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PubMed2007

Longitudinal study of the simultaneous secretion of melatonin and leptin during normal puberty.

BACKGROUND/AIMS: Pubertal changes are a consequence of the activation of the hypothalamic-pituitary-gonadal axis due to an increase in the frequency and magnitude of pulses of gonadotropin-releasing hormone (GnRH), which may depend on the intrinsic properties of the neurons of the hypothalamic arcuatus nucleus, or on the influence of neurotransmitters and/or neuromodulators. We evaluated the serum concentrations of melatonin and leptin in healthy prepubertal and adolescent subjects of both sexes, to define their participation at the initial stages and during the progression of pubertal development. METHODS: 80 pediatric subjects (47 females and 33 males), aged 6-18 years, were divided into 2 groups, prepubertal (n = 25) and adolescent (n = 55), according to the absence or presence, respectively, of physical signs of pubertal development. The subjects were assessed on two occasions: at the time of their inclusion in the study, and 12-18 months later when the subject had advanced one pubertal stage according to the Tanner classification. Blood was obtained in fasting for clinical purposes and for the hormonal study. Melatonin and leptin were measured by radioimmunoanalysis. RESULTS: As described previously, melatonin decreases at the onset of puberty and during pubertal development. Both the absolute melatonin value and the decrease between evaluations tended to be greater in females; the variations were correlated with neither an increase in body weight nor with the degree of pubertal development. The concentration of leptin increased in both sexes with the progression of puberty, this value being 40% greater in women, and correlated with the indicators of an increase in body volume and fat accumulation. Although its concentration remained stable between evaluations for both sexes, among the males the association between leptin and pubertal development took place at the start of the process, while for the females we observed a significant overall association between pubertal stage and leptin concentration, this association being stronger at more advanced Tanner stages. Neither at the onset of puberty nor during its course did we observe any significant relation between melatonin concentration and any of the Tanner stages, whether for males or for females. Neither was there any correlation between the absolute values or rates of modification of melatonin and leptin. CONCLUSION: According to the evolutionary dynamics of their respective concentrations, both initially and during pubertal progress, melatonin and leptin do not interact in the initiation or progression of human pubertal development, and do not seem to play a key role in this process.

Adipose Tissue↗
PubMed1992

Central administration of neuropeptide Y induces precocious puberty in female rats.

To examine the role of neuropeptide Y (NPY) in the regulation of puberty, the effects of various doses of NPY or saline injected into the 3rd ventricle of peripubertal female rats were determined. A single injection of NPY at a dose range of 10-20 micrograms into the 3rd ventricle of 30-day-old female rats advanced the time of vaginal opening (VO) and first ovulation by 4 days, as compared to saline-treated controls. Ova number and ovarian, adrenal and uterine weights at first estrous were similar in all animals regardless of treatment. The NPY-treated precocious animals showed lower body weight than did the VO-matched controls, but showed similar body weight as that of age-matched controls. Determination of plasma luteinizing hormone (LH) levels in the peripubertal female rats revealed that plasma LH was increased transiently immediately after NPY administration. Also, NPY-treated rats which had precocious puberty showed elevated pituitary and plasma LH levels on the day of VO. These results suggest that NPY can activate the hypothalamic-pituitary-gonadal axis to precociously initiate puberty.

Age Factors↗
PubMed1987

Treatment of central precocious puberty with an LHRH agonist (Buserelin): effect on growth and bone maturation after three years of treatment.

The LHRH analog Buserelin was used to treat 27 children (21 girls, 6 boys) with central precocious puberty. Nineteen patients had idiopathic precocious puberty and 8 had organic lesions (hamartoma, hydrocephalus or suprasellar arachnoid cyst). All patients received 20 or 30 micrograms/kg/day s.c. of Buserelin, and we obtained plasma E2 less than 20 pg/ml, vaginal maturation index less than 30 in girls or plasma testosterone less than 0.3 ng/ml in boys. The mean growth rate decreased from 9.3 +/- 0.5 to 4.6 +/- 1.3 cm/year after 3 years. The velocity of skeletal maturation decreased so that the final height prediction improved by a mean value of 1.6 SD. As the follow-up increases, this study confirms that LHRHa therapy is effective and potentially improves the final height of children presenting active and severe central precocious puberty.

Aging↗
PubMed1989

Lack of adrenarche in two children with precocious puberty secondary to hypothalamic hamartoma.

