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PubMed2002

The neuroendocrinology of human puberty revisited.

The fundamental aspects of the hypothalamic luteinizing hormone-releasing hormone (LHRH)(1) [1]pulse generator-pituitary gonadotrophin-gonadal apparatus in mammals have striking commonalities. There are, however, critical, substantive differences in the neuroendocrinology of puberty among species. The onset of puberty in the human is marked by an increase in the amplitude of LH pulses, an indirect indicator of the increase in amplitude of LHRH pulses. The hypothalamic LHRH-pituitary gonadotrophin complex is functional by at least 0.3 gestation in the human foetus; the sex difference in the fetal and neonatal pattern of LH and FSH secretion is an apparent consequence of imprinting of the fetal hypothalamus-pituitary-gonadotropin apparatus by fetal testosterone. Until about 6 months of age in boys and 12-24 months in girls, the testes and ovaries respond to the increased LH in boys and follicle-stimulating hormone (FSH) in girls by secreting testosterone and oestradiol, respectively, reaching levels that are not again achieved before the onset of puberty. Striking features of the ontogeny of the human hypothalamic pulse generator are: (1) its development and function in the foetus; (2) the continued function of the hypothalamic LHRH pulse generator-pituitary gonadotrophin-gonadal axis in infancy; (3) the gradual damping of hypothalamic LHRH oscillator activity during late infancy; (4) its quiescence during childhood - the so-called juvenile pause; (5) during late childhood the gradual disinhibition and reactivation of the LHRH pulse generator, mainly at night; (6) the increasing amplitude of the LHRH pulses, which are reflected in the progressively increased and changing pattern of circulating LH pulses, with the approach of and during puberty. The intrinsic central nervous system (CNS) mechanisms responsible for the inhibition of the LHRH pulse generator during childhood (the juvenile phase) involve the major role of an inhibitory neuronal system - the CNS inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and GABAergic neurons, as revealed by studies in the rhesus monkey by Terasawa and her associates. With the onset of puberty, the disinhibition and reactivation of the LHRH pulse generator is associated with a fall in GABAergic neurotransmission and a concomitant increase in the input of excitatory amino acid neurotransmitters (including glutamate) and possibly astroglial-derived growth factors. Despite remarkable progress over the past three decades, large gaps remain in our understanding of the neurobiological, genetic and environmental mechanisms involved in the control of the onset of puberty. The role of leptin in the control of the onset of puberty is reviewed. Severe leptin deficiency is associated with hypogonadotrophic hypogonadism; it appears that a critical level of leptin and a leptin signal is required to achieve puberty. The weight of evidence supports the hypothesis that leptin acts as one of several permissive factors and not a trigger in the onset of human puberty. The application of these advances provides a framework for the described classification of sexual precocity and delayed puberty.1 GnRH is synonymous with LHRH.

Animals↗
PubMed1988

Variations in duration of pubertal growth: a mechanism compensating for differences in timing of puberty and minimizing their effects on final height. Belgian Study Group for Paediatric Endocrinology.

It is unclear how important age at onset of puberty is for adult stature. The growth effects of differences in timing of puberty have been studied on a bone age basis in 22 hypopituitary boys and on a chronological age basis in male subjects with early, normal or delayed onset of puberty. Very early onset of puberty results in short adult stature. This is because a marked reduction of prepubertal height gain is only partially compensated for by an increase in pubertal height gain. In contrast, very late onset of puberty determines no increase or a minor increase in adult stature. This results from a reduction in pubertal height gain, counterbalancing the increased prepubertal height gain. Differences in duration of growth are the major factor accounting for the different height gains observed in relation to timing of puberty, while mean growth rate shows only minor changes. The differences in duration of pubertal growth are paralleled by differences in the rate of bone maturation, which therefore do not account for differences in duration of puberty. It is concluded that, except in severely precocious puberty, manipulation of the timing of puberty is unlikely to affect final height to any great extent.

Adolescent↗
PubMed1985

Pathogenesis and management of abnormal puberty.

