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PubMed1991

Low growth hormone levels are related to increased body mass index and do not reflect impaired growth in luteinizing hormone-releasing hormone agonist-treated children with precocious puberty.

To test the hypothesis that GH deficiency might explain the low growth velocity of some LHRH agonist (LHRHa)-treated children with central precocious puberty, we measured stimulated (n = 81) and spontaneous (n = 32) GH levels during or after LHRHa treatment. GH stimulation tests in the children who were receiving LHRHa treatment were performed after 2 days of ethinyl estradiol administration. Thirty-one of 81 children (38%) who underwent GH stimulation tests had subnormal responses (less than or equal to 7 micrograms/L) to all tests administered (at least 2 stimuli), including 22 of 67 (33%) who had precocious puberty that was idiopathic or associated with hypothalamic hamartoma. Eleven of 32 children (34%) who underwent measurement of the mean nighttime spontaneous GH level had levels below the normal range for prepubertal children (less than 1.2 microgram/L). Despite the high incidence of subnormal GH levels, there appeared to be no relationship between the GH levels of these children and their growth characteristics. The height, growth velocity, bone maturation rate, predicted height, and insulin-like growth factor-I levels were not different between the children with low GH levels and the children with normal GH levels. Conversely, the GH levels were not different between the children with subnormal growth rates and the children with normal growth rates. Thus, variation in the growth rates of these LHRHa-treated children with central precocious puberty could not be explained by variation in the stimulated or spontaneous secretion of GH. In attempting to understand the high incidence of low GH levels in children with precocious puberty, we examined the relationship between GH level and body mass index (BMI). Both the stimulated (r = -0.33; P less than 0.002) and the spontaneous (r = -0.61; P less than 0.0002) GH levels were inversely related to BMI. Moreover, the children with precocious puberty as a group had significantly elevated BMI [1.2 +/- 0.1 (+/- SE) SD units] compared to normal children of the same age (P less than 0.0001). Thus, increased body mass may explain the high incidence of subnormal GH levels in these patients, and normative GH levels adjusted for body mass are needed before it can be concluded that the apparently subnormal GH levels in LHRHa-treated children with precocious puberty are in fact low.

Adolescent↗
PubMed1995

Gonadotropin releasing hormone agonist (nafarelin) test to differentiate gonadotropin deficiency from constitutionally delayed puberty in teen-age boys--a clinical research center study.

The objective of this study was to determine whether the hormonal response to a GnRH agonist (nafarelin) challenge differentiates hypogonadotropinism from delayed puberty as well as the sleep test does. We studied boys ages 13.25-17.6 yr with prepubertal constitutional delay of puberty (CDP, n = 11), prepubertal gonadotropin deficiency (GnD, n = 10), pubertal CDP (PCDP, n = 11) and partial GnD (PGnD, n = 2). These disorders were defined on the basis of the following independent criteria: CDP = isolated delayed puberty with documentation of subsequent pubertal progression; GnD = panhypopituitarism or anosmia with absence of subsequent pubertal progression; PCDP = isolated delayed puberty in an early pubertal child; and PGnD = arrest of puberty in boys with partial hypopituitarism. CDP was compared with GnD and PCDP was compared with PGnD by analysis of variance and two-tailed t tests. Each patient had a nafarelin test with measurement of LH, FSH, and testosterone responses at intervals after nafarelin administration. Most patients had a sleep test with measurement of LH and testosterone levels at intervals overnight. CDP and GnD patients could not be distinguished by pubertal staging criteria. All but 1 patient with CDP had an LH response higher than that of GnD patients 4 h postnafarelin (P = 0.003). An incremental response to nafarelin of LH (delta LH at 4 h) below 4.8 IU/L was the best discriminant; it distinguished GnD from CDP in 95% of the cases and PGnD from PCDP completely. During the sleep test, all patients with CDP and 2 of 8 with GnD exhibited a significant increase in plasma LH. An incremental increase in LH during sleep (mean LH asleep minus mean LH awake) of less than 0.35 IU/L, near the limit of sensitivity of the method, differentiated GnD from CDP similarly to the nafarelin test. We conclude that the LH response to nafarelin distinguished gonadotropin deficiency from constitutional delay of puberty as well as the sleep test did and with certain advantages. The diagnostic reliability of the GnRH agonist test deserves to be determined prospectively in teen-agers with isolated GnD and partial hypopituitarism.

