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At least 19 recordsLinked to original sources
PubMed1998

Gonadotrophin and prolactin secretory dynamics in girls with normal puberty, idiopathic precocious puberty and precocious puberty due to hypothalamic hamartoma.

OBJECTIVE: This study was designed to test the hypothesis that hypothalamic hamartoma causes precocious puberty through a different neuroendocrine mechanism than that of normal puberty or of idiopathic precocious puberty. DESIGN AND PATIENTS: We compared the pattern of gonadotrophin secretion among 4 girls with precocious puberty due to hypothalamic hamartoma, 27 girls with idiopathic precocious puberty, and 14 girls with normal puberty. All subjects were breast stage 3 or 4. Blood samples were obtained every 20 min for 4 h during the day (1.000 hours to 1400 h) and night (22.00 hours to 0200 h). MEASUREMENTS: LH, FSH, and prolactin were measured in each blood sample. Girls also underwent LHRH-stimulation with measurement of LH and FSH before and after stimulation. RESULTS: There were no significant differences in mean LH level, LH peak amplitude, or LH or FSH peak frequency during either the day or the night among the three diagnostic groups. However, the mean +/- SD LHRH-stimulated peak LH levels were greater in girls with hypothalamic hamartoma than in girls with normal puberty or with idiopathic precocious puberty (194 +/- 142 vs 85 +/- 60 or 66 +/- 54 IU/l, respectively, P < 0.05). The LHRH-stimulated peak FSH level in girls with hypothalamic hamartoma exceeded the level for the normal pubertal girls (31 +/- 19 vs 17 +/- 7 IU/l, P < 0.05), but not the level for the girls with idiopathic precocious puberty (25 + 12 IU/l). The peak LH to peak FSH ratio in the girls with hypothalamic hamartoma exceeded the ratio for the girls with idiopathic precocious puberty (7.3 +/- 3.9 vs 2.6 +/- 3.0 IU/l, P < 0.05), but not the ratio for the normal pubertal girls (5.0 + 2.9). There were no significant differences in mean prolactin level, peak amplitude or frequency, or in the ratio of mean night to mean day prolactin, among the 3 diagnostic groups. CONCLUSIONS: We conclude that spontaneous gonadotrophin and prolactin secretion are similar among girls with hypothalamic hamartoma, idiopathic precocious puberty, or normal puberty. However, the increased LHRH-stimulated peak LH in the girls with hypothalamic hamartoma suggests subtle differences in neuroendocrine regulation that may underlie their more rapid pubertal maturation.

Adolescent↗
PubMed1998

Relationships between age at puberty and interval from weaning to estrus and between estrus signs at puberty and after the first weaning in pigs.

The study comprises observations in 464 Swedish Yorkshire pigs at puberty and after the first weaning. The aim was to study relationships between age at puberty and weaning to estrus interval and between estrus signs at puberty and after the first weaning. The estrus signs were checked, and blood samples for progesterone determination were drawn regularly around puberty and after the first weaning. Gilts expressing early puberty (youngest one-third) showed a greater ability to return to estrus and to ovulate within 10 d after weaning than gilts expressing late puberty (oldest one-third) (P = .01). A positive genetic correlation was found between age at puberty and the interval from weaning to the first detected estrus (WEI) (rg = .45). The genetic correlation between age at puberty and the ability to show the standing reflex and to ovulate within 10 d after weaning was negative (rg = -.50). The heritability of the ability to show the standing reflex and to ovulate within 10 d after weaning was .31. Gilts not showing a standing reflex at puberty also had a higher incidence of ovulation without a standing reflex within 10 days after their first weaning (21.4 vs 6.2%, P = .001). There was a significant positive correlation between the total duration and the intensity of the reddening and swelling of the vulva at puberty and after the first weaning. This study demonstrates relationships both between age at puberty and WEI and between some estrus signs at puberty and after the first weaning.

Aging↗
PubMed2001

Precocious puberty in children with tumours of the suprasellar and pineal areas: organic central precocious puberty.