In the prepubertal child, the hypothalamic-pituitary-gonadal (H-P-G) axis is functional and extremely sensitive to negative feedback inhibition by low circulating levels of sex steroids. This feedback system may be under the control of unknown CNS inhibitory mechanisms. Clinical signs of puberty are preceded by increased pulsatile secretion of hypothalamic gonadotropin-releasing hormone (GnRH) followed by increased pituitary responsiveness to GnRH. Gonadotropin secretion, particularly LH, increases in both sexes, especially during sleep, resulting in gonadal stimulation, secretion of sex steroids, and progressive physical maturation. When any phase of the H-P-G axis malfunctions, abnormal puberty can result. Abnormal puberty may be precocious or delayed. When puberty is precocious it may be isosexual or heterosexual, complete or partial, intermittent (unsustained), or progressive. True (central) precocious puberty is usually progressive, and hormonally reflective of normal puberty, although occurring at an earlier age, whereas intermittent or unsustained precocious puberty usually is associated with immature patterns of gonadotropin secretion, or with complete gonadotropin suppression as in precocious pseudopuberty (ovarian or adrenal tumors). Cranial axial tomography, gonadotropin response to GnRH, and pelvic ultrasound in girls are useful tools to aid in the differential diagnosis of these conditions. Intermittent, or unsustained, puberty in girls is usually self-limited, requiring no medical or surgical intervention. True progressive central precocity may now be managed with GnRH analogues, which effectively arrest pubertal changes as well as slow rapid linear growth and skeletal maturation. Although a maturation lag usually explains most patterns of delayed puberty, it is often challenging to exclude other conditions that may contribute to slow pubertal progression, such as chronic illness, excessive exercise, emotional stress, anorexia, or drug use. Elevated serum gonadotropin levels direct further evaluation toward etiologies of gonadal failure, including gonadal dysgenesis, Klinefelter syndrome, and chemotherapy/irradiation damage. Both low gonadotropins and absence of or immature gonadotropin response to GnRH administration after a bone age of 11 years in girls and 13 years in boys point toward hypopituitarism or isolated hypogonadotropic hypogonadism. Management with administration of gradually incremented amounts of sex steroids at an appropriate psychologic age usually leads to enhanced linear growth, physical maturation, and improved self-esteem.

Adrenal Gland Neoplasms↗
PubMed1997

[Significance of ultrasonographic examinations in the diagnosis of premature and normal puberty in girls].

Dynamic and individual course of the processes being associated with puberty and also the necessity of establishing instantaneous diagnosis of disturbances occurring at that period made it indispensable to apply simple and non-invasive diagnostic methods. The aim of the study was to estimate the usefulness of ultrasonographic measurements of the first- and second-rate genital features in the course of normal puberty, as well as differentiating, on the basis of the said measurements, various forms of premature puberty. Ultrasonographic examination of the internal genital organs allows for their precise assessment, without any simultaneous invasiveness ascribed to the method. The study material comprised 248 girls. The normal puberty was evaluated in 138 girls. The studied girls were divided into groups by resorting to gynaecological criteria, it means, from the age proceeding since the menarche, considered as being modern and highly objective criteria of development. The study also included 64 girls with different forms of premature puberty, as well as a group of 46 healthy girls lodging in the same age compartment. All the studied persons were evaluated with regard to measurements of the ovary length, width, thickness and volume. The ratio of volume of the left ovary to the right one was calculated, with the size and the number of ovarian follicles being evaluated by employing the four-grade scale in own modification (F1 < 2 mm diameter, F2 < 3 mm, F3 < 5 mm, F4 > 5 mm). At evaluating the uterus, the accomplished measurements included the length of uterine cervix, the length, width, thickness and the volume of the body of the uterus. Next, the ratio of the cervical length to the body of uterus was calculated. The presence or absence of endometrium in the uterine cavity as well as within the cervical canal was estimated too. In menstruating girls the investigations were performed between 7-9 day of the cycle. The ultrasonographic examinations were carried out with a trans abdominal probe, the frequency being 3.5 or 5 MHz, with apparatus of Brüel & Kjaer or Acusson Companies. The established results were elaborated statistically. In the course of normal puberty the ovarian development is dynamic and involves both glands (Tab. 1-4). At the same period the body of the uterus increases while the cervical length remains unchanged (Tab. 6-9). The termination of the morphological development concerning the first- and second-rate genital features occurs at the time of gynaecological age +2. The girls with premature puberty of the central origin as compared with the control group display higher degree of development of the first- and second-rate genital features (Tab. 10-14). These differences are not observed in girls with premature development of mammary glands (Tab. 11-15) and also with premature growth of public hair (Tab. 12-16). The results of the studies have made it possible to provide the following conclusions: the ultrasonographic examinations of the first- and second-rate genital features constitute a valuable aid for determining the stages of normal puberty, thus facilitating the detection and differentiation of the disturbances. The ultrasonographic examination claims to be a basic diagnostic method for various forms of premature puberty.

