[Study of sexual maturation in Langdon-Down disease. Puberty and precocious puberty in mongoloid feeble-mindedness].
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Adolescent↗
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[Experiments in biological engineering to induce puberty in young female swine. 4: Ovulation period after puberty in animals aged about 200 days, using different combinations of gonadotropic hormones].
44 prepuberal gilts were treated with gonadotropic combinations and investigated for ovarian dynamics. 400 PMS + 200 HCG (Suigonan-Vemie) induced ovulations at the 4th day p.i., 100 FSH + 100 HCG resp. 200 FSH + 200 HCG at the 6th day p.i. At the 8,-11th day p.i. the PMS/HCG-treated animals showed corp. lut, in 100, the FSH/HCG-treated in 50 resp. 87% of the cases. A second injection of 250 HCG 3 days after 200 FSH + 200 HCG increased the number of animals which had ovulated. Zystic ovaries (larger than or equal to 11 mm) developed in all groups. Declaration of gonadotropins in "international units".
Age Factors↗
Sexual precocity in boys: accelerated versus slowly progressive puberty gonadotropin-suppressive therapy and final height.
The indication for GnRH analog treatment in boys with central sexual precocity is based mainly on the age of onset of puberty. Our aim was to determine whether the rate of pubertal progression should also be taken into consideration. Included in the study were 81 boys with central sexual precocity: 27 with true precocious puberty (onset at <9 yr) and 54 with early puberty (onset at 9-10.5 yr). At the time of analysis, all had completed puberty, and 66 (22 central precocious puberty, 44 early puberty) had achieved final height. Progression of puberty (Tanner stage 2 to 3) was accelerated (0.5-1.32 yr) in 42 boys (16 central precocious puberty, 26 early puberty) and slow (1.7-2.9 yr) in 39 (11 central precocious puberty, 28 early puberty). The boys with accelerated puberty had significantly elevated T levels (central precocious puberty and early puberty, P < 0.001), faster growth rate (change in height SD score/duration: central precocious puberty, P < 0.05; early puberty, P < 0.01), and faster bone maturation rate (change in bone age/duration: central precocious puberty, P < 0.05; early puberty, P < 0.001). All 42 boys with accelerated puberty were treated with GnRH analog for 2.3-4.2 yr; the duration to completion of puberty and the height gain after therapy was discontinued were similar for the boys with central precocious puberty and early puberty. The 39 boys with slow puberty received no treatment and had a prolonged course of puberty (central precocious puberty, 5.05 +/- 0.3 yr; early puberty, 4.72 +/- 0.77 yr; average normal, 3.5 yr). The final height achieved in the 35 (11 central precocious puberty, 24 early puberty) untreated boys was within the range of their respective target height. The 31 (11 central precocious puberty, 20 early puberty) treated boys also achieved their genetic target height. Predictions based on the Bayley-Pinneau method at Tanner stage 3 for all boys and at discontinuation of therapy for treated boys overestimated the achieved final height (P < 0.001). In conclusion, boys with sexual precocity, whether central precocious puberty or early puberty, may have either accelerated or slow pubertal development. The decision to institute suppressive therapy should be based also on the rate of pubertal progression. Treatment should be offered only to those (either central precocious puberty or early puberty) with accelerated growth and bone maturation rates and rapid increase in T levels. Suppression therapy apparently converts accelerated puberty into nonsustained slow puberty and probably prevents compromised final height.
Body Height↗
Increased risk of precocious puberty in internationally adopted children in Denmark.
