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At least 865 records · Page 48Linked to original sources
PubMed1999

Effects of puberty on bone age maturation in a girl after medulloblastoma therapy.

BACKGROUND: Craniospinal radiotherapy for malignant brain tumors can result in a variety of neuroendocrine disturbances, among which are the development of growth hormone deficiency and early puberty, which can markedly reduce adult height. METHODS: The authors report the case of a girl who received craniospinal radiotherapy for a medulloblastoma at the age of 3.4 years. At 9.1 years, growth hormone therapy was started, and spontaneous onset of puberty (Tanner stage B2) occurred at age 10.3 years. Interval until menarche was short, at only 0.9 years. RESULTS: Although chronologic age at appearance of Tanner stages was within the normal range, the patient showed a rapid acceleration in skeletal maturation, resulting in adult short stature. CONCLUSION: Bone age seems to be a more precise parameter for biologic maturation in some patients after craniospinal irradiation than is clinical assessment of pubertal stages. Thus, if progression of bone age and decreasing final height predictions are noted, puberty should be stopped with gonadotropin-releasing hormone analogs, even if pubertal development seems to be adequate for chronologic age, because this increases the remaining time for growth hormone treatment.

Age Determination by Skeleton↗
PubMed1998

Developmental changes in the relationship between IGF-I and body composition during puberty.

To examine the hypothesis that anthropometric measures and physical fitness influence circulating insulin-like growth factor-I (IGF-I) during puberty, we measured IGF-I, free IGF-I, IGFBP-1, and IGFBP-3 concentrations in 156 healthy girls (9-16 years old) characterized by aerobic capacity (VO2max), fat-free mass (FFM), percent fat mass and pubertal development. IGF-I, free IGF-I and IGFBP-3 increased with pubertal development while IGFBP-1 declined. Percent fat mass correlated inversely with IGFBP-1 (r = -0.57) and directly with insulin (r = 0.50), while VO2max correlated inversely with percent fat mass (r = -0.63), body mass index (BMI, r = -0.57), and FFM (r = -0.40). When subdivided by Tanner stage, IGF-I correlated directly with weight, height, BMI, and FFM in pre-pubertal girls, but these relationships all diminished or disappeared completely by late puberty. Inverse correlations between IGF-I and percent fat mass, and direct correlations between IGF-I and VO2max as observed previously in adults, were not seen until late puberty. These data suggest that in pre-pubertal and early pubertal girls, IGF-I concentrations in blood reflect overall somatic size. This relationship between IGF-I and body size diminishes with sexual maturation, while correlations between IGF-I and both fitness and fatness emerge.

Adolescent↗
PubMed2002

[Neuroendocrine mechanisms of puberty onset].

An increase in pulsatile release of GnRH is essential for the onset of puberty. However, the mechanism controlling the pubertal increase in GnRH release is still unclear. The GnRH neurosecretory system is already active during the neonatal period but subsequently enters a dormant state by central inhibition in the juvenile period. When this central inhibition is removed or diminished, an increase in GnRH release occurs with increase in synthesis and release of gonadotropins and gonadal steroids, followed by the appearance of secondary sexual characteristics. Recent studies suggest that disinhibition of GnRH neurons from GABA (gamma-aminobutyric acid) appears to be a critical factor in female rhesus monkey. After central inhibition is removed, increases in stimulatory input from glutamatergic neurons as well as new stimulatory input from norepinephrine and NPY neurons and inhibitory input from beta endorphin neurons appear to control pulsatile GnRH release as well as gonadal steroids. Nonetheless, the most important question still remains: what determines the timing to remove central inhibition? Because many genes are turned on or turned off to establish a complex series of events occurring during puberty, the timing of puberty must be regulated by a master gene or genes, as a part of developmental events.

Animals↗
PubMed1998

Puberty and depression: the roles of age, pubertal status and pubertal timing.

BACKGROUND: Previous work has indicated that the 2:1 female:male sex ratio in unipolar depressive disorders does not emerge until some time between ages 10 and 15. METHODS: Data from four annual waves of data collection from the Great Smoky Mountains Study (GSMS) involving children aged nine to 16 were employed. RESULTS: Pubertal status better predicted the emergence of the expected sex ratio than did age. Only after the transition to mid-puberty (Tanner Stage III and above) were girls more likely than boys to be depressed. The timing of this transition had no effect on depression rates. Before Tanner Stage III, boys had higher rates of depression than girls, and the prevalence of depression appeared to fall in boys at an earlier pubertal stage than that at which it began to rise in girls. In addition, recent transition to Tanner Stage III or higher had a transient effect in reducing the prevalence of depression in boys. CONCLUSIONS: The period of emergence of increased risk for depression in adolescent girls appears to be a relatively sharply demarcated developmental transition occurring in mid-puberty. Previously reported effects of the timing of puberty (which have tended to be transient) appeared less important in increase of risk for depression than pubertal status.