Child↗
PubMed1996

Age at onset of puberty following high-dose central nervous system radiation therapy.

OBJECTIVE: To determine if a relationship exists between age at irradiation, sex of the patient, and age at onset of puberty and pubarche in children treated with high-dose radiation to the central nervous system. DESIGN: Case series. SETTING: Tertiary care institutional practices and clinics. PATIENTS: Thirty-six children treated with high-dose irradiation (hypothalamic pituitary dose, 30-72 Gy) by conventional (n = 29) or hyperfractionated (n = 7) schedules. Girls were treated before age 8 years and boys before age 9 years. Twenty-six of the 36 children also received chemotherapy. All tumors were distant from the hypothalamic-pituitary region. MAIN OUTCOME MEASURE: Age at onset of puberty and pubarche. RESULTS: In girls, the median age at onset of puberty was 9.3 years vs 10.9 years for controls (P < .01); pubarche occurred at 9.4 years vs 11.2 years for controls (P < .01). In boys, the median age at onset of puberty--genital II--was 11.0 years vs 11.5 years for controls (P = .30); pubarche occurred at a median age of 10.5 years vs 12 years for controls (P = .25). A censored-data normal linear regression model was used to account for children (n = 6) who had not reached puberty. Age at diagnosis (P < .01) and sex (P = .01) were significant predictors of age at onset of puberty. Body mass index SD score (z score) was inversely related to age at onset of puberty (r = -0.77) and was greater at onset of puberty in girls than in boys. CONCLUSION: In children who have received high-dose cranial radiation therapy, a significant positive correlation exists between age at diagnosis and age at onset of puberty in boys and girls.

Adolescent↗
PubMed2000

Reference data of forearm bone mineral density in healthy Japanese male and female subjects in the second decade based on calendar age and puberty onset: Japanese Population Based Osteoporosis (JPOS) study.

Osteoporosis is a major public health problem in Japan. The second decade is an important period in which to attain a high peak bone mass. However, normal values of forearm bone mineral density (BMD) are not well known in children and adolescents. BMD at one-third of forearm length proximal to the ulnar end plate (BMD1/3) and the ultradistal forearm (BMDud) was measured using dual-energy X-ray absorptiometry (DXA) in 1207 (631 males, 576 females) Japanese subjects aged 9-18 years. Puberty onset was assessed by questionnaire, by obtaining the time that pubic hair appeared in males and the time that menstruation started in females. BMD1/3 and BMDud increased steadily with age in males. In relation to puberty development, these parameters also increased after puberty onset although the increase in BMD1/3 was not statistically significant after the fifth year from puberty onset and that of BMDud was not significant after the sixth year from puberty onset. BMD1/3 and BMDud increased with age and then plateaued in females. The increase in BMD1/3 was not statistically significant after 15-16 years of age and that of BMDud was not significant after 13-14 years of age. In relation to puberty development, the increase in BMD1/3 leveled out after the fourth year from puberty onset and that of BMDud also plateaued after the third year from puberty onset. We provide reference values of forearm BMD in Japanese children and adolescents by DXA according to calendar age and puberty development. Peak bone mass of the forearm may be in the late second decade in Japanese females.

Absorptiometry, Photon↗
PubMed1993

Neurobehavioral relationships and puberty: another transformation?