BACKGROUND: Studies have indicated that internationally adopted children have an increased risk of developing precocious puberty, but no epidemiologic risk estimates have previously been calculated. We aimed to assess the risk of developing precocious puberty in intercountry adoptees, children immigrating with their family, and descendants of immigrants living in Denmark. METHODS: Patients who were registered with the diagnosis of precocious puberty during the period 1993-2001 were identified through the national patient registry. The background population of children born from 1983 to 2001 were identified through the unique Danish Civil Registration System and subsequently categorized as being Danish (N = 1,062,333), adopted (N = 10,997), immigrating with their family (N = 72,181), or being descendants of immigrants (N = 128,152). The incidence rate ratio of precocious puberty was estimated by log-linear Poisson regression. All rate ratios were adjusted for age and its interaction with gender and calendar year. P values were based on likelihood ratio tests, and 95% confidence intervals were calculated by Wald's test. RESULTS: In the study period, 655 children developed precocious puberty during 5,627,763 person-years at risk. Adopted children were followed during 39,978 person-years at risk, during which 45 girls and 6 boys developed precocious puberty. The risk of developing precocious puberty was significantly increased 10 to 20 times in adopted girls compared with girls with Danish background. The risk of developing precocious puberty depended on the country of origin. In children immigrating with their family, the risk of developing precocious puberty was only marginally increased. Older age at adoption significantly increased the risk of precocious puberty in adoptees independent of region of origin. The incidence rate ratio was significantly higher in children adopted after the age of 2. In children immigrating with their family, we found no effect of age at migration. DISCUSSION: In this large, nationwide, register-based study including 655 cases of precocious puberty, we found that intercountry boys and girls were 10 to 20 times more likely to develop precocious puberty compared with the Danish reference group. Older age at adoption significantly increased the risk of precocious puberty. Uncertainty of the exact age is a well-known problem in adopted children, and systematic underestimation of age might bias the result. However, using the worst-case scenario that all children who according to the Danish Civil Registration System were adopted after 2 years of age were in fact 1 year older, we still observed a highly increased risk of precocious puberty associated with adoption and especially with adoption after 2 years of age. Surprisingly, the risk of precocious puberty was not increased in the large group of children adopted from Korea. One case of precocious puberty was identified among Korean children, whereas > 20 cases of precocious puberty would have been expected if the risk for a Korean child was at the same level as observed among adopted children from India and South America. In the study population, 99% of Korean children were adopted before 2 years of age, which may contribute to explaining our finding. In Korea, children appointed for adoption are often living in foster care settings from birth to adoption, whereas most other countries are reported to take care of the children in orphanages before adoption. It can only be speculated whether a relation between preadoption living conditions and later risk of precocious puberty exists. Genetic factors play a key role in the timing of puberty, and large variations in age at menarche are observed worldwide. Age at menarche is reported to be in the same age range in South Korea as in well-off populations in other parts of the world, indicating that the different risk of precocious puberty observed between Korean and other adoptees probably cannot be explained by genetic factors alone. The finding that the risk of precocious puberty was significantly increased among adoptees in contrast to what was seen in children immigrating with their families contradicts a direct effect of migration. An increasing number of studies have shown long-term effects of certain prenatal and postnatal growth patterns, including advancement in pubertal maturation after poor intrauterine growth and catch-up growth during childhood. Different growth patterns and dietary habits between adoptees and children immigrating with their families might contribute to explain our findings. It has been hypothesized that stressful psychosocial factors in infancy and childhood may lead to earlier pubertal maturation. In general, adoptees have experienced several traumatic life events, and it may be speculated that these events alter the susceptibility for developing precocious puberty. CONCLUSIONS: Foreign-adopted children originating from regions other than Korea had a 15- to 20-fold increased risk of precocious puberty compared with Danish-born children, whereas adoptees originating from Korea had no increased risk of precocious puberty. In addition, children immigrating with their families had no increased risk of precocious puberty. The effect of country of origin might be explained by genetic factors or by different environmental exposures and living conditions in the different countries. Older age at adoption increased the risk for premature onset of puberty, which may suggest that environmental factors influence the risk of precocious pubertal development in adopted children.
Adoption↗
Serum leptin levels in males with delayed puberty during short-term pulsatile GnRH administration.