Adolescent↗
PubMed1991

Do parent-child relationships change during puberty?

This article reviews changes in parent-child relationships during puberty, emphasizing the developmental processes that might be implicated in these changes. Evidence suggests increases in conflict and less warm interactions in relationships between parents and children during puberty. Changes are assumed to be short term, although little longitudinal research has directly addressed the issue of long-lasting effects. Other developmental changes occurring for the adolescent, the parent, or both (such as social cognitive or self-definitional change), as well as other relationship changes, personality characteristics, and the sheer number of life events or transitions have all been posited as potential contributors to changes in the parent-child relationship for young adolescents. These possible contributors, however, have seldom been studied in conjunction with pubertal changes. Such integrative research is necessary to test various models through which puberty, social relationships, social cognitive, self-definitional, and other processes influence one another and are influenced by one another during the transition to adolescence.

Adolescent↗
PubMed2000

Puberty begins with a characteristic subcutaneous body fat mass in each sex.

OBJECTIVE: To observe whether there exists a characteristic body fat mass at pubertal onset. DESIGN: Longitudinal clinical follow-up (between ages of 10 and 15 y) with an annual visit in a sample of 469 children. They were grouped according to age of purbertal onset: boys with pubertal onset at the ages of 11 (n=59), 12 (n=88), 13 n=89) and 14 y (n=46), and girls with pubertal onset at the age of 10 (n=68), 11 (n=66), 12 (n=37) and 13 (n=16). METHODS: Height, weight, upper arm circumference and four skinfold thicknesses were recorded annually. In boys testicular volume index was measured, and genital development was assessed on the Tanner scale; in girls mammary development was measured also using the Tanner scale. The sum of four skinfolds, body mass index, upper arm fat estimate and percentage body fat were calculated. RESULTS: Boys presented a positive relation between the age of pubertal onset and body mass index (P<0.001), which was not observed in girls. Body mass index thus varied according to the onset of puberty in boys (P<0.001), but not in girls. The sum of four skinfolds, the upper arm fat estimate index and the percentage of body fat mass did not differ according to age of pubertal onset either in girls (P=NS) or in boys (P=NS). The characteristic adiposity of the puberty onset is progressively acquired during the previous years in all the groups. CONCLUSIONS: Puberty seems to begin with a characteristic subcutaneous body fat mass that is independent of the age of onset. This study supports the hypothesis of a close link between maturation and the development of an energy store in the form of adipose tissue in both sexes.

Adipose Tissue↗
PubMed2001

Socio-economic status and puberty are the main factors determining anaemia in adolescent girls and boys in East Java, Indonesia.

OBJECTIVE: To determine prevalence and contributing factors of anaemia in adolescents. DESIGN: Cross-sectional study of anaemia prevalence, socio-economic status and puberty. SETTING: Schools in East Java, Indonesia. SUBJECTS: Male and female adolescent pupils (age 12-15 y; n=6486). RESULTS: Anaemia prevalence was 25.8% among girls (n=3486), 24.5% among pre-pubertal boys (n=821), and 12.1% among pubertal boys (n=2179). Socio-economic status, indicated by type of school attended, was an important factor determining the risk of anaemia. Girls had a higher risk when they attended a poor school (OR poorest school, 1.00; other schools, 0.67-0.87), had reached puberty (OR, 1.25), had lower retinol intake (OR 1st-4th quartiles-1.00, 0.97, 0.89, 0.77) and higher vitamin A intake from plant sources (OR 1st-4th quartiles-1.00, 1.10, 1.31, 1.04). Boys had a higher risk of anaemia when they attended a poor school (OR poorest school 1.00, other schools 0.54-0.63), were younger (OR per year=0.79), had not yet reached puberty (OR not yet, 1.00; already, 0.78), were shorter (OR per cm 0.95), had smaller mid-upper-arm circumference (MUAC) (OR per mm 0.99) and lower retinol intake (OR 1st-4th quartile 1.00, 0.67, 0.74, 0.68). CONCLUSIONS: Anaemia in adolescents should be reported separately for pre-pubertal and pubertal subjects and for different ages, and the population's socio-economic status should be specified. The results of this survey call for treatment of anaemia in adolescents. Given Indonesia's current situation, micronutrient intake of adolescents should be increased using supplements for all girls and for pre-pubertal boys. SPONSORSHIP: This survey was funded by USAID through the OMNI project.