In a follow-up study of the Groningen Perinatal Project (GPP) on minor neurological dysfunction (MND) at 12 and 14 years the onset of puberty appeared to play a role. The children were selected on the presence (n = 185) and absence (n = 185) of MND at 9 years. Puberty was defined by the presence of three or more physical puberty signs. With the onset of puberty the incidence of MND decreased. The neurobehavioral relationships became more explicit after the onset of puberty. All types of MND were related to behavioural and cognitive problems at this developmental stage. In normal children, boys showed an increase of strength during puberty whereas the movements of girls became more fluent. The apparent changes in neurological function during puberty were interpreted as a transformation of the central nervous system. The possible causes are discussed. The conclusion is that gonadal hormones and especially oestrogens, play a role. The fact that two-thirds of the children with MND and behavioural problems outgrow the problems during puberty, can be of great help. Finally, any longitudinal study of brain function, which includes the age of puberty, should pay attention to the pubescent stage.

Adolescent↗
PubMed1998

Age at puberty and risk of testicular germ cell cancer (Ontario, Canada).

OBJECTIVES: Incidence rates of testicular cancer are increasing among postpubescent men. This suggests that putative exposures may operate early in life and have changed over time. The age at which endocrine activity accelerates (age at puberty) may be such an exposure. This study was undertaken to investigate the relationship between age at puberty and testicular cancer risk. METHODS: A population-based case-control study was conducted in the province of Ontario, Canada which included males, aged 16 to 59 years, diagnosed with testicular germ cell cancer between 1987 and 1989, and age-matched controls. Data were collected on 502 cases, 346 case mothers, 975 controls, and 522 control mothers. Surrogate measures for age at puberty included age at starting to shave, appearance of hair, growth spurt, and voice change. RESULTS: A protective effect of later puberty was evident for all four measures of puberty as reported by both subjects and mothers, and greater protection was conferred when the greatest number of later puberty events were reported. Risk associated with earlier puberty was inconclusive. CONCLUSIONS: As age at puberty is decreasing in the population, the proportion of boys experiencing the protective effect of later puberty may be diminishing. This may help explain the increasing incidence of testicular cancer.

Adolescent↗
PubMed2002

Skin-prick test findings in atopic asthmatic children: a follow-up study from childhood to puberty.

In a prospective cohort study we investigated the course of allergic sensitization from childhood to puberty in a group of children with atopic asthma. An attempt was made to correlate the findings with the persistence of asthma. A total of 150 children with atopic asthma established at 7 years of age were evaluated when 8-10 years of age. A battery of skin-prick tests (SPTs) to common environmental allergens, a detailed clinical history for asthma severity classification, and spirometric analyses, were performed. In 127 of these children a re-evaluation was performed at puberty. A variety of statistical methods were used to analyze the results regarding changes in skin test reactivity to individual aeroallergens and atopic index (degree of atopy), as well as to determine any correlation between these changes and the persistence of asthma in puberty. A wide spectrum of modification in skin reactivity to common environmental allergens was observed, including the complete loss of sensitization to some allergens or the development of a new one to others. Specifically, 34% of asthmatic children sensitive to Dermatophagoides pteronyssinus and 52.7% sensitive to cat lost their sensitivity in puberty, while only 7.5% and 11.1%, respectively, became sensitized (p = 0.03 and p = 0.001, respectively). In contrast, regarding pollen sensitivity, 30.2% and 24% of asthmatic children became sensitive in puberty to olive pollen and grasses mix, respectively, and only 11.7% and 12.5%, respectively, lost their sensitivity to these allergens (p = 0.04). No correlation was shown between the skin test reactivity changes to individual allergens and the persistence of asthma, but a significant correlation was found between atopic index to indoor allergens in childhood and the persistence of asthma at puberty (p = 0.04). Interestingly, multi-sensitivity to allergens (>/= 4 allergens) in childhood was also found to correlate with the persistence of asthma at puberty [p = 0.05, odds ratio (OR) = 2.65, 95% confidence interval (CI) 1.2-7.2]. Our findings indicate that significant modification of skin reactivity to common environmental allergens in atopic children with asthma in puberty can occur. However, no association between these changes and the persistence of asthma could be demonstrated, although children with indoor allergic sensitization and multi-reactivity were found to have a higher probability of maintaining their asthma in puberty.