Adolescent↗
PubMed2000

Diurnal rhythms of luteinizing hormone, follicle-stimulating hormone, testosterone, and estradiol secretion before the onset of female puberty in short children.

To investigate hormonal changes before the onset of female puberty, we measured LH and FSH in serum samples drawn every 20 min for 24 h and measured testosterone and estradiol hourly for 24 h. Seventeen girls (13 prepubertal and 4 early pubertal) of short stature, from 5.1-11.4 yr of age, participated in this study. LH and FSH were measured using a time-resolved immunofluorometric assay, and testosterone and estradiol were measured using a sensitivity RIA capable of detecting testosterone and estradiol concentrations of 10 and 2 pg/mL, respectively. Diurnal rhythms of LH, FSH, and testosterone were apparent in all subjects, including those aged 5-6 yr. Serum LH and FSH concentrations showed night-day variation in a pulsatile fashion. The serum testosterone concentration was elevated in the early morning in all subjects. The serum estradiol concentration was elevated in the early morning in 4 of 13 prepubertal subjects and all 4 early pubertal subjects. The diurnal pattern of the serum estradiol concentration was similar to that of the serum testosterone concentration. Mean 24-h LH and testosterone concentrations in prepubertal subjects who did not attain puberty for at least 1 yr were 0.07 U/L and 65 pg/mL, respectively, whereas those in prepubertal subjects who attained puberty within 1 yr (0.14 U/L and 106 pg/mL, respectively) were significantly higher. Furthermore, mean 24-h LH, FSH, testosterone, and estradiol concentrations increased with the onset of puberty. In conclusion, the diurnal rhythms of LH, FSH, and testosterone already exist at 5-6 yr of age, and serum LH and testosterone levels increase before the onset of puberty. These results suggest that preparation for the onset of female puberty may begin in 5- to 6-yr-old girls.

Aging↗
PubMed2005

Examining bone surfaces across puberty: a 20-month pQCT trial.

UNLABELLED: This follow-up study assessed sex differences in cortical bone growth at the tibial midshaft across puberty. In both sexes, periosteal apposition dominated over endosteal resorption. Boys had a greater magnitude of change at both surfaces, and thus, a greater increase in bone size across puberty. Relative increase in cortical bone area was similar between sexes. INTRODUCTION: Generally, sex differences in bone size become most evident as puberty progresses. This was thought to be caused, in part, by greater periosteal apposition in boys, whereas endosteal apposition prevailed in girls. However, this premise is based on evidence from cross-sectional studies and planar measurement techniques. Thus, our aim was to prospectively evaluate sex-specific changes in cortical bone area across puberty. MATERIALS AND METHODS: We used pQCT to assess the tibial midshaft (50% site) at baseline and final (20 months) in girls (N = 68) and boys (N = 60) across early-, peri-, and postpuberty. We report total bone cross-sectional area (ToA, mm2), cortical area (CoA, mm2), marrow cavity area (CavA, mm2), and CoA/ToA ratio. RESULTS: Children were a mean age of 11.9 +/- 0.6 (SD) years at baseline. At the tibia, CoA ranged from 230 +/- 44, 261 +/- 50, and 258 +/- 46 in early-, peri-, and postpubertal girls. In boys, comparable values were 223 +/- 36 (early), 264 +/- 38 (peri), and 281 +/- 77 (postpubertal). There was no sex difference for ToA or CoA at baseline. Increase in ToA and CoA was, on average, 10% greater for boys than girls across maturity groups. The area of the marrow cavity increased in all groups, but with considerable variability. The increase in CavA was significantly less for girls than boys in the early- and postpubertal groups. Change in CoA/ToA was similar between sexes across puberty. CONCLUSION: Both sexes showed a similar pattern of change in CoA at the tibial midshaft, where periosteal apposition dominated over endosteal resorption. Boys showed a greater magnitude of change at both surfaces, and thus, showed a greater increase in bone size across puberty. The relative increase in cortical area was similar between sexes. These pQCT findings provide no evidence for endosteal apposition in postmenarchal girls.

Adolescent↗
PubMed2000

Spontaneous, but not induced, puberty permits adequate bone mass acquisition in adolescent Turner syndrome patients.