Adolescent↗
PubMed1999

Serum leptin concentration, body composition, and gonadal hormones during puberty.

BACKGROUND: Recent evidence has suggested that leptin concentration is associated with gonadal hormone levels, and that changes in leptin concentration may trigger the onset of reproductive function in children. However, the concurrent changes in body composition during puberty make the independent associations between leptin and gonadal hormone concentrations in children difficult to resolve. METHODS: To investigate the nature of associations between leptin levels and pubertal maturation, serum concentrations of leptin, estradiol, and testosterone and body composition measures were examined in a sample of 152 healthy pre-pubertal, pubertal, and post-pubertal children. RESULTS: Leptin concentration was nearly three-fold higher in post-pubertal girls than in pre-pubertal girls, but was relatively similar in pre- and post-pubertal boys. Significant sex differences in leptin concentration existed in prepubertal, pubertal and post-pubertal children, and these remained significant after controlling for adiposity. After adjusting for total body fat, fat-free mass and age, testosterone concentration was negatively associated with leptin levels in pubertal boys, while estradiol concentration was positively associated with leptin level in pubertal girls. CONCLUSIONS: Girls have higher serum leptin concentration before, during, and after puberty than boys, even after accounting for the development of greater female adiposity. Although other factors may be involved, sexual dimorphism in leptin concentrations during puberty appears to be partly due to a stimulatory effect of estradiol on leptin concentration in females and a suppressive effect of testosterone on leptin concentration in males.

Adipose Tissue↗
PubMed2006

The impact of childhood body mass index on timing of puberty, adult stature and obesity: a follow-up study based on adolescent anthropometry recorded at Christ's Hospital (1936-1964).

OBJECTIVE: To examine the impact of childhood body mass index (BMI) on timing of puberty, adult stature and obesity. DESIGN: A retrospective school-based cohort follow-up study. SUBJECTS: A total of 1520 men born between 1927 and 1956 with serial height and weight measurements from the age of 9 to 18, followed up in adulthood at a mean age of 63 years. MEASUREMENTS: Prepubertal (child) BMI; age at peak height velocity (APHV); adult leg length, waist and hip circumference (self-reported), and height and weight (measured). RESULTS: Boys with a higher childhood BMI tended to have an earlier puberty (per s.d. increase in child BMI: -0.31 years, 95% confidence interval (CI): -0.23 to -0.39, P < 0.001). Childhood BMI correlated strongly and positively with adult adiposity, as measured by BMI (1.24 kg/m(2), 95% CI: 1.04-1.45, P < 0.001), waist (1.94 cm, 95% CI: 1.50-2.37, P < 0.001) and hip (1.91 cm, 95% CI: 1.55-2.28, P < 0.001). It correlated inversely with leg length (-0.40 cm, 95% CI: -0.68 to -0.12, P = 0.005), but not significantly with height or trunk length. Boys with a later puberty tended to be taller (per s.d. increase in APHV: 0.57 cm, 95% CI: 0.17-0.97, P = 0.006) and less adipose as adults (-0.55 kg/m(2), 95% CI: -0.33 to -0.77, P < 0.001). CONCLUSION: The long-term consequences of childhood obesity into adulthood are well known, but the potential impact on early pubertal maturation is less well appreciated. The factors that contribute to the onset and persistence of childhood obesity require more public health focus.

Adolescent↗
PubMed1997

Prepubertal and pubertal growth, timing and duration of puberty and attained adult height in patients with congenital hypothyroidism (CH) detected by the neonatal screening programme for CH--a longitudinal study.