Air Pollution, Indoor↗
PubMed1991

A novel testis-stimulating factor in familial male precocious puberty.

BACKGROUND: Familial male precocious puberty is a gonadotropin-independent form of precocious puberty that occurs only in males. The cause of the disorder is unknown. To examine the hypothesis that the plasma of boys with familial male precocious puberty contains a novel stimulator of testicular testosterone production, we developed a bioassay using adult male cynomolgus monkeys. METHODS: We collected plasma from 12 boys with familial male precocious puberty, 7 normal prepubertal boys of similar ages and with similar plasma gonadotropin levels, and 1 boy with hypogonadotropic hypogonadism and infused it into the testicular artery of adult male cynomolgus monkeys that had been pretreated with gonadotropin-releasing-hormone antagonist to inhibit the endogenous secretion of gonadotropins. Testicular venous effluent was collected at 15-minute intervals for 3 or 5 hours for the measurement of testosterone. RESULTS: The mean (+/- SE) peak testosterone response, as compared with base line, was significantly greater in the monkeys infused with plasma from the 12 boys with familial male precocious puberty than in the monkeys infused with plasma from the 7 normal prepubertal boys and the boy with hypogonadotropic hypogonadism (385 +/- 51 vs. 184 +/- 25 percent, P less than 0.005) in the three-hour studies. Plasma from 92 percent of the boys with familial male precocious puberty and 12.5 percent of the normal prepubertal boys stimulated a response greater than 195 percent of base-line values. In the animals studied for five hours after receiving a second dose of antagonist, the mean peak testosterone response, as compared with base line, was significantly greater in the monkeys infused with plasma from three boys with familial male precocious puberty than in the monkeys infused with plasma from three normal prepubertal boys (363 +/- 81 vs. 115 +/- 6 percent, P less than 0.01). The mean area under the testosterone-response curve was significantly larger in the monkeys infused with plasma from the boys with familial male precocious puberty in the five-hour studies (154 +/- 34 vs. -58 +/- 10 percent, P less than 0.005), but not in the three-hour studies. CONCLUSIONS: These findings support the presence of a circulating testis-stimulating factor in the plasma of boys with familial male precocious puberty. The production of such a factor would explain the biologic nature of the disorder.

Animals↗
PubMed1992

Osteopenia in men with a history of delayed puberty.

BACKGROUND AND METHODS: The effect of delayed puberty on peak bone mineral density in men is unknown. To determine whether such a delay reduces normal peak bone density and leads to osteopenia during adulthood, we measured radial bone mineral density by single-photon absorptiometry and spinal bone mineral density by dual-energy x-ray absorptiometry in 23 men who had a history of constitutionally delayed puberty and 21 men who underwent normal puberty. Their mean ages were 26 and 24 years, respectively. The groups were matched for other factors known to affect bone mass. RESULTS: The mean (+/- SD) radial bone mineral density was significantly lower in the men with a history of delayed puberty than in the normal men (0.73 +/- 0.07 vs. 0.80 +/- 0.05 g per square centimeter; P less than 0.0002). Spinal bone mineral density was also significantly lower in the men with delayed puberty than in the normal men (1.03 +/- 0.10 vs. 1.13 +/- 0.11 g per square centimeter; P less than 0.003). Radial bone density was at least 1 SD below the mean value for the normal men in 15 of the 23 men with a history of delayed puberty, and spinal bone density was similarly decreased in 10 of the 23. CONCLUSIONS: Adult men with a history of constitutionally delayed puberty have decreased radial and spinal bone mineral density. These findings suggest that the timing of puberty is an important determinant of peak bone density in men. Because the peak bone mineral density achieved during young adulthood is a major determinant of bone density in later life, men in whom puberty was delayed may be at increased risk for osteoporotic fractures when they are older.

Absorptiometry, Photon↗
PubMed2006

Age at puberty and adult blood pressure and body size in a British birth cohort study.