Leptin may be a possible trigger for puberty. In normal males, it has been shown that leptin increases from the pre-pubertal to the early pubertal stage, and then declines in the late pubertal stage. We examined leptin levels in six male adolescents (mean age 16.3+/-0.6 yr; range 14.2-17.6 yr) with delayed puberty (constitutional delay of puberty no.=2; idiopathic hypogonadotropic hypogonadism no.=4) during 120 days of subcutaneous pulsatile GnRH administration. A group of subjects in pre-puberty (no.=11), early-puberty (n=10) and mid-puberty (no.=7) were evaluated as controls. Morning blood samples were taken for determination of leptin, testosterone, LH and FSH levels. In delayed puberty subjects blood samples were taken every 30 days after the start of GnRH administration. At each examination BMI and testicular volume were evaluated. A follow-up examination was performed in the 6 patients 1.3-7.5 yr after the end of the 120 days of GnRH therapy. At baseline evaluation in delayed puberty mean leptin levels were 11.3+/-2.0 microg/l (median 11.3 microg/l; range 4.7-17.3 microg/l) and were higher than those found in pre-puberty (p=0.04) and mid-puberty (p=0.001). During GnRH administration there was no change in BMI and leptin levels but there was an increase in gonadotrophin levels, testosterone and testicular volume. One hundred and twenty days after, mean serum leptin were 10.1+/-2.1 microg/l (median 9.1 microg/l; range 3.4-16.8 microg/l). At the end of the study, leptin levels were higher in delayed puberty than in mid-puberty (p=0.002). At the follow-up examination leptin levels were 4.3+/-1.3 microg/l (median 3.4 microg/l; range 1.4-9.1 microg/l) (p=0.03 vs end of 120 days GnRH therapy) while testosterone and BMI were not changed. In conclusion 120-day pulsatile GnRH administration induced in males with delayed puberty physiological-like pubertal changes but not the decline in leptin levels reported during the progression of puberty. Therefore, in males with delayed puberty an impairment in the phenomenon of leptin decline associated with progression of puberty could be suggested. However after retrospective diagnosis of pubertal delay and long-term therapy in subjects with idiopathic hypogonadotropic hypogonadism leptin levels declined. These data seem to indicate that time more than increase in testosterone levels and testicular volume is the determinant of leptin decline at puberty.
Adolescent↗
Puberty in children with idiopathic growth hormone deficiency on growth hormone treatment: preliminary analysis of the data from the Kabi Pharmacia International Growth Study.
In total, 524 children (335 boys, 189 girls) with idiopathic growth hormone deficiency (GHD) who had entered puberty after at least 1 year of growth hormone (GH) treatment were studied. Spontaneous onset of puberty occurred in 319 boys and 174 girls, and puberty was induced in 16 boys and 15 girls. Median chronological and bone ages at onset of spontaneous puberty were 14.8 and 13.4 years in boys, and 13.3 and 11.8 years in girls, respectively. Age at onset of spontaneous puberty was correlated to age at start of GH treatment. Puberty was induced at a median chronological age of 16.0 years in boys and 14.4 years in girls. Height velocity increased in the year before spontaneous puberty in boys and girls, and rose further to a maximum (median, 8.3 cm/year) in the first year of puberty in boys. In girls, the maximum height velocity occurred in the year before puberty (median, 6.5 cm/year). Height velocity increased in the year before spontaneous puberty in boys and girls, and rose further to a maximum (median, 8.3 cm/year) in the first year of puberty in boys. In girls, the maximum height velocity occurred in the year before puberty (median, 6.5 cm/year). Height velocity during the first year of puberty was inversely correlated to age at puberty onset (r = -0.56, p = 0.0001). After medical induction of puberty, height velocities in the first year of puberty were 5.4 and 3.4 cm/year for boys and girls, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
[Ovarian cysts and tumors as the cause of isosexual pseudoprecocious puberty].