Lumbar L2-L4 bone mineral density (BMD) values were measured in 37 adolescent and young adult Turner syndrome patients. Nine had developed spontaneous puberty and had had regular menses since menarche (12.55 years +/- 1.17 years) to the time of BMD evaluation (14.96 years +/- 1.26 years). In the other 28, puberty was induced with increasing doses of oral ethinyl estradiol (2.5-10.0 microg/day, for 2 years) and later administration of estrogen/gestagen therapy up to the time of BMD evaluation. In 18, the adolescent group, menarche appeared at 14.68 years +/- 0.63 years and BMD was evaluated at 17.77 years +/- 0.70 years, and in the other 10, the young adult group, menarche appeared at 14.47 years +/- 0.53 years and BMD was evaluated at 20.90 years +/- 0.68 year. BMD values were in the normal range in those who had developed spontaneous puberty (Z score values, -0.24 +/- 0.22) and in the osteopenia range in those in whom puberty was induced (Z score values, -2.09 +/- 0.79 and -2.18 +/- 0.32 for the adolescent and young adult groups, respectively) p < 0.0001. Height Z score values were similar in all three groups (-3.45 +/- 0.77, -3.15 +/- 0.83, and -3.08 +/- 0.33, respectively). No significant differences in calcium intake or physical activity were found among groups. Neither the karyotype distribution nor growth hormone (GH) therapy (five in the spontaneous puberty and six in the induced puberty groups had been treated for a 3.5- to 4.4-year period) explained the differences in BMD values. Because the main difference between groups was the availability of estrogens to bone tissue from infancy to menarche and of estrogens/gestagens from then on up to the time of BMD evaluation, our results suggest that normal gonadal function from infancy to adulthood may be required for adequate bone mass peaking. Early detection of osteopenia and improvement in general measures for adequate bone mass peaking (calcium intake and physical activity) should be considered mandatory in the health care of these patients.

Absorptiometry, Photon↗
PubMed2005

Relation of beta2-adrenoceptor polymorphisms at codons 16 and 27 to persistence of asthma symptoms after the onset of puberty.

BACKGROUND: It has long been recognized that many children with asthma outgrow the disease after the onset of puberty, but little is known about genetic factors influencing this outcome. OBJECTIVES: The aim of the present study was to determine whether the polymorphisms at codons 16 and 27 of the beta2-adrenoceptor are significant predictors of the persistence of asthma during adolescence. DESIGN AND PARTICIPANTS: We used data from the prospective Tucson Children's Respiratory Study. Children were genotyped for the polymorphisms at codons 16 and 27. The presence of wheezing/asthma was assessed by questionnaire from age 6 years up to the reported onset of puberty (prepubertal period) and after the onset of puberty up to age 16 years (adolescence). RESULTS: Among children who wheezed in the prepubertal period (n = 168), subjects homozygous for Gly at codon 16 were at significantly increased risk for persistent wheezing after puberty, as compared with carriers of the other genotypes (relative risk [RR], 1.43; 95% confidence interval [CI], 1.06 to 1.92; p = 0.019). This relation was present among boys (RR, 2.17; 95% CI, 1.41 to 3.36) but not girls (RR, 0.85; 95% CI, 0.55 to 1.30), and increased linearly according to the frequency of wheezing episodes after the onset of puberty. These findings persisted after adjusting for ethnicity and other potential confounders and after selecting only white children. The polymorphism at codon 27 showed no relation with risk for persistent wheezing. CONCLUSIONS: This study provides evidence for a strong gender-specific effect of the Gly16 polymorphism on the persistence of asthma after the onset of puberty.

Adolescent↗
PubMedDate not supplied

Precocious puberty: clinical and endocrine profile and factors indicating neurogenic precocity in Indian children.