OBJECTIVE: To investigate the association between age at puberty and blood pressure at age 53 years. DESIGN: A prospective birth cohort study with regular contacts through childhood and adulthood until the age of 53 years. PARTICIPANTS: A total of 1193 men and 1204 women, from a sample of 5362 born in Britain in March 1946. MAIN OUTCOME MEASURE: Blood pressure at age 53 years. RESULTS: Regression models indicated that men who had reached puberty latest had a lower mean systolic blood pressure (SBP; P = 0.03) and diastolic blood pressure (DBP; P = 0.01) at 53 years than others. The mean SBP (95% confidence interval) was 6.4 mmHg (1.8, 10.9) greater in the earliest puberty group compared with the latest; for DBP the difference was 4.6 mmHg (1.9, 7.4). The associations were not accounted for by current body size, even though later puberty was associated with a decreasing body mass index (BMI) at 53 years. Neither were they accounted for by prepubertal body size, birth weight, or childhood and adult social class. Although women who reached puberty early had a higher BMI and shorter stature at 53 years compared with other women, they did not have higher blood pressure. CONCLUSIONS: Better health behaviours in men reaching puberty late may explain the association between age at puberty and blood pressure. Alternatively, age at puberty may be a marker of the whole growth trajectory, distinguishing characteristics important in the later development of high blood pressure. The association of early puberty with high adult BMI in both sexes highlights the importance of controlling obesity in those who mature early.

Aging↗
PubMed1995

Investigation of delayed puberty.

Delayed puberty is defined arbitrarily on the basis of statistical consideration, when no signs of puberty have occurred at 2.0 SD (13.4 years in girls and 13.8 in boys) above the mean chronological age for the onset of puberty. The vast majority of these patients have no endocrine abnormality and their pubertal development and growth spurt are simply consequences of primary delay (constitutional delay of growth and puberty (CDGP)) or secondary delay due to a chronic disease of childhood, such as asthma. However, a small proportion may have pathological causes of delayed puberty which must be careful identified as specific management may be required. Associated with delayed puberty, the growth spurt is always delayed which is why the condition is described as delayed growth and puberty. Short stature and lack of sexual development may lead to emotional and social difficulties and in some patients their consequences can persist when 'normal' height and full sexual maturation are attained. Recent data also suggest that a delay in the 'tempo' of pubertal maturation may interfere with the normal bone accretion occurring during puberty, later causing osteoporosis. Such findings suggest that a new approach in delayed puberty may be necessary not only for psychological reasons but also for optimizing bone mass accretion.

Adolescent↗
PubMed1994

Cranial irradiation and early puberty.

Low doses of cranial irradiation (18-24 gray) employed in the management of acute lymphoblastic leukemia may cause early or precocious puberty, predominantly in girls. To determine whether this sexual dichotomy exists at higher irradiation doses (25-47 gray), the onset of puberty was identified in 46 GH-deficient children (30 males) previously irradiated for a brain tumor not involving the hypothalamic-pituitary axis and compared with the normal pubertal standards of Marshall and Tanner. Age at irradiation was at least 2 SD below the mean age of pubertal onset in normal children. There was a significant linear association between age at irradiation and age at onset of puberty. The onset of puberty occurred at an early age in both sexes (mean, 8.51 yr in girls and 9.21 yr in boys plus 0.29 yr for every year of age at irradiation). For example, the estimated age at onset of puberty in a boy irradiated at 2 yr of age would be 9.79 yr, and that for a boy irradiated at 9 yr of age would be 11.82 yr. In the context of GH deficiency, which is usually associated with a delay in the onset of puberty, this is abnormal. At each age of irradiation, the estimated age at the onset of puberty was approximately 0.7 yr earlier in girls than boys. A similar trend was seen for bone age, which was abnormally early at the time of pubertal onset (mean, 7.39 yr in girls and 8.66 yr in boys plus 0.25 yr for every year of age at the time of irradiation). At the doses of irradiation employed in the treatment of brain tumors, radiation-induced early puberty is not restricted to girls. The clinical consequence of early puberty in the management of poor growth associated with radiation-induced GH deficiency is to foreshorten the time available for treatment with GH.

Age Factors↗
PubMed1999

Diurnal rhythms of luteinizing hormone, follicle-stimulating hormone, and testosterone secretion before the onset of male puberty.