INTRODUCTION: Precocious puberty in girls is generally defined as appearance of secondary sexual characteristics before eight years of age. Menarche before the ninth birthday may serve as an additional criterion. Precocious puberty is divided in central precocious puberty and pseudoprecocious puberty. Central precocious puberty (GnRH dependent) occurs because of premature activation of hypothalamic-pituitary-gonadal axis and activity of gonadotrophins. Pseudoprecocious puberty (GnRH independent) is caused by activity of sexual steroids that are not the result of gonadotrophin activity. OBJECTIVE: Objective of our study was to examine the etiology, clinical and laboratory manifestations of isosexual pseudoprecocious puberty in girls. METHOD: In the period between 1995 and 2004, clinical and laboratory sings of 34 girls with precocious puberty were studied at the Endocrine Department of the Institute of Mother and Child Health Care of Serbia. Initial evaluations included height measurement, staging of puberty, bone age assessment and pelvic ultrasound. Important diagnostic sonographic parameters of precocious puberty were the volumes of ovaries and uterus as well as ovarian structure. The initial hormonal evaluation included measuring of plasma oestradiol, luteinizing hormone (LH) and follicle stimulating hormone (FSH). The luteinizing hormone releasing hormone (LHRH) stimulation test was used to evaluate LH and FSH responsiveness (60 microg/m2 LHRH-Relefact LHRH, Ferring). Blood samples were collected at 0, 20 and 60 minutes. Basal and GnRH stimulated LH and FSH were determined by immunoradiometric assay. Estradiol concentration was measured using the fluoroimmunometric assay. RESULTS: Thirty-four girls aged 6 months to 9 years (mean age 4.5 years) with precocious puberty were studied during the period of 9 years. Eleven girls presented with breast development, six with vaginal bleeding and seventeen with signs of puberty. On the basis of clinical signs, bone age, estradiol levels and LHRH test, premature thelarche was diagnosed in eleven patients (32.4%), premature menarche in six (17.6%) and central precocious puberty in ten girls (29.4%). Seven girls (20.6%) presented with pseudoprecocious puberty. Pelvic ultrasound examination revealed unilateral ovarian cysts in six patients and granulosa cell tumor in one. Elevated estrogen serum levels and failure of gonadotropin responses after gonadotropin releasing hormone were the classical findings in patients with isosexual pseudoprecocious puberty during the acute period of disease. In four patients, the cyst decreased spontaneously after several months, while in two patients, the cyst was removed by laparotomy. Surgical treatment was performed in a patient with granulosa cell tumor. CONCLUSION: Our work demonstrates that autonomous functional ovarian follicle cyst is the most often cause of isosexual pseudoprecocious puberty. Short period of observation is suggested because the cyst can resolve spontaneously. On the other hand, juvenile granulosa cell tumor, as highly malignant tumor, should be removed as soon as diagnosis is established.
Child↗
The NIH experience with precocious puberty: diagnostic subgroups and response to short-term luteinizing hormone releasing hormone analogue therapy.
Between 1979 and 1983, 129 children (95 girls) with precocious puberty were referred to the National Institutes of Health and received treatment for at least 6 months with the long-acting LHRH analogue D-Trp6-Pro9-NEt-LHRH. The majority (107 of 129) of the children had central precocious puberty mediated by activation of the hypothalamic-pituitary-gonadal axis in association with hypothalamic hamartomas (24 of 107) or other central nervous system lesions (21 of 107), or idiopathic precocious puberty (62 of 107). Hypothalamic hamartomas or other central nervous system lesions were a frequent cause of central precocious puberty in girls (27 of 87), but idiopathic precocious puberty was still the most frequent diagnosis (63%). Idiopathic precocious puberty was uncommon in boys (6%). The patients with peripheral precocious puberty included six girls with McCune-Albright syndrome and six boys with familial male precocious puberty. These children had peripheral sex steroid secretion in the absence of hypothalamic-pituitary-gonadal axis maturation. The children with combined peripheral and central precocious puberty included nine children with congenital adrenal hyperplasia and one girl with a virilizing adrenal tumor. In the patients with central precocious puberty or combined peripheral and central precocious puberty, LHRHa therapy caused suppression of gonadotropin and sex steroid levels (P less than 0.001), stabilization or regression of secondary sexual characteristics, and decreases in growth rate and in the rate of bone age maturation (P less than 0.005). Patients with peripheral precocious puberty, however, had no significant change in gonadotropin or sex steroid levels, growth rate, or the rate of bone age maturation, and no improvement in secondary sexual characteristics. Thus, LHRHa is an effective treatment of central precocious puberty and combined peripheral and central precocious puberty, but is ineffective in the therapy of peripheral precocious puberty.
Adrenal Hyperplasia, Congenital↗
Puberty stage and spontaneous descent of acquired undescended testis: implications for therapy?