The objective of this study was to evaluate the clinical and endocrine profile of patients with precocious puberty followed up in a tertiary care hospital. Records of 140 patients (114 girls, 26 boys) with precocious puberty were reviewed. Clinical features including age of onset, stage of pubertal development, presenting symptoms, features suggestive of CNS involvement and family history were analyzed. Endocrine investigations included basal and GnRH-stimulated levels of LH and FSH as well as 17OHP, DHEA, hCG and thyroid profile. Abdominal and pelvic ultrasonography and CNS imaging were correlated with clinical features. Girls outnumbered boys in this series (4.4:1). Neurogenic central isosexual precocious puberty (CIPP) was more common in boys (10 out of 18, 55.6%) than girls (16 out of 77, 20.8%). The most common cause of neurogenic CIPP was hypothalamic hamartoma present in five girls and four boys. Other causes of neurogenic CIPP included neurotuberculosis, pituitary adenoma, hydrocephalus, post radiotherapy, CNS tumors and malformations. Peripheral precocious puberty (PPP) was secondary to adrenal causes in boys and ovarian cysts in girls. Benign variants of precocious puberty, such as premature thelarche and premature adrenarche, were present in 23 and six girls, respectively. Hypothyroidism was present in four girls and McCune-Albright syndrome in one girl. Girls with neurogenic CIPP had a lower age of onset as compared to idiopathic CIPP (3.6 +/- 2.7 years vs 5.4 +/- 2.5 years, p = 0.014). The lowest age of onset was seen in girls with hypothalamic hamartoma (1.6 +/- 0.9 years). Forty-seven girls with CIPP (seven neurogenic and 40 idiopathic) presented after the age of 6 years. Features of CNS involvement, in the form of seizures, mental retardation, raised intracranial tension or focal neurological deficits, were present in seven girls (43.8%) and four boys (40%), and gelastic seizures were present in three children. Girls with CIPP had greater bone age advancement (3.4 +/- 1.5 years) and negative height standard deviation for bone age (-2.7 +/- 1.5) than those with PPP (1.9 +/- 1.6 years and -1.3 +/- 1.3) and premature thelarche (0.4 +/- 0.4 years and -0.8 +/- 0.8). Patients with neurogenic CIPP had significantly higher levels of baseline and GnRH-stimulated levels of LH and FSH and LH:FSH ratio than those with idiopathic CIPP. Occurrence of neurogenic CIPP in seven girls with an age of onset after 6 years emphasizes the need for CNS imaging in these girls contrary to the current recommendations. The fact that 65.6% cases of idiopathic CIPP presented after the age of 6 years raises the possibility that these patients may be physiological variants of normal puberty. Pointers to neurogenic CIPP included early age of onset in girls, clinical features of CNS involvement, and elevated basal and stimulated LH levels and LH:FSH ratio.

Age Determination by Skeleton↗
PubMed1995

High prevalence of abnormal adrenal response in girls with central precocious puberty at early pubertal stages.

Abnormal adrenal response is often observed in girls with precocious adrenarche (1). We studied the adrenal response in 112 girls with idiopathic true central precocious puberty (CPP) at early stages of puberty compared to that in 21 girls with normal puberty (controls). The aims of this study were to determine the prevalence of abnormal adrenal response at early stages of puberty, the possible correlation of abnormal adrenal response with pubertal signs at onset of puberty and with plasma androgen levels, and a possible association with the activity of the hypothalamic-pituitary-gonadal (HPG) axis. All participants underwent a combined i.v. adrenocorticotropic hormone (ACTH)-gonadotropin-releasing hormone (GnRH) test at Tanner stage 2-3: 62 of the CPP girls before and 50 during treatment with GnRH analog. The stimulated levels of 17-hydroxypregnenolone (17OHPreg) and the stimulated 17OHPreg/17-hydroxyprogesterone ratio were analyzed and compared to previously reported norms. The result revealed three patterns of adrenal response: normal (17OHPreg < or = 24 nmol/l and 17OHPreg/17OHP ratio < or = 7) in 50/112 (44.6%) CPP patients and 17/21 (80.9%) controls; exaggerated (17OHPreg > 24 nmol/l, 17OHPreg/17OHP ratio < or = 7) in 50/112 (44.6%) CPP patients and 3/21 (14.3%) controls; and non-classical 3 beta-hydroxysteroid dehydrogenase deficiency (17OHPreg > 24 nmol/l and 17OHPreg/17OHP ratio > 7) in 12/112 (10.8%) CPP patients and 1/21 (4.8%) controls. The clinical features at onset of puberty were comparable in all girls with the CPP in spite of the different adrenal response patterns.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxypregnenolone↗
PubMed1997

Prostate specific antigen in boys with precocious puberty before and during gonadal suppression by GnRH agonist treatment.