Adrenarche, which occurs earlier than gonadarche in normal children, is marked by increases in plasma dehydroepiandrosterone and its sulfate (DHAS). Adrenarche and gonadarche can be dissociated in various situations, e.g. central precocious puberty, indicating that they are controlled by independent mechanisms. This report concerns 2 children with central precocious puberty secondary to hypothalamic hamartoma. Their plasma basal DHAS values, compared to other cases with central precocious puberty not secondary to hamartoma, remained low for chronological age and bone age over a follow-up of 6.3 (case 1) and 9.2 9.2 years (case 2): in case 1 (boy), DHAS was 9 micrograms/dl at chronological age 7.7 and bone age 13 years; in case 2 (girl), DHAS was 11 micrograms/dl for chronological age 10.5 and bone age 13.5 years. GH secretion was normal. Basal plasma cortisol levels as the levels during hypoglycemia and after corticotropin stimulation were all normal. These data suggest that hypothalamic hamartoma may affect the central control of adrenarche. They may also contribute to the diagnosis of hypothalamic hamartoma.

Adrenal Glands↗
PubMed1990

Relationships between puberty and growth at adolescence in growth-hormone-deficient males: effect of growth hormone and of associated gonadal suppression therapy.

125 boys with idiopathic GH deficiency who received GH treatment were followed until they reached their final height. In 85 patients who had spontaneous puberty (group I), the mean final height was 151.5 +/- 6.6 cm. In 23 patients with combined GH and gonadotropin deficiency (group II) whose pubertal development was induced artificially at age 19.4 +/- 2.1 years, the mean final height was 163.7 +/- 3.9 cm (p less than 0.01 vs. group I). Final height was strongly related to height at the onset of pubertal development in combined groups I and II when the time of gonadal replacement treatment was taken as the onset of pubertal development in group II. In 17 patients (group III) who developed spontaneous puberty, gonadal suppression treatment was started at their early stage of puberty and was continued for a mean duration of 4.3 +/- 1.1 years. The mean final height in group III was 157.9 +/- 3.0 cm (p less than 0.01 vs. group I, group II). Longitudinal growth pattern analysis demonstrated that this beneficial effect on final height by gonadal suppression treatment was attributed to the elongation of pubertal growth spurt and pubertal height gain.

Adolescent↗
PubMed1992

Prediction of advanced puberty by height velocity in children with acute lymphoblastic leukemia.

Pubertal development was retrospectively evaluated in 58 children with cancer, mostly acute lymphoblastic leukemia (ALL), who are in complete remission and off chemotherapy. Six girls [5 patients with ALL, and 1 with malignant lymphoma (NHL)] showed advanced puberty (25.0%, 6 of 24 female patients with ALL and NHL) through the evaluation of their growth velocity. No evidence for advanced puberty was seen in the males. All 6 girls had received cranial irradiation for central nervous system prophylaxis and systemic chemotherapy including glucocorticoid. The mean age at onset of the pubertal growth spurt in these 6 girls was significantly lower than for girls with a solid tumor [6.90 +/- 0.10 and 9.00 +/- 0.77 (mean +/- SD) years, respectively (p < 0.01)]. By simply evaluating the height velocity, we could predict advanced puberty which was ultimately associated with short stature.

Adolescent↗
PubMed1992

Final height attainment and gonadal function in girls with precocious puberty treated with cyproterone acetate.

Thirty-four girls with precocious puberty (27 idiopathic, 6 cerebral, 1 McCune-Albright syndrome) were treated with cyproterone acetate (CPA) for 1.2-8.4 years (3.71 +/- 0.31; mean +/- SEM) at a daily dosage of 66-150 mg/m2 (103.7 +/- 6.2). The mean chronological age (CA) and bone age at the beginning of treatment were 5.99 +/- 0.31 and 8.6 +/- 0.39 years, respectively, and 9.78 +/- 0.19 and 12.44 +/- 0.22 years, respectively, at the end of therapy. At the last evaluation, mean CA was 14.23 +/- 0.4 years, and 32 girls had reached final height. The control group consisted of 10 girls with idiopathic precocious puberty who, at their parents' request, were not treated. Mean CA at the onset of pubertal signs was 6.05 +/- 0.25 years. All patients had reached final height at the time of the last observation. There was no significant difference between final height of treated (152.43 +/- 1.36 cm) and untreated (149.55 +/- 1.99 cm) girls. Final height was significantly lower than target height in both treated (155.08 +/- 0.92 cm; p < 0.025) and untreated (156.45 +/- 1.29 cm; p < 0.0005) patients, but the mean height of treated patients is nearer to target height than that of untreated ones. A positive correlation was found between final height and target height both in treated (p < 0.005) and untreated (p < 0.05) patients. After the discontinuation of CPA treatment all girls resumed the progressive course of puberty.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1992

Insulin and growth factors adaptation to normal puberty.

Insulin and IGF-1 production were measured throughout childhood and puberty and into adult life. Basal insulin and IGF-1 secretion increased during puberty, falling back to prepubertal levels in adulthood. However, fasting glucose levels remained constant, implying an increase in tissue resistance to insulin coinciding with puberty.

