months to several years after Herbst treatment. The newly formed bone was stable and no TMJ problems were observed. The change in morphology and the double contour of the condyle can be interpreted as bone modelling. The newly formed bone on the posterior part of the condyle can be explained as a response to hypertropic chondrocytes, and that on the posterior part of the ramus as a response of resting osteoblasts to mechanically induced changes in the condyle (adaptive bone growth). In two cases, remodelling resorption was found in the anterior part of the condyle after Herbst treatment, again as a sign of adaptation to changed mechanical influence. In both cases, later refilling with bone was registered during the remodelling process. The biomechanical effect of Herbst treatment on the mandible is also analogous with an impeded matrix rotation combined with relocation of the mandible.

Adaptation, Physiological↗
PubMed1993

Cosegregation of missense mutations of the luteinizing hormone receptor gene with familial male-limited precocious puberty.

Familial male-limited precocious puberty is a male-limited autosomal dominant condition. It is characterized by increased testosterone synthesis in the absence of testicular stimulation by luteinizing hormone (LH). We hypothesised that an abnormal configuration of the LH receptor might autonomously activate G protein coupling, and thereby cause the overproduction of testosterone in this condition. To test this hypothesis, we screened for mutations in a part of the LH receptor gene that is important for G protein binding. DNA sequence variation was detected in 2 out of 5 families with male-limited precocious puberty by the single strand conformation polymorphism technique. Direct sequencing demonstrated different single nucleotide substitutions in the sixth transmembrane region of the LH receptor gene. The mutations cosegregated with the disorder in both families (lod score 5.76 without recombination). Both mutations cause an amino acid substitution in the sixth transmembrane domain, close to the C-terminal portion of the third cytoplasmatic loop, a region which is important for the binding of G proteins. We conclude that familial male-limited precocious puberty cosegregates with missense mutations in the LH receptor gene. These findings support the hypothesis that increased activity of the LH receptor is the pathogenetic mechanism that causes the abnormal pubertal development in this condition.

Amino Acid Sequence↗
PubMed1997

Ontogeny of gonadotrophin and inhibin secretion in normal girls through puberty based on overnight serial sampling and a comparison with normal boys.

We measured luteinizing hormone (LH) and follicle stimulating hormone (FSH) by immunofluorometric assays and alpha-inhibin by radioimmunoassay in serum sampled every 10 min throughout the night (2100-0500 h) from 44 normal girls. Mean overnight LH values rose log-linearly from a mean of 0.2 IU/l in prepubertal girls to 3.0 IU/l in late pubertal girls. Log2 mean overnight FSH rose rapidly through early puberty and then remained constant; mean FSH rose from 1.0 IU/l in prepubertal girls to approximately 2.8 IU/l in Tanner III-V girls. Mean overnight inhibin increased through puberty, rising from 151 ng/l in prepubertal girls to 432 ng/l in fully pubescent girls. Within each of the first three Tanner stages, LH differed approximately 100-fold between the smallest and largest mean concentrations but differed <10-fold within stages IV or V. Such within-pubertal stage variability was less pronounced for FSH, which differed approximately 16-fold among Tanner I subjects and 4-10-fold at later stages, and for inhibin, which varied approximately 4-fold within each Tanner stage. The frequency of LH pulses during overnight sampling increased significantly during puberty, but the frequency of FSH and inhibin pulses remained constant. We compared the results from girls to those from 50 normal boys [Manasco et al. (1995) J. Clin. Endocrinol. Metab., 80, 20462052]. At each pubertal stage, girls had approximately the same mean overnight LH values as boys; girls had higher mean overnight FSH, particularly during Tanner stages II-IV; and boys had mean overnight alpha-inhibin immunoreactivity approximately 1.5 times that of girls at each pubertal stage. Still, hormone concentrations for individuals of both sexes intergraded at each pubertal stage.

Adolescent↗