UNLABELLED: In healthy boys, the pituitary-gonadal axis exhibits diurnal variation in early puberty. Serum testosterone levels are higher during the night and low or immeasurable during the day. These fluctuating levels of circulating androgens in early pubertal boys are difficult to monitor. Prostate specific antigen (PSA) is a marker of the androgen-dependent prostatic epithelial cell activity and it is used in the diagnosis and surveillance of adult patients with prostatic cancer. We have measured PSA concentrations in serum from boys with precocious puberty before and during gonadal suppression with GnRH agonists to evaluate the effect of normal and precocious puberty on PSA levels and to study the correlation between testosterone and PSA in boys. METHODS: PSA was measured by an ultrasensitive immunofluorometric assay with a detection limit of 0.03 microgram/l. Testosterone was measured by an RIA with a sensitivity of 0.23 nmol/l, and sex hormone binding globulin was measured by a time-resolved immunofluorescence assay (sensitivity 0.23 nmol/l). Five boys with central precocious puberty (CPP) were studied before and after 12 months of GnRH agonist treatment. Sixty healthy boys (12 in each Tanner stage of puberty) and 37 healthy young males served as controls. RESULTS: PSA levels were immeasurable in all prepubertal boys, whereas PSA levels increased with increasing stage of pubertal maturation. There was a significant correlation between PSA and testosterone and free androgen indices (r = 0.61 and r = 0.65 respectively, both P < 0.001). All 5 boys with CPP had significantly elevated PSA levels which decreased to very low or immeasurable levels after GnRH agonist treatment. CONCLUSION: PSA may be a useful marker of testosterone activity in boys with normal or precocious puberty.

Adolescent↗
PubMed2001

Leptin levels show diurnal variation throughout puberty in healthy children, and follow a gender-specific pattern.

OBJECTIVE: To investigate the levels and diurnal rhythm of serum leptin in healthy children, and to investigate the association between leptin levels and sex steroids. METHODS: Four girls and four boys, all healthy volunteers, were followed longitudinally throughout puberty. Their chronological ages ranged from 8.7 to 19.5 years, and body composition, expressed as weight-for-height standard deviation scores (SDS), ranged between -1.7 and +2.4. Serum leptin, oestradiol and testosterone concentrations were measured by radioimmunoassay at 1000, 1400, 1800, 2200, 0200 and 0600 h. RESULTS: In all girls and boys, both prepubertally and during pubertal development, serum leptin levels increased during the night, with no difference in relative peak amplitude. In boys, the leptin concentrations increased until the initiation of puberty and then declined, whereas in girls, the concentrations increased throughout puberty. The inter-individual variation in mean leptin levels among girls decreased to 11% at the time of menarche. A positive correlation was found for both oestradiol and testosterone versus leptin in girls throughout puberty (r=0.64 and r=0.71 respectively, P<0.001). A negative correlation was found between leptin and testosterone in boys in mid- and late puberty (r=-0.66, P<0.01). No correlation was found between oestradiol and leptin in boys or between testosterone and leptin in pre- and early pubertal boys. CONCLUSION: Serum leptin concentrations show diurnal variation throughout pubertal development in both girls and boys. The changes in leptin levels during puberty follow a gender-specific pattern, probably due to an influence of sex steroids on leptin production.

Adolescent↗
PubMed2005

The neuroendocrine timing of puberty.

Puberty is the attainment of fertility, a process encompassing morphological, physiological and behavioural development. The increased hypothalamic secretion of the gonadotrophin-releasing hormone decapeptide (GnRH) is essential for the activation of the pituitary-gonadal axis at puberty. The GnRH secretory network initially develops and is temporarily active during species-specific periods of fetal/neonatal development, so puberty is the secondary reactivation of an existing system. From a neurobiological perspective, the timing of puberty is therefore a function of changes in the neural systems controlling GnRH release. The large variability between individuals in the onset and progression of puberty indicates that the timing of puberty is not simply a function of chronological age. Rather, the neurotransmitter and neuromodulatory systems that impact upon the GnRH secretory network convey information about metabolic fuels, energy stores and somatic development and, for many species, information about season and social environment. The clear links demonstrated between metabolic fuel availability and reproductive function in many animal models provides evidence that the earlier onset of pubertal development observed in girls in certain US study populations is likely to relate to the increasing prevalence of overweight and obesity in adolescents.

Adolescent↗
PubMed1999

Growth, puberty, and endocrine functions in patients with sporadic or familial neurofibromatosis type 1: a longitudinal study.