UNLABELLED: During the past 11 y, 115 children younger than 8/9 y of age (female/male) with tumours of the suprasellar or pineal areas were followed in our clinic to study the incidence of precocious puberty. In addition, type of central lesion, clinical characteristics and gonadotropic secretion were studied in order to elucidate the different mechanisms of gonadal activation. A control group of 21 patients with idiopathic precocious puberty and a control group of 10 age-matched patients with suprasellar tumours without precocious puberty were also studied. Precocious puberty associated with organic central lesions was found at diagnosis in 30 patients (26%), in 9 out of 48 patients with glial cell tumours (18.7%), 6 out of 9 patients with germ cell tumours (66.6%), 11 out of 11 patients with hypothalamic hamartomas (100%) and in 4 out of 4 patients with subarachnoid cysts or arachnoidocele (100%). Precocious puberty was not found in any of 36 patients with craniopharyngioma. With the exception of one patient with pineal germinoma, all lesions were localized to the suprasellar area. In all patients with hypothalamic hamartoma, precocious puberty was diagnosed before 4 y of age, while in most patients with the other lesions, it was diagnosed after this age. Height SDS, weight increase and advancement of bone age were similar in both idiopathic and organic central precocious puberty. Maximal LH responses to GnRH in idiopathic and organic central precocious puberty were similar except for germ cell tumours. Patients with suprasellar tumours without precocious puberty had lower maximal LH (but not FSH) responses to GnRH, with the exception of germ cell tumours. In the latter, elevation of serum beta-hCG indicates that this gonadotropin was responsible for gonadal stimulation. In hypothalamic hamartomas, the prepubertal hiatus in the activity of the GnRH pulse generator was absent. The mechanism of this failure in the inactivation of GnRH is unknown. Data suggest that in glial cell tumours and in subarachnoid cysts, an unknown factor, probably secreted by the tumours, advances the tempo of GnRH maturation. Therefore, the aetiology of organic central precocious puberty is multiple and is directly related to location and type of lesion. CONCLUSION: This clinical information suggests that the onset of puberty is not the result of the disruption of a putative pulse generator inhibitory influence but the consequence of secretion of stimulatory substances by the lesions.

Age of Onset↗
PubMed1995

Effects of growth rate on carcass composition and lipid partitioning at puberty and growth hormone, insulin-like growth factor I, insulin, and metabolites before puberty in beef heifers.

The effect of three rates of gain on carcass composition, lipid partitioning, age and BW at puberty, and concentrations of growth hormone (GH), IGF-I, insulin, glucose, and NEFA in plasma were evaluated in 38 Angus x Hereford heifers. Heifers were allotted by BW and age to three treatments with a replication in each of 2 yr: full-fed (n = 13; FF) to gain 1.36 kg/d; limit-fed (n = 12; LF) to gain .68 kg/d; maintenance-full-fed (n = 13; MFF) to gain .23 kg/d for 16 wk, then full-fed to gain 1.36 kg/d. Heifers were slaughtered within 10 d after the onset of puberty. At slaughter, kidney, pelvic, and heart fat (KPH) and udder (UDDER) were separated from carcass, as was fat surrounding viscera (OM). After 48 h at 4 degrees C a carcass side was dissected into subcutaneous fat (SC), intermuscular fat (SEAM), soft tissue (SFT = inseparable lean and fat), LEAN, and BONE. In yr 1, LF heifers (431 d) were older (P < .05) than MFF heifers (371 d) at puberty, but age of FF heifers (389 d) did not differ (P > .10) from that of LF and MFF heifers. In yr 2, FF heifers (351 d) were younger (P < .05) than LF and MFF heifers (398 and 434 d, respectively). The FF heifers had greater (P < .05) BW and a greater (P < .01) percentage of lipid in the carcass at puberty than LF and MFF heifers. During the first 16 wk of treatment, concentrations of NEFA were greater in heifers with slower daily gains (MFF > LF > FF; P < .01). Concentrations of NEFA were lesser and concentrations of IGF-I and insulin were greater in plasma of FF than in that of MFF heifers during the 10 wk before puberty. Treatment significantly altered age, BW, carcass composition, and lipid partitioning at puberty in beef heifers. We conclude that the percentage of body fat is not the sole regulator of puberty, and age may be an important modulator in determining the onset of puberty in beef heifers.

Aging↗
PubMed1985

Somatomedin-C in normal puberty and in true precocious puberty before and after treatment with a potent luteinizing hormone-releasing hormone agonist.