OBJECTIVE: We have evaluated parameters of growth, the pubertal process and attained adult height in patients with congenital hypothyroidism (CH) of various aetiologies, diagnosed by the neonatal screening programme, and followed up longitudinally. To the best of our knowledge, no such data are available in the published literature. Our aim was to define the most important factors affecting these parameters. PATIENTS AND MEASUREMENTS: Thirty patients with CH (20 females and 10 males) diagnosed by neonatal screening (dysgenetic (n = 15), ectopic thyroid (n = 11), and enzymatic defect (n = 4)), treated with levo-thyroxine (L-T4) since the age of < or = 4 months, and followed up at intervals of 1-6 months for a mean period of 11.4 (range 5-19.6) years were evaluated. Detailed anthropometric measurements were performed by the same trained nurse, and pubertal stages were evaluated according to Tanner's criteria for breast or genitalia and pubic hair. Serum T4 and TSH levels were measured at each clinic visit using commercial kits. Bone age (BA) was determined at 6-12 months intervals using the Greulich & Pyle method. Seventeen patients attained adult height at the time of the report. RESULTS: Mean L-T4 dose of 7.9 (range 5.2-14.0) to 2.4 (range 1.3-3.4) micrograms/kg/day at various ages corrected the serum free T4(f-T4) levels to normal (> 10 pmol/l) in 95% of determinations, and the TSH level was reduced to < 10 mIU/l in 54% of the determinations during the follow-up period. Length at initiation of therapy (mean -0.15, (range -2.5-2.1) SDS), height at onset of puberty (mean -0.4, (range -1.8-1.8) SDS) and adult height (mean 0.2 (range -1.4-2.0) SDS, n = 17) were within the normal range (0.00 +/- 2 SDS). Onset and duration of puberty were normal in both sexes, and total pubertal growth contributed 19.1% (M) and 16.4% (F) to adult height. Peak height velocity (mean 10-6 (range 7.3-15.1) (M) and mean 8.0 (range 6.2-15.5) (F) cm/year) was within the normal range and occurred at the expected BA (14y; M and 12y; F). The attained average adult height was in close proximity to the average target height in both males and females. A significant positive correlation was found between the average L-T4 daily dose administered during the first 6 months of treatment and the attained adult height. CONCLUSIONS: Early detection by neonatal screening and treatment of congenital hypothyroidism enables normal prepubertal and pubertal growth and achievement of normal adult height, following normal puberty. Adult height in congenital hypothyroidism is significantly correlated with parental height and the mean L-T4 daily dose administered over the first 6 months of treatment. A dose of at least 8.5 micrograms/kg/day is recommended during this period. Periodical adjustments of L-T4 daily dose should be guided by clinical observation and serum free T4 levels.

Adolescent↗
PubMed2002

Regulation of puberty.

Pubertal development is the last phase of a continuum of changing gonadotrophin releasing hormone (GnRH) activities. Whether or not puberty tends to start at a younger age, as has been recently described in a population of black Americans, remains under debate. Such early onset has not been confirmed in different European countries. Ideas about the underlying mechanisms responsible for the reawakening of GnRH release at the onset of puberty have changed significantly during the last decades. At this moment, the common opinion is that neuronal outgrowth of both GnRH and other regulatory neurons results in changing interactions and activities. Sex steroids, as well as various central neurotransmitters, play a role in modulating GnRH release. Active release after birth is followed by the restraint of childhood. A re-onset of GnRH excitatory activities heralds the onset of puberty. This chapter gives an overview of the many factors involved.

Endocrine Glands↗
PubMed2002

Inhibins in childhood and puberty.

Inhibin is a heterodimeric glycoprotein that consists of an alpha-subunit linked to either a betaA subunit (inhibin A) or to a betaB subunit (inhibin B) and it exists in at least six different isoforms. These isoforms can not be measured separately by immunoassays. In boys, serum inhibin B levels change in concert with the increase in gonadotrophins. Associated with the postnatal activation of gonadotrophin secretion, the early inhibin B secretion is sustained until the age of 18-24 months; thereafter serum concentrations subside. In boys, between Tanner stages G1 and G2, serum inhibin B concentration again increases, but then plateaus. Inhibin A levels in human males are below the detection limit, but in girls, during the postnatal activation of gonadotrophin secretion, both serum inhibin A and inhibin B concentrations are measurable. Serum inhibin B levels correlate positively with age several years before the clinical onset of puberty, suggesting increasing follicular activity in late prepuberty. During female puberty, the inhibin B level increases from Tanner stage B1 through stage B3, suggesting high follicular activity before the development of ovulatory menstrual cycles, but serum inhibin A levels become measurable later in puberty, in agreement with the idea that inhibin A is mainly produced by the corpus luteum.

Adolescent↗
PubMed2002

Early puberty in girls.

Early puberty is not well defined in paediatric endocrinology. This chapter reviews the current insights on definitions, patient groups and treatment modalities in girls with early puberty. It is concluded that there is no clear evidence for a beneficial effect of gonadotrophin releasing hormone agonist (GnRHa) treatment in auxological terms. A clinical approach is presented, including both auxological and psychological items. Further research is needed to answer the question of whether early puberty should be treated with GnRHa.

Adolescent↗
PubMed2002

Oestrogens and puberty.