OBJECTIVE: This study prospectively evaluates parameters of growth, puberty, and attained adult height in children with sporadic or familial occurrence of neurofibromatosis type 1 (NF-1), followed up longitudinally, to define the most important factors affecting these parameters. PATIENTS AND METHODS: The study was made up of 89 patients (55 boys, 34 girls) with sporadic (n = 45) or familial NF-1 (13 affected fathers and 31 affected mothers). The average age at referral was 8.9 years (range 8.5-15 years), and the average follow-up period was 8.5 years (6-15 years). A total of 28 patients attained adult height at the time of the report. Anthropometric measurements and bone age determinations were performed at 6- to 12-month intervals. As indicated, central nervous system (CNS) imaging was performed on 60 patients. Serum levels of thyroid stimulating hormone, free T4, lutheinizing hormone, follicle stimulating hormone, testosterone or estradiol, cortisol, and prolactin were measured in all patients periodically, and the pituitary growth hormone reserve was assessed in 32 short patients. RESULTS: CNS pathology was found in 23 of the 89 patients. A total of 6 patients required neurosurgery, and 2 patients had cranial irradiation. Of these patients, 3 were receiving recombinant growth hormone and thyroxin replacement therapy and 5 patients with precocious puberty were treated with a gonadotropin-releasing hormone analog. All other patients had normal endocrine tests. Precocious puberty was recorded in 5 patients and was more common among the familial cases. The 5 patients with precocious puberty also had CNS pathology. Short stature (<10th percentile) was observed in 25.5% of the patients during the prepubertal period with a significant gradual reduction of their relative height for age (standard scores) during puberty. Short adult height was noted in 12 (43%) of 28 patients, and only 50% of the 28 patients attained an adult height that was appropriate for their respective target height. Short stature was more common among patients with familial NF-1, particularly if the father was affected, and among those patients with CNS pathology. Parental short stature was observed in 39% of the mothers and in 33% of the fathers (59% and 54% among the affected parents, respectively). Tall stature (>90th percentile) was observed in 4 of 89 patients (4.5%), who all had CNS tumors. A highly significant correlation was found among all adult height-predicting parameters (r =.79), and attained adult height was best correlated with the target height (r =.7; n = 28). CONCLUSIONS: Short adult height is an important characteristic of NF-1 and deserves to be emphasized in the evaluation and follow-up of these patients during childhood. Short adult height is strongly linked with familial background of NF-1, in particular if the affected parent is the father, and is affected adversely by the relatively poor pubertal growth. Despite normal pituitary gland and thyroid function tests in most children and adolescents with NF-1, increased incidence of precocious puberty was observed. As the clinical expression in the second generation is more pronounced, the underlying mechanism seems to be mediated by genetic factors that are yet undefined.

Adolescent↗
PubMed2000

Predicting heart growth during puberty: The Muscatine Study.