We assessed spontaneous descent of acquired undescended testis (UDT) at puberty. 299 Boys (aged 1.2-16.5 years, mean 9.4) with 350 acquired-UDT were examined annually during a 12.6-year period (mean 3.1). An acquired-UDT was defined as a previously intrascrotal testis which can no longer be manipulated into a stable scrotal position. Each year, position of the testis and pubertal development according to Tanner's stages were assessed. Early puberty was defined as puberty stage G2 (testicular volume 4-9 mL), mid-puberty as puberty stages G3 (testicular volume 10 mL) and G4 (testicular volume 11-15 mL), and late puberty as puberty stage G5 (testicular volume >15 mL). Follow-up was completed if spontaneous descent had occurred, if mid-pubertal orchidopexy (ORP) had to be performed, if the boy was lost for follow-up, or if pre-pubertal ORP was performed in another hospital. In 139 boys with 164 acquired-UDT follow-up was meanwhile completed. Twelve boys with 14 UDT were lost for follow-up. In an additional 16 boys with 21 UDT, ORP was performed in another hospital. In 98 of the remaining 129 (76.0%) acquired-UDT spontaneous descent at puberty occurred. Mean follow-up was 2.5 years (range 0.2-8.5). In 70 of 98 testes (71.4%) descent occurred in early puberty, in 26 of 98 testes (26.5%) in mid-puberty, and in two testes in late puberty. In 31 of 129 testes (24.0%) ORP had to be performed at mid (30 cases) or late (one case) puberty. In this series, 98 of 129 acquired-UDT (76.0%) descended spontaneously at puberty, whereas in 31 of 129 (24.0%) pubertal ORP was performed. If ORP is postponed until puberty stage G3 (testicular volume of 10 mL) three of four acquired-UDT will descend spontaneously.
Adolescent↗
Contact with oestrous female pigs stimulates and synchronises puberty in gilts.
Three experiments, using a total of 132 pre-pubertal gilts, were carried out to investigate the influence of contact with oestrous female pigs on the attainment of puberty by gilts. Experiment 1 compared the effect of removing the gilts from their groups as they reached puberty in response to exposure to a boar, with leaving the gilts in their groups for five to 15 days after puberty or five to 15 days after second oestrus. All the groups exposed to boars reached puberty significantly earlier than controls (P less than 0.05) but there was no difference between these groups in their mean age at puberty. However, the synchrony of puberty was significantly greater among the gilts which remained in their groups after puberty (P less than 0.01) or second oestrus (P less than 0.001) than among the gilts which were removed at puberty. Experiment 2 investigated the influence of housing pre-pubertal gilts with penmates induced into puberty with injections of oestradiol benzoate. Puberty was significantly advanced by the presence of penmates regularly exhibiting oestrous periods. Experiment 3 compared the effect of daily exposure to an anoestrous ovariectomised sow, an oestrous ovariectomised sow or a boar, on the attainment of puberty by gilts. Gilts exposed to either an oestrous sow or a boar were significantly younger at puberty than isolated control animals (P less than 0.05) whereas the mean age at puberty of gilts exposed to an anoestrous sow was not significantly different from that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects on C3H mouse mammary cancer of changing from a high fat to a low fat diet before, at, or after puberty.
A low fat/low calorie (LF/LC) diet is a relative inhibitor of murine mammary cancer. Because the mammary gland may be most sensitive to the action of a carcinogen at or near the age of puberty, we studied whether beginning a LF/LC diet before puberty would decrease C3H/OuJ mouse mammary cancer incidence more than if such a diet was begun at or after puberty. We also studied whether the advancement of the age of puberty by a high fat/high calorie (HF/HC) diet would in itself be a mammary cancer risk factor and whether dietary fat levels would affect mammary cancer metastases. In the first study, mice were changed from a HF/HC diet to a LF/LC diet at 12 days of age, puberty, or 60 days of age. Other groups were always HF/HC or always LF/LC. In a second experiment, mice were fed a high fat diet for the same length of time, i.e., from 21 to 75 days of age (before and through puberty) or 75 to 129 days of age (well after puberty). In one aspect of the first study, puberty was advanced by feeding a HF/HC diet until the first day of puberty. However, tumor latency, incidence, and multiplicity were not statistically different from those of the LF/LC control. Other results of the first study indicated, in general, that mice consuming a LF/LC diet beginning at or before puberty had a longer tumor latency and a lower tumor incidence and multiplicity than mice either beginning a LF/LC diet at 60 days of age or continuously fed a HF/HC diet. Lung metatases were greater in mice fed a HF/HC diet continuously compared to LF/LC continuously. In the second study, beginning the high fat diet before or after puberty did not result in statistically significant differences in tumor latency, incidence, or multiplicity. It was concluded that the longer a LF/LC diet was fed, the lower was the mammary cancer risk. An early puberty in itself was not a mammary cancer risk factor and mouse puberty had no particular significance as an age before which a LF/LC diet should begin.