Adaptation, Physiological↗
PubMed1994

Psychosocial milestones in normal puberty and adolescence.

Puberty and adolescence are not generally times of great stress and turmoil. The storm-and-stress theory has a long history, but can no longer be supported by recent empirical research. A modern approach to the psychosocial changes of these phases is based on the concept of developmental tasks in an age-appropriate and stage-appropriate way. Biological processes can influence an individual's psychological and psychosocial state, but psychological and psychosocial events may also influence the biological systems. Therefore, the timing and outcome of pubertal processes can be modified by psychosocial factors. The most important psychological and psychosocial changes in puberty and early adolescence are the emergence of abstract thinking, the growing ability of absorbing the perspectives or viewpoints of others, an increased ability of introspection, the development of personal and sexual identity, the establishment of a system of values, increasing autonomy from family and more personal independence, greater importance of peer relationships of sometimes subcultural quality, and the emergence of skills and coping strategies to overcome problems and crises. All these changes can be looked on as developmental tasks during normal development, but they can also help in understanding developmental deviations and psychopathological disorders. From the viewpoint of developmental psychopathology, several psychiatric disorders of puberty and adolescence can be seen in a new light.

Adolescent↗
PubMed1995

Central precocious puberty following feminizing right ovarian granulosa cell tumor.

A 7-month-old girl presented with ascites and breast enlargement due to right ovarian granulosa cell tumor. After tumor removal, the clinical signs of incomplete precocious puberty regressed. Four years later, the patient reappeared with signs of precocious puberty. Our investigations proved that this was not due to tumor recurrence, but it was a true central precocious puberty. She responded well to therapy with a luteinizing hormone releasing hormone agonist, and 3 years after onset of this therapy, she is growing at a normal prepubertal rate.

Antineoplastic Agents, Hormonal↗
PubMed1995

Precocious puberty and decreased melatonin secretion due to a hypothalamic hamartoma.

Hypothalamic hamartomata are benign malformations of the brain consisting of heterotopic nervous tissue, and are often associated with precocious puberty and gelastic seizures in early childhood. We report for the first time the melatonin plasma values of a girl with central precocious puberty and gelastic seizures due to a hypothalamic hamartoma. The melatonin plasma levels were low for the chronological age but appropriate for the pubertal status, making a causal relationship between lowered melatonin plasma levels and precocious puberty possible.

Female↗
PubMed1997

Final height of girls with central precocious puberty, untreated versus treated with cyproterone acetate or GnRH analogue. A comparative study with re-evaluation of predictions by the Bayley-Pinneau method.

This study was designed to determine the benefit of therapy on final height (FHt) in girls with central precocious puberty (CPP). A total of 102 patients were evaluated--28 untreated, 26 treated with cyproterone acetate (CyA), and 48 treated with GnRH analogue (GnRHA)-and their achieved FHt was compared to the respective target height (THt). Of the untreated girls, half (14/28) had a slow course of puberty and reached THt +/- 0.5 SD (FHt 160.2 +/- 7.1, THt 159.5 +/- 6.6 cm); the other half (14/28) had an accelerated course of puberty with a FHt well below THt (FHt 150.8 +/- 4.3, THt, 159.2 +/- 5.9 cm) and in most cases (14/28) below the height-SDS of both parents. The treated girls (both regimens) reached THt above (CyA group: FHt 157.8 +/- 5.1, THt 156.8 +/- 5.1 cm; GnRHA group: 159.6 +/- 6.3, THt 157.7 +/- 5.7 cm). We conclude that without treatment the FHt of girls with CPP may be significantly compromised and that therapy is more beneficial if started before bone age exceeds 12 years. Our data also showed that for final height predictions in CPP the Bayley and Pinneau tables for average children should be used, regardless of the advanced bone age of the patients.

Administration, Oral↗
PubMed1997

Puberty in children with intrauterine growth retardation.

There is a remarkable scarcity of data concerning puberty in children born with intrauterine growth retardation (IUGR). What little there is suggests that puberty occurs at a normal age compared with the general population, but a little early compared with other short children. The pattern of puberty is quite normal in children born with IUGR, with normal inter-relationships between the various events, although the growth spurt is, on average, a little less intense than in the normal population. In general, adult height is significantly compromised, partly because of the rather attenuated pubertal growth spurt.

Adolescent↗
PubMed1996

Maternal uniparental isodisomy of human chromosome 14 associated with a paternal t(13q14q) and precocious puberty.