OBJECTIVES: During childhood, heart growth is closely associated with somatic growth including increases in body weight, fat-free body mass (FFM), and height. However, with age, greater variability in heart size in relationship to body size is observed, presumably attributable to the increased effect of cardiac workload. At this time, little is known as to what functional attributes (eg, aerobic fitness) contribute to cardiac workload and the relative contribution of these attributes to heart growth during childhood and adolescence. In this article, we report cross-sectional and longitudinal relationships among aerobic fitness, body size, blood pressure (BP), and left ventricular mass (LVM) through puberty including the predictors of heart growth during puberty and the tracking of LVM from pre-puberty to late and post-puberty. Describing the predictors of heart size and heart growth and establishing the likelihood that a large heart, relative to peers, may (or may not) remain a large heart should aid pediatricians in discerning between normal developmental increases in LVM and increases in LVM suggestive of excessive heart growth (left ventricular hypertrophy). METHODOLOGY: Using a repeated-measures design, we assessed aerobic fitness, FFM, fatness, weight, height, sexual maturation, resting BP, peak exercise BP, and LVM in 125 healthy children (mean baseline age: 10.5 years) for a period of 5 years. All subjects were either in prepuberty or early puberty at the beginning of the study. At follow-up, 110 subjects attempted all research procedures (87% of the initial cohort). Using anthropometry and bioelectrical impedance, we measured FFM, fatness, weight, and height quarterly (once every 3 months) for a total of 20 examinations. Resting BP and LVM (2-dimensional echocardiography) were also assessed quarterly. Aerobic fitness, peak exercise BP, and sexual maturation (staging of secondary sex characteristics and, for boys, serum testosterone) were measured annually (5 examinations). The same field staff conducted all examinations. Statistical methods included Spearman rank correlation coefficients (r(s)) calculated to estimate how well the year 5 LVM was predicted by LVM at earlier years. We also categorized the LVM data into tertiles and reported the percentage who remained in the extreme tertiles in year 5, given they began in that tertile in year 1. Gender-specific stepwise multivariate analysis was used to evaluate predictors of follow-up LVM and predictors of changes in LVM. The latter model examined whether the variability in the changes in LVM, as quantified by subject-specific slopes, could be explained by changes in predictor variables, also quantified by subject-specific slopes. RESULTS: At baseline and at follow-up, boys tended to be taller, leaner, more aerobically fit, and had greater LVM than girls. Rate of change for these variables was also greater in boys than girls. For example, LVM increased 62% in boys and 48% in girls. At year 5, subjects had advanced at least 1 stage in genital or breast development and over 80% of the subjects were in late- or post-puberty. Significant and strong tracking of heart size (r(s) =.65-.87) was observed. The likelihood that a subject would be in an extreme tertile for heart size at follow-up was approximately doubled if he or she started there at baseline. In boys, baseline FFM explained 54% of the variability in follow-up LVM. Change in aerobic fitness and change in FFM explained 55% of the variability in change in LVM. In girls, baseline aerobic fitness and fatness explained 45% of the variability in follow-up LVM. Because FFM did not enter in this model, we constructed an alternative model in which baseline aerobic fitness adjusted for FFM was entered. Using this approach, 43% of the variability in follow-up LVM was explained by baseline FFM, fatness, and adjusted aerobic fitness. Change in FFM explained 58% of the variability in change in LVM. (ABSTRACT TRUNCATED)

Adolescent↗
PubMed1994

Changes in gonadotrophin secretion during childhood and puberty.

The changes in gonadotrophin secretion in childhood and puberty involve changes in the pulsatile pattern as well as mean concentration. We have examined pulsatile secretion using 24-h LH profiles in 78 children aged 4.2-15.6 years and six adult men. The profiles were analysed by a method which gives an estimate of peak and baseline levels and by spectral analysis. Prepubertal children were divided into groups by age and pubertal children by pubertal stage. Baseline LH levels in children aged 4.2-6.9 years were higher than in those aged 7.1-9.8 years. Pulse frequency in both groups was slow (periodicities 140-200 min). In the oldest prepubertal group there was an increase in peak levels with increased spectral power at periodicities of 100-120 min. Pulse frequency did not change in puberty (periodicity 120-160 min). Girls demonstrated an increase in both peak and baseline LH concentrations in early puberty. Boys had an increase in only peak levels in early puberty; there was no increase in baseline concentrations until a testicular volume of 10 ml was attained. In conclusion, these data show that LH levels do not reach a nadir until 8 years of age. We have detected a sex difference in the pattern of LH secretion seen in early puberty, and this mirrors clinical findings. The mature pattern attained by the end of puberty in both sexes is probably important for fertility.

Adolescent↗
PubMed1987

CT of cerebral abnormalities in precocious puberty.

True precocious puberty occurs as a result of the premature release of luteinizing hormone-releasing hormone from the hypothalamus, which stimulates the secretion of the pituitary gonadotropins, which in turn stimulate the gonadal sex steroids. The differential diagnosis of true precocious puberty includes cerebral and idiopathic categories. This differentiation, which cannot be made endocrinologically due to similarities in pituitary gonadotropin and sex steroid levels, may be facilitated by high-resolution CT. A CT study of 90 children (73 girls and 17 boys) with true precocious puberty was performed at the NIH to detect cerebral causes of their precocious puberty. Thirty-four cerebral abnormalities were demonstrated in 32 children, 16 boys and 16 girls. These included hypothalamic hamartomas (17), hypothalamic astrocytoma (one), optic chiasm lesions (six), ventricular abnormalities (eight), arachnoid cyst (one), and teratoma (one). The CT appearance of these cerebral abnormalities is discussed and related to the endocrinologic findings and natural history of true precocious puberty. A practical neuroradiologic approach to the evaluation of children with precocious puberty is presented.