To explore further the relationship of gonadal sex steroids to the rise in somatomedin-C (Sm-C) during puberty, we studied a group of children with true precocious puberty before and after treatment which suppressed sex steroid output. Plasma estradiol and testosterone and serum acid-ethanol-extractable Sm-C were determined by specific RIAs in 7 boys and 12 girls with true precocious puberty before and at regular intervals during treatment with a potent LHRH-agonist (LHRH-A), D-Trp6-Pro9-NEt-LHRH. For comparison, Sm-C and sex steroid concentrations were determined in 266 normal adolescents and 37 normal prepubertal children, 1-9 yr of age. The mean +/- SEM Sm-C levels in normal male individuals peaked at 15 yr (2.46 +/- 0.23 U/ml) and at pubertal (genital) stage III (2.29 +/- 0.19 U/ml), and those in normal females reached their highest concentration at 12-15 yr of age and at pubertal (breast) stage III (2.47 +/- 0.15 U/ml). Sm-C concentrations correlated better with pubertal (genital or breast) stage than with chronological age for both sexes and better with testosterone levels in males than with estradiol levels in females. The mean +/- SEM Sm-C concentrations in both males and females with true precocious puberty were 2.07 +/- 0.16 U/ml before therapy and decreased significantly to 1.52 +/- 0.13 U/ml after 6 months of therapy. The mean Sm-C level of the patients remained significantly elevated for chronological age, but decreased into the normal range for bone age after 6-12 months of therapy. Sm-C correlated significantly with testosterone and estradiol levels, but not with growth rate. Mean nighttime GH secretion decreased significantly after 6 months of LHRH-A therapy. In summary, children with true precocious puberty have Sm-C elevations typical of normal puberty. The decrease in Sm-C levels after suppression of gonadal sex steroid output with LHRH-A is evidence that sex steroids are necessary to induce this elevation in Sm-C concentration. The decrease in GH secretion during LHRH-A therapy suggests that the effect of sex steroids on Sm-C levels during normal puberty is mediated, at least in part, through stimulation of GH secretion.

Adolescent↗
PubMed1995

Correlation of the periodontal status 6 years after puberty with clinical and microbiological conditions during puberty.

The purpose of this study was to assess the oral clinical and microbiological status of young adults 6 years after puberty and to compare these findings with the conditions observed during puberty. Clinical and microbiological parameters were monitored in 42 individuals 10 x between the ages of 11 and 14 years. 33 individuals were re-examined 10 years after the start of this monitoring. Microbiology included 2 subgingival samples per subject taken from the mesiobuccal aspects of the upper 1st molars. The samples were subject to continuous anaerobic culturing. Individuals with a marked and sustained increase in mean papillary bleeding scores during puberty (group A, n = 16) differed 6 years later from individuals without pronounced puberty gingivitis (group C, n = 8) in several aspects. Individuals in group A had a significantly higher gingival bleeding tendency and an increased number of sites with more than 3 mm attachment loss. The subjects in group C showed the lowest anaerobic total cultivable counts. Spirochetes were detected only in group A subjects (4 samples in 3 individuals). In all positive sites, spirochetes had been identified at least 8 out of 10 times during puberty. A. actinomycetemcomitans was present in only one individual of group A. P. gingivalis had not been detected during puberty; none of the samples were P. gingivalis positive 6 years later. P. intermedia was found in 27% of all samples, isolates belonging to the P. melaninogenica group of black pigmenting anaerobes had a frequency of 6%, 6 years after puberty.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1998

Irreversible increase of serum IGF-1 and IGFBP-3 levels in GnRH-dependent precocious puberty of different etiologies: implications for the onset of puberty.