Animals↗
Late or delayed induced or spontaneous puberty in girls with Turner syndrome treated with growth hormone does not affect final height.
Although it has been well established that GH treatment increases final height (FH) in girls with Turner syndrome (TS), the optimal ages to start GH therapy and introduce estrogens for pubertal induction have not been defined. We evaluated retrospectively the influence of the age at onset of GH treatment and age at onset of puberty on FH of 186 adult TS women treated during childhood with GH. Puberty started spontaneously in 38 patients, and it was induced in 148 girls with ethinyl estradiol (mean +/- SD starting dose, 66 +/- 32 ng/kg.d). Patients with spontaneous or induced puberty were divided into quartiles on the basis of age at initiation of GH treatment (3-10, 10-12, 12-14, and 14-19 yr). FH was 151.7 +/- 6.0 cm; there were no FH differences between patients with induced or spontaneous puberty, nor were there differences between the age quartiles. Puberty started earlier in the girls with spontaneous puberty than in those with induced puberty (12.4 +/- 1.3 yr vs. 14.5 +/- 1.9 yr; P < 0.0001). The age at onset of puberty was not related to FH. Pubertal growth was 15.4 +/- 4.6 cm in the girls with spontaneous puberty and 8.6 +/- 4.3 cm in the girls with induced puberty (P < 0.0001). We conclude that GH treatment results in a significant increase in FH in most TS girls. Under the conditions of GH treatment and induction of puberty that we have used, the age at start of GH treatment was not related to FH; in addition, late or delayed induced or spontaneous puberty did not affect FH.
Adolescent↗
Control of puberty by excitatory amino acid neurotransmitters and its clinical implications.
Excitatory amino acids, glutamate in particular, have a marked stimulatory effect on the reproductive axis, particularly at puberty. Glutamate, N-methyl-D-aspartate (NMDA), and kainate stimulate gonadotropin-releasing hormone (GnRH) secretion in immature mammals and NMDA receptor stimulation results in precocious puberty in rats and monkeys. Puberty is characterized by an increased sensitivity of GnRH to glutamate as well as an increase in glutaminase activity in the hypothalamus. Glutamatergic and GABAergic regulation of GnRH secretion seem strongly interdependent around puberty. In addition to the transsynaptic glutamatergic regulation of GnRH secretion, a coordinated activity of glutamatergic neurons and astroglial cells has been shown to play an active role in puberty. The participation of kainate receptors in the estradiol-induced advancement of puberty suggest that these receptors may be involved in the estradiol-mediated activation of GnRH secretion at puberty. A case of precocious puberty associated with hyperglycinemia illustrates the NMDA involvement in puberty in humans. In this patient, the occurrence of precocious puberty was thought to result from excessive stimulation by glycine of the NMDA receptors linked to the GnRH neurons. Glutamate plays several roles in the hypothalamic mechanism of puberty as it has been shown in animal models, but there are still few clinical data supporting the role of glutamate in human puberty.
Adolescent↗
Analysis of puberty and pubertal growth in healthy boys.
The aim of this study was to provide normative data for the onset and tempo of puberty in healthy boys. The analyses are based on data that were collected and evaluated biannually on 1112 Turkish school children aged from 8 to 18 years and a subsample of 30 boys who had reached final height (FH). The data were analyzed cross-sectionally in the total group and longitudinally in the subsample. Mean age and height (Ht) at onset of puberty were 11.6 +/- 1.2 years and 146.1 +/- 7.7 cm, respectively. Peak height velocity (HtV) was 10.1 +/- 1.6 cm. Total pubertal height gain was 26.4 +/- 4.3 cm. The duration of puberty was 4.9 +/- 0.6 years. Height at onset of puberty was positively correlated with FH (p < 0.0001) and with duration of puberty (p = 0.03). Body mass index at onset of puberty correlated negatively with age at onset of puberty (p < 0.009) and with the duration of puberty (p = 0.05) but not with FH. In conclusion, these results provide normative data for Ht and HtV for each testicular volume stage for boys in puberty. Height at onset of puberty is the most important determinant of FH. There is no secular trend for the onset of puberty. Weight does seem to affect the onset and tempo of puberty but not FH.