Astrocytoma↗
PubMed2001

Peripheral nerve function is increasingly impaired during puberty in adolescents with type 1 diabetes.

OBJECTIVE: To evaluate the impact of puberty on peripheral nerve function in adolescents with type 1 diabetes. RESEARCH DESIGN AND METHODS: Of 138 eligible patients with type 1 diabetes, 100 patients (age >9 years and diabetes duration >2 years) attending an outpatient diabetes clinic and 100 age- and sex-matched healthy control subjects took part in this cross-sectional study. Peripheral motor and sensory nerve conduction tests, cardiovascular reflex tests on the autonomic nervous system, and measurements of vibration-perception threshold (VPT) were performed. RESULTS: Nerve conduction velocity (NCV) in the distal motor and sensory nerves, the motor nerve distal latency, and the sensory nerve action potential (SNAP) amplitude were impaired in the adolescent patients with type 1 diabetes. The deterioration in motor NCV, H-reflex latency, and SNAP amplitude became more conspicuous in late puberty and postpuberty and was related to poor metabolic control. A total of 10 patients had distal diabetic polyneuropathy (DP) neurophysiologically, and these patients had significantly lower heart-rate variation in the deep breathing test than the other patients. Three of the patients with DP had peripheral neurological signs or symptoms. A slight difference in the VPT between the patients and control subjects was observed after puberty. CONCLUSIONS: Increasing subclinical motor nerve impairment can be detected during late puberty and after puberty, and sensory NCV and SNAP amplitude are reduced in adolescents with type 1 diabetes. Poor metabolic control during puberty appears to induce deteriorating peripheral neural function in young patients with type 1 diabetes.

Action Potentials↗
PubMed1989

[Three cases of Klinefelter syndrome in childhood--endocrinological and gonadal changes in puberty].

Three children at the ages of 4, 10 and 12 years, with external genital malformation, were diagnosed to be with the Klinefelter syndrome by chromosome analysis. To clarify the pubertal changes in this syndrome, all of them were studied for physical and endocrinological examinations and two underwent testicular biopsy. Before puberty any remarkable abnormality were not observed in the hypothalamus-pituitary-gonadal axis and in the physical status. After the onset of puberty they started showing increases of the basal levels of plasma FSH and LH with over-response to LH-RH stimulation test. During the period of this study the levels of plasma testosterone were in the normal range and increased gradually with age. One boy showed a transient high level of plasma testosterone at early puberty. The reactions of plasma testosterone to HCG stimulation of all cases showed the normal pattern. The histological examination of the testis revealed that the number of spermatogonia was reduced in both cases compared with that of normal boys reported by Mancini et al. These findings indicate that most endocrinological and histological abnormalities in adult Klinefelter syndrome occur after the onset of puberty. These changes may be induced at puberty by hypergonadotrophic condition which result from slightly impaired testicular function which is present before puberty.

Age Factors↗
PubMedDate not supplied

[Surgical treatment of GnRH secretory hypothalamic hamartomas causing precocious puberty].

Hypothalamic hamartomas (HHs) are benign lesions often associated with central precocious puberty. Resection of HHs has been recommended as a treatment option for selected cases, however recent reports stressed the role of effective medical management with a long-acting GnRH agonist. This paper describes incomplete response to the initial GnRH therapy and results of total resection of HHs. Five children two boys and three girls with physical signs of puberty at a mean age of 20.2 months (range 5-36 months) have been treated at our institution. All children had a pedunculated mass below the tuber cinereum. Two children were initially treated with GnRH agonist and had received follow-up care for 11 and 12 months respectively. These patients had incomplete regression of endocrinological disturbances to prepubertal level. Both patients were subsequently operated on. All five children underwent total surgical removal of HHs. The hamartomas were excised through pterional approach. Postoperatively two children showed transient third nerve palsy and one diabetes incipidus. There was no permanent disability due to surgical intervention. The clinical and biochemical symptoms and signs of precocious puberty completely regressed postoperatively including two cases treated initially with GnRH analog. The children have been followed for 1 to 6 years and no recurrence of puberty was observed. Surgical excision of pedunculated HHs is still a valuable option in the treatment of precocious puberty in small children. This alternative should be considered if the initial GnRH therapy failed to suppress++ puberty and reduce bone age advancement.

Brain Diseases↗