Oestrogens induce the development of female reproductive tissues. Endogenous human oestrogens include oestradiol, oestrone and oestriol. Oestrogen signalling in target tissues is dependent on the tissue concentration of oestrogen and the interaction of oestrogen receptors with an array of cell-specific co-regulator proteins. The diverse mechanisms of oestrogen signalling are complex and incompletely understood. In puberty, oestrogen is derived from both gonadal and peripheral sources. Originally, oestrogen was only thought to drive feminization in females; now, oestrogen is known to be important for pubertal development of males as well. Oestrogen is required for normal maturation of the neuroendocrine-gonadal axis and bone in both sexes, and a variety of other tissues are also responsive to oestrogen. Abnormal puberty can be associated with either excessive or inadequate oestrogen production. Girls deficient in oestrogen should receive replacement in physiological doses. Aromatase inhibitors and anti-oestrogens may prove to be useful therapeutic tools in some types of abnormal puberty.

Estradiol Congeners↗
PubMed2002

Leptin and the onset of puberty: insights from rodent and human genetics.

Deficiency of the adipocyte-derived hormone leptin in ob/ob mice results in severe, early-onset obesity and infertility. Administration of leptin results in complete reversal of the phenotype, suggesting that leptin is needed for the development of puberty in rodents. In humans, mutations in the genes encoding leptin and the leptin receptor result in obesity syndromes and hypogonadotropic hypogonadism. I have shown that administration of recombinant human leptin results in the onset of puberty at an appropriate developmental age in human congenital leptin deficiency. This work suggests that leptin is a metabolic gate for the onset of puberty in humans. Leptin's actions may be mediated by central pathways and by direct action on peripheral organs.

Animals↗
PubMed2003

Pitfall in diagnosing growth hormone deficiency in a hypochondroplastic patient with a delayed puberty.

Hypochondroplasia is a clinically and genetically heterogeneous skeletal dysplasia with less obvious disproportion in childhood and a reduced pubertal growth spurt. We report on a young hypochondroplastic man who had been misdiagnosed and treated as being growth hormone (GH) deficient in the early phase of puberty. The delay of his puberty which is unusual in hypochondroplasia might have confused the results of provocative GH testing. At the age of 17 years measurement of body proportions revealed an increased upper to lower body segment ratio. Skeletal radiographs showed a lack of increase in the interpedicular distance from the first to the fifth lumbar vertebra, anteroposterior shortening of the lumbar pedicles, short femoral necks, a fibula longer than the tibia, and short tubular bones. As the clinical and radiographic features suggested the diagnosis of a skeletal dysplasia, a DNA sequence analysis of the fibroblast growth factor receptor 3 gene on chromosome 4 p16.3 was performed, which identified the missense mutation C1620 G in the tyrosine kinase domain resulting in an Asn540Lys substitution. Hypochondroplastic children with this common mutation (N540K) were previously found to respond to GH treatment with an increase in sitting height compared to leg length, which accentuated the existing disproportion. We want to emphasise that in children with normal serum IGF-I and IGFBP-3 levels accurate measurements of body proportions and skeletal radiographs in disproportionate cases are more important than reiterative GH stimulation tests, which prepubertally and in the early phase of puberty often show subnormal responses.

Child↗
PubMedDate not supplied

[Gelastic epilepsy and precocious puberty in hamartoma of the hypothalamus].

Four cases of hypothalamic hamartoma leading to gelastic epilepsy, precocious puberty and behavioural disorders are reported. Cerebral neuroradiologic examinations revealed a tumor-like mass attached to the hypothalamus in the region of the mamillary bodies in all cases. Precocious puberty developed in the two girls at 4 and 13 months but in neither of the two boys, who both suffered behaviour disturbances in the form of aggressive outbursts. A total resection of the tumors of both boys led to histologic confirmation of hamartoma. One boy was free of seizures upon follow-up, whereas seizure frequency in the other boy was reduced, while his aggressivity increased. The cases are discussed in context of current therapeutic conceptions of gelastic epilepsy and central precocious puberty.

Aggression↗
PubMed1990

[Diagnostic differentiation between precocious puberty and premature thelarche using ultrasonography and the stimulated LH/FSH quotient].

True precocious puberty represents a serious developmental disorder necessitating immediate therapeutic measures, whereas premature thelarche is a harmless variation from the norm. For the differential diagnosis the ultrasonographic evaluation of the internal genitalia is of value. Girls with precocious puberty reveal a statistically significantly greater uterus length and volume as well as ovarian size. The stimulated LH/FSH quotient allows verification of the diagnosis. This value is found always to be greater than 1 in precocious puberty and always less than 1 in premature thelarche.

Adolescent↗