Adolescent↗
Serum inhibin B in healthy pubertal and adolescent boys: relation to age, stage of puberty, and follicle-stimulating hormone, luteinizing hormone, testosterone, and estradiol levels.
Inhibin B levels were measured in serum from 400 healthy Danish prepubertal, pubertal, and adolescent males, aged 6-20 yr, in a cross-sectional study using a recently developed immunoassay that is specific for inhibin B, the physiologically important inhibin form in men. In addition, serum levels of FSH, LH, testosterone, and estradiol levels were measured. Serum levels of inhibin B, FSH, LH, testosterone, and estradiol all increased significantly between stages I and II of puberty. From stage II of puberty the inhibin B level was relatively constant, whereas the FSH level continued to increase between stages II and III. From stage III of puberty the FSH level was also relatively constant, although there was a nonsignificant trend of slightly decreased FSH levels at pubertal stage V compared to stage IV. The levels of serum LH, testosterone, and estradiol increased progressively throughout puberty. In prepubertal boys younger than 9 yr, there were no correlation between inhibin B and the other three hormones. In prepubertal boys older than 9 yr, a significant positive correlation was observed between inhibin B and FSH, LH, and testosterone. However, at this pubertal stage, each hormone correlated strongly with age, and when the effect of age was taken into account, only the partial correlation between inhibin B and LH/testosterone remained statistically significant. At stage II of puberty, the positive partial correlation between inhibin B and LH/testosterone was still present. At stage III of puberty, an negative partial correlation between inhibin B and FSH, LH, and estradiol was present, whereas no correlation between inhibin B and testosterone could be observed from stage III onward. The negative correlation between inhibin B and FSH persisted from stage III of puberty onward, whereas the correlation between inhibin B and LH and between inhibin B and estradiol was nonsignificant at stages IV and V of puberty. In conclusion, in boys, serum inhibin B levels increase early in puberty; by pubertal stage II the adult level of inhibin B has been reached. The correlation of inhibin B to FSH, LH, and testosterone changes during pubertal development. Early puberty is characterized by a positive correlation between inhibin B and LH/testosterone, but no correlation to FSH. Late puberty (from stage III) is characterized by a negative correlation between inhibin B and FSH (which is maintained in adult men), a diminishing negative correlation between inhibin B and LH, and no correlation between inhibin B and testosterone, suggesting that developmental and maturational processes in the hypothalamic-pituitary-gonadal axis take place, leading to the establishment of the closed loop feedback regulation system operating in adult men. The positive correlation between inhibin B and LH/ testosterone at the time when serum inhibin B levels rise early in puberty suggests that Leydig cell factors may play an important role in the maturation and stimulation of Sertoli cells in the beginning of pubertal development.
Adolescent↗
[Endocrine biochemistry of puberty].
Puberty corresponds to the development of gonads and secondary sexual characteristics, and on a biological point of view, to the functional maturation of the gonadal axis. Puberty begins at the age of 11.5 to 12 years in males and 10.5 to 11 years in females. Depending on secondary sexual characteristics, particularly pubic pilosity, puberty is classified in five stages (Tanner's stages). During puberty growth velocity increases in response to gonadal steroid secretion. From a biochemical point of view, three steps are involved in the development of the hypothalamo-hypophysogonadal axis: 1. nocturnal hypothalamic GnRH secretion increases and becomes pulsatile (a peak every 60 to 90 min); 2. the pituitary gonadotrophins FSH and LH follow the same pattern of secretion as GnRH; increase of GnRH and FSH/LH secretion is due to a decrease in hypothalamo-hypophysal sensitivity to the negative feed back exerted by circulating gonadal steroids; 3. secretion of estradiol in females and testosterone in males increases, as a consequence of pituitary stimulation. Hormonal exploration of puberty is mainly based on the measurement of FSH-LH and testosterone or estradiol. SDHA is also measured to investigate adrenal androgen secretion, which increases three or four years before puberty; this is related to the maturation of adrenal androgenic function (adrenarche). Dynamic tests are used to evaluate the biological stage of puberty (LH-RH test) and to measure the functional capacity of the testes. Pubertal abnormalities can theoretically be divided into precocious and delayed puberty. In the former, clinical and biological characteristics are used to define: dissociated puberties, central precocious puberty and peripheral precocious puberty. In the latter, hypogonadism has either a central origin (hypogonadotropic hypogonadism) or peripheral origin (hypergonadotropic hypogonadism).