To investigate hormonal change before the onset of male puberty, we measured LH and FSH in serum samples drawn every 20 min for 24 h and measured testosterone hourly for 24 h. Forty-six boys (32 prepubertal and 14 pubertal) of short stature, between 4.4-19.3 yr of age, participated in this study. LH and FSH were measured using a time-resolved immunofluorometric assay, and testosterone was measured using high sensitivity RIA capable of detecting a testosterone concentration of 0.01 ng/mL. Diurnal rhythms of LH, FSH, and testosterone were apparent in all subjects, including those aged 4-5 yr. Serum LH and FSH concentrations showed night-day variation in a pulsatile fashion. The serum testosterone concentration was elevated at early morning in all subjects. Mean 24-h LH, FSH, and testosterone concentrations of prepubertal subjects who did not attain puberty for at least 3 yr were 0.10 U/L, 0.63 U/L, and 0.06 ng/mL, respectively, whereas those of prepubertal subjects who attained puberty within 1 yr (0.54 U/L, 1.68 U/L, and 0.10 ng/mL, respectively) were significantly higher. Furthermore, mean 24-h LH, FSH, and testosterone concentrations increased with developing puberty. All of the 46 subjects showed positive cross-correlation between the LH and testosterone time series. The mean lag time from the LH to the testosterone time series in the prepubertal subjects who attained puberty within 1 yr (4.7 +/- 2.4 h, mean +/- SD) was shorter than that in the prepubertal subjects who attained puberty after at least 3 yr (7.3 +/- 2.2 h). This lag time decreased with developing puberty, plateauing at 1.4 +/- 0.9 h at midpuberty. Thus, the diurnal rhythms of LH, FSH, and testosterone already exist at 4-5 yr of age; serum LH, FSH, and testosterone levels increase before the onset of puberty; and a time delay is observed between the LH and testosterone time series that decreases before the onset of puberty.

Adolescent↗
PubMed2000

Serum inhibin A and inhibin B in healthy prepubertal, pubertal, and adolescent girls and adult women: relation to age, stage of puberty, menstrual cycle, follicle-stimulating hormone, luteinizing hormone, and estradiol levels.

Biochemical assessment of gonadal function during maturation in girls and in adult women can be troublesome. With the recent advent of specific assays for the gonadal peptides inhibin A and inhibin B, it might be possible to achieve a clearer picture of events. We therefore determined serum levels of inhibin A, inhibin B, FSH, LH and estradiol in a cross-sectional study of 403 healthy schoolgirls (aged 6 -20 yr) in relation to age and stage of puberty and in 181 healthy nonpregnant women (aged 20-32 yr) in relation to stage of the menstrual cycle. In addition, inhibin A and inhibin B were measured daily throughout the menstrual cycle in 10 healthy adult women. Levels of inhibin B are low or undetectable in prepubertal girls (median, 26.5 pg/mL; 95% prediction interval, <20-100 pg/mL), increase sharply through pubertal stage II to peak in stage III (median, 84 pg/mL; 95% prediction interval, 28-227 pg/mL) and thereafter decline through pubertal stages IV and V. These changes presumably reflect increasing ovarian stimulation through early puberty, resulting in an increased number of developing follicles, follicles reaching a later stage of development before undergoing atresia, or both. Declining levels in late puberty and adulthood probably reflect the onset of the menstrual cycle and the subsequent appearance of the luteal phase, where inhibin B levels are low. Inhibin A levels are undetectable or very low in early puberty (median, <7 pg/mL; 95% prediction interval, <7-14) pg/mL), increasing gradually through pubertal stages to reach their highest values in adult women (median, 21.5 pg/mL; 95% prediction interval, <7-129 pg/mL). Levels of inhibin A greater than 19 pg/mL are only seen in postmenarcheal girls in puberty and in adult women, again consistent with inhibin A being primarily produced by the corpus luteum. Determining cut-off levels of serum inhibin B regarding whether a girl had entered puberty resulted in similar (low) sensitivities and specificities as those found for cut-off levels of LH or estradiol due to the large overlap between serum values in Tanner stages I and II. Correlations between inhibin A and inhibin B and FSH, LH, and estradiol within pubertal stages are presented. In early puberty both inhibin A and inhibin B correlated positively with LH and FSH. In late puberty inhibin A correlated negatively with FSH and did not correlate with LH; inhibin B still correlated positively with both FSH and LH, now most strongly with FSH. In adult women during the menstrual cycle, serum inhibin B levels increased during the follicular phase, indicating the greatest production by follicles in early stages of development. In contrast, serum inhibin A levels peaked during the luteal phase, indicating the greatest production by the corpus luteum. In conclusion, serum inhibin A and inhibin B levels in normal puberty in girls show consistency with our knowledge of the manner in which these hormones are secreted within the menstrual cycle in adult women. The presented reference values may be of use in the clinical evaluation of pubertal development in girls.