Cytogenetic and molecular investigation of a boy with precocious puberty and motor developmental delay revealed a 45,XY,t(14q14q) or i(14q) karyotype with no paternal chromosome 14 contribution. VNTR analysis of loci on four other chromosomes excluded non-paternity with greater than 99% confidence. Results of VNTR and CA repeat analyses of ten loci along the entire length of chromosome 14 were consistent with homozygosity at all loci, suggesting that the chromosomal rearrangement was a maternal isochromosome for 14q. As the proband's father had a balanced Robertsonian translocation, t(13q14q), we suggest that the origin of the maternal uniparental disomy (UPD) was fertilization by a nullisomy 14 sperm with formation of the isochromosome in the early embryo. Also, the proband has several clinical features in common with six previously reported liveborn cases of maternal UPD 14: hypotonia and motor developmental delay, mild dysmorphic facial features, low birth weight and growth abnormalities, and, more specifically, precocious puberty among the four cases old enough to assess. The emergence of a syndrome associated with maternal UPD 14 suggests the possibility of genomic imprinting of regions of chromosome 14, especially a gene involved in the onset of puberty.

Adolescent↗
PubMed1989

Ovarian cysts in precocious puberty.

We describe a 7-year-old girl with precocious puberty in whom a single large cyst (5 cm) and several small cysts (8-10 mm) in the single remaining ovary were detected by the ultrasound examination. Endocrinological examinations confirmed the diagnosis of central precocious puberty. Pathologic findings after the removal of the cystic lesions revealed that the large cyst was derived from degenerated follicular cysts and the small cysts were identical to follicular cysts: all were considered to have been formed by gonadotropin stimulation. In general, surgical removal of an ovarian follicular cyst in central precocious puberty is inappropriate. However, in this unusual patient who had a degenerated large cyst, surgery seemed to be appropriate because of a previously removed teratoma in the contralateral ovary.

Child↗
PubMed1992

Puberty and insulin-dependent diabetes mellitus.

Puberty and IDDM interact at many different levels, each affecting the other. Pediatricians, diabetologists, and patients with IDDM must be aware of these interactions and be prepared to adjust their management of IDDM accordingly. Glycemic control in the young prepubertal patient has not been associated with the development of subsequent diabetic microvascular disease. However, extremely tight glycemic control (percent HbA1 in the nondiabetic range) may expose patients to more severe and more frequent hypoglycemic episodes. This may be particularly detrimental for the very young (less than age 3 years) patient whose brain growth and myelinization has not yet been completed. Glycemic control must be maintained in the prepubertal diabetic patient to ensure normal physical and psychological growth, to avoid hospitalizations, and to allow participation in school and other age-appropriate activities. During puberty, health-care professionals and patients should anticipate more difficulty in maintaining glycemic control. Insulin doses commonly need to be increased, sometimes dramatically. Timing of insulin injections will frequently need to be adjusted to blunt the dawn phenomenon. Patients should be allowed to give themselves additional doses of regular insulin (5% to 10% of their total daily dose) when their blood-sugar levels are intermittently elevated to blunt the increased variability in blood-sugar levels seen during puberty. The use of supplemental regular insulin to correct intermittent hyperglycemia is preferable to withholding food in the adolescent patient, since overzealous food restriction can in itself lead to problems with linear growth and pubertal development.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Dental development in precocious puberty.

One hundred and one children with precocious puberty were given an oral examination. Dental root development was assessed using panoramic radiographs. All mandibular canines, pre-molars, and molars which could be visualized without apparent distortion were included. The patients were grouped for analysis according to the etiology of their precocity, e.g., McCune-Albright syndrome, familial male, congenital adrenal hyperplasia, central nervous system lesions, and idiopathic precocious puberty. Dental development was significantly retarded relative to their chronological age in patients with idiopathic precocious puberty. However, no significant abnormal dental development was detected in any of the other groups. Individual oral-facial growth and development remain the primary considerations for timing orthodontic treatment.

Age Determination by Skeleton↗
PubMed2004

Puberty, ovarian steroids, and stress.

Puberty is accompanied by a number of changes, among them increased risk for development of major depression. The most common etiology of major depression is stressful life events, being present in approximately 90% of first episodes of depression. The hypothalamic-pituitary-adrenal (HPA) axis is one of the major systems involved in responses to stress, and this system is clearly influenced by ovarian hormones. Normal women demonstrate resistance to negative feedback of both cortisol in the fast-feedback paradigm and dexamethasone in the standard delayed-feedback paradigm. Depressed premenopausal women show greater increases in baseline cortisol than postmenopausal depressed women and than depressed men. Studies in rodents suggest a similar resistance to glucocorticoid feedback but suggest that estradiol can function to inhibit stress responsiveness. Studies of premenopausal depressed women demonstrate lower estradiol, which suggests that there is less inhibitory feedback of estradiol on the HPA axis, while normal progesterone continues to augment stress responses further. The onset of these reproductive hormonal changes modulating stress systems at puberty may sensitize girls to stressful life events, which become more frequent at the transition to puberty and young adulthood.

Animals↗