Child↗
Onset of puberty in pasture-raised Thoroughbreds born in southern hemisphere spring and autumn.
REASONS FOR PERFORMING STUDY: There is little information on age, weight and time of year of puberty in Thoroughbred horses, and the interpretation of such data is difficult due to the wide variety of descriptions of the onset of puberty. OBJECTIVES: To examine the age, bodyweight and date of onset of puberty in Thoroughbreds born in spring and autumn. METHODS: Bodyweight data and blood samples were collected in 59 pasture-raised Thoroughbred horses. Five autumn-born and 18 spring-born colts and 3 autumn-born and 33 spring-born fillies were examined from birth to age 13 and 17 months. A testosterone concentration >2 s.d. above the baseline concentration was indicative of onset of puberty in colts; and progesterone concentration >2 ng/ml and at least 3 times greater than the previous progesterone concentration was indicative of a first ovulation in fillies. RESULTS: Spring-born fillies and colts were older and heavier than autumn-born fillies and colts at puberty. The age at onset of puberty in spring- and autumn-born foals was 291-408 days and 212-270 days, respectively. The weight at puberty in spring-born foals was 302-409 kg, and in autumn-born foals was 277-344 kg. However, the mean date at onset of puberty was not significantly different between spring- and autumn-born horses, with puberty occurring in October (New Zealand spring). CONCLUSIONS AND POTENTIAL RELEVANCE: Seasonal changes in photoperiod affect the timing of onset of puberty, provided a minimum threshold bodyweight has been reached. Spring-born horses reached this threshold weight during the winter months and remained reproductively inactive until after the stimulus of increasing day-length occurred. The autumn-born horses reached the threshold weight to support puberty at the same time as stimulatory photoperiod and, therefore, reached puberty significantly younger and lighter than the spring-born horses.
Age of Onset↗
Fetal nutrition and timing of puberty.
Over the last decade growing evidence has been documented on the relationship between intrauterine growth retardation (IUGR) and pubertal development indicating changes in timing and progression of puberty. These changes in pubertal development are part of a growing list of IUGR-related diseases, which includes type 2 diabetes mellitus, cardiovascular disease, short stature and polycystic ovary syndrome. The influence of IUGR on the mechanisms behind the onset of puberty is still elusive. In the absence of prospective studies on gonadotropin-releasing hormone pulse patterns in IUGR children, other markers of pubertal development such as age at menarche in girls and progression of puberty have been employed. We investigated pubertal development and DHEAS levels in children born small for gestational age (SGA) after third trimester growth retardation and children born appropriate for gestational age (AGA). A faster progression of puberty was found in girls but not in boys. DHEAS levels tended to be higher in SGA children than in AGA children. In animal studies using two rat models, growth and onset of puberty based on perinatal undernutrition were also investigated. In one model intrauterine growth retardation was induced by ligation of the uterine arteries (IUGR) at day 17 of gestation and in the other model postnatal food restriction (FR) was induced by increasing litter size after birth until weaning. In both models, the rats showed a persistent growth failure. Onset of puberty was defined by vaginal opening (VO) in female rats and by balanopreputial separation (BPS) in male rats. At onset of puberty IUGR and FR rats had a lower body weight compared to controls, indicating that no threshold for body weight is needed for the onset of puberty. In the IUGR female rats, the onset of puberty was delayed and in the FR female rats the onset of puberty was in time. In both IUGR and FR female rats VO and first cycle were uncoupled. In IUGR female rats, at VO, at first cycle and at the age of 6 months the ovaries showed a decline in number of follicles indicating that intrauterine malnutrition in the female rat has a permanent influence on the growth and development of follicles. In the FR female rats, at VO, the ovaries showed a normal number of follicles but an abnormal maturation pattern. At the time of first cycle and at the age of 6 months normalization in follicle growth pattern was observed. These findings suggest that postnatal undernutrition has a transient influence on follicle growth and development. In male rats, both models showed delayed onset of puberty and impaired testicular function, as shown by decreased testosterone levels. These data indicate that early malnutrition during different critical developmental time windows may result in different long-lasting effects on pubertal development in both humans and rats.
Animals↗