Adolescent↗
PubMed2000

Delayed growth and puberty in patients with Gaucher disease type 1: natural history and effect of splenectomy and/or enzyme replacement therapy.

BACKGROUND: Growth retardation in childhood was only recently recognized as a prominent feature of Gaucher disease type 1, but there are few data on both the pubertal development and the final outcome of growth and sexual maturation. OBJECTIVE: To investigate the natural pattern of growth and puberty in patients with Gaucher disease type 1 and the effect of splenectomy and enzyme replacement therapy. METHODS: We retrospectively analyzed growth and puberty in 57 patients with Gaucher disease type 1; 52 were followed since childhood and/or prepuberty and 42 have reached sexual maturity and final height. In the analysis we considered severity of disease, time of splenectomy, and start of enzyme replacement therapy. RESULTS: Deceleration of growth at age 3-5 years was observed in 30 of 57 patients followed since early childhood while untreated: height-SDS decreased from -0.34 +/- 0.42 at age 0-3 years to -1.93 +/- 0.95 (P < 0.01) at age 7-10 years and was more pronounced with severe disease. A high prevalence (59.6%) of delayed puberty, which was more frequent with severe disease, was observed in 47 patients followed before and throughout puberty. No primary endocrine pathology was found. All patients, untreated as well as treated, with growth and pubertal delay had a spontaneous catch-up, achieved full sexual maturation, and most (83.3%) reached a final height within the range of parental height-standard deviation score. Splenectomy (partial and/or total) performed in 20 patients while still growing had a beneficial effect on growth, which was temporary in some and did not affect puberty. ERT improved growth in 11 patients who started therapy before puberty, as evidenced by a progressive increase in the height-SDS, and seemed to normalize the onset of puberty. CONCLUSIONS: Growth retardation in childhood and delay of puberty are characteristic of Gaucher disease type 1 and are more frequent with severe disease. There is a spontaneous catch-up later in life and most patients reach a final height within their genetic growth potential. Enzyme replacement therapy apparently normalizes growth and possibly also the onset of puberty.

Adolescent↗
PubMed1988

Management of idiopathic growth hormone deficient patients during puberty.

Boys with idiopathic GH deficiency, treated with hGH and entering spontaneous puberty, have an onset of puberty and peak height velocity (PHV) at a late chronological age but normal bone age. PHV occurs at G3 with testicular volumes of 6-12 ml. The size of PHV and the height gain after G2 are similar to those of a normal delayed adolescent. In contrast, idiopathic GH deficient girls have an onset of puberty and PHV nearer to a normal chronological age and at an early bone age. PHV occurs at B2 and its size and the height gain after B2 are similar to those of normal girls. The length of time of pubertal growth is shorter in both GH deficient boys and girls. Very late induction of puberty in idiopathic GH deficient boys results in psychosocial damage and in bodily disproportion. It is suggested that induction of puberty be considered no later than 14.5 years in boys and 13.5 years in girls with the use of low-dose sex steroids. The decision to induce puberty should be taken to avoid psychosocial problems and be independent of proof of associated gonadotrophin deficiency. In GH deficient girls with early puberty, therapies to delay puberty may be considered. There are theoretical grounds for increasing the GH dose given during puberty, but present dose-response studies fail to include controls for important biological variables and are so far inconclusive. Cost-effectiveness is an important consideration. Increasing the frequency of injections probably improves the growth effect for a given dose of GH.

Adolescent↗