In normal puberty, as well as in precocious puberty, serum GH, IGF-1 and IGFBP-3 are increased as a consequence of the increase in sex hormone secretion. However, the effect of suppressing sex hormones on serum GH and IGF-1 in precocious puberty is controversial. On the other hand, the interest in the interaction between the GH-IGF-1 system and the hypothalamic-pituitary gonadal axis has been reinforced by experimental evidence which indicates that IGF-1 might be involved in the regulation of the onset of puberty. We have studied 11 girls with GnRH-dependent precocious puberty (Gr1), before and during treatment with GnRH analog for 1.43+/-0.81 years, and 4 children (3 boys and 1 girl) with GnRH-dependent precocious puberty secondary to congenital adrenal hyperplasia (Gr2), before and during treatment with hydrocortisone (HC) alone for 0.32+/-0.23 years, and during combined treatment with GnRH analog, for 1.87+/-1.43 additional years. The etiology of precocious puberty in Gr1 was either idiopathic or associated with several brain lesions (hydrocephalia, hypothalamic hamartoma, suprasellar astrocytoma). During follow-up, clinical status as well as gonadotropin suppression, tested with the acute GnRH test, was checked every 3 months. Peptides and steroid hormones were determined by radioimmunoassay. Normal values for serum IGF-1 and serum IGFBP-3 were established in our laboratory from a population of 165 clinically controlled subjects, aged 0.5-15 years. In Gr1, treatment arrested breast development and blunted LH and FSH response to GnRH in all subjects. In Gr2, during HC treatment, all patients had a pubertal type of response to the acute GnRH test which was suppressed during combination treatment. In Gr1, serum IGF-1 SDS for chronological age (CA), but not IGFBP-3 SDS CA, was significantly high before GnRH analog treatment (mean+/-SD 1.33+/-1.84 and -0.68+/-1.55, p < 0.05 and p = NS, respectively). IGF-1 SDS CA remained high and IGFBP-3 SDS CA remained normal during treatment (1.34+/-2.0 and 0.73+/-1.93). In Gr2, serum IGF-1 and IGFBP-3 SDS CA were high before treatment (3.11+/-0.74 and 1.31+/-1.43, p < 0.02 and p < 0.05, respectively), and they remained high during HC or combined treatment. In the two groups, serum IGF-1 SDS BA and serum IGFBP-3 SDS BA levels were similar to control subjects before and during treatments. In Gr1, mean serum dehydroepiandrosterone sulfate (DS) was within prepubertal preadrenarche values but serum androstenedione (delta4) was significantly higher (6.35+/-3.45 nmol/l) than in our own normal control group (1.84+/-1.18, n = 20), both before and during treatment (p < 0.02). In Gr2, serum DS and serum delta4 were high before treatment but they decreased to prepubertal values during combined treatment. It is concluded that (1) the CNS maturational events which change the regulation of serum IGF-1 and IGFBP-3 are induced by the pubertal increase in sex steroids in a nonreversible way and (2) the high adrenal steroid levels present in CAH induce a nonreversible activation of the GH-IGF-1 axis and of the GnRH pulse generator.

Adrenal Cortex Hormones↗
PubMed1997

A longitudinal assessment of hormonal and physical alterations during normal puberty in boys. V. Rising leptin levels may signal the onset of puberty.

Leptin, the product of the ob gene, is an adipocyte-derived hormone that signals the amount of adipose tissue energy stores to the brain and exerts major effects on energy homeostasis and neuroendocrine function. Leptin has recently been shown to affect reproductive function in leptin-deficient and normal rodents. As puberty, the process of sexual maturation and acquisition of reproductive competence, has been proposed to be triggered by the attainment of a critical amount and/or distribution of fat, we examined whether changes in circulating leptin levels could represent the hormonal signal responsible for triggering the onset of puberty in humans. Eight prepubertal boys (Tanner genital stage 1 or early stage 2 at the initiation of the study) were evaluated longitudinally for 2.5-5.1 yr depending on when Tanner stage 5 of genital development was achieved. Sera for the determination of leptin, testosterone, and dehydroepiandrosterone sulfate were obtained every 4 months during the period of the study. Compared to baseline prepubertal levels (8 months before the onset of puberty, as defined by the initial rise in testosterone above the detection limit of the assay), leptin levels rose by approximately 50% just before the onset of puberty and decreased to approximately baseline values after the initiation of puberty (P < 0.01, by ANOVA), remaining stable for more than 2 yr. These changes occurred despite constantly increasing body mass index (P < 0.05, by ANOVA). No significant association between leptin and dehydroepiandrosterone sulfate concentrations was detected. In conclusion, the levels of circulating leptin are consistent with the hypothesis that this molecule is an important signal responsible for triggering the onset of puberty. The stimulus for a surge in leptin levels just before the onset of puberty is currently unknown.

Body Mass Index↗
PubMed2002

Idiopathic precocious puberty versus puberty in adopted children; auxological response to gonadotrophin-releasing hormone agonist treatment and final height.

OBJECTIVE: The objective of this study was to evaluate the characteristics of puberty and response to gonadotrophin-releasing hormone (GnRH) agonist treatment in adopted children compared with children with idiopathic precocious puberty (IPP). METHODS: We studied 17 girls with central IPP (group A) and 11 girls adopted from Asia and Central and South America (group B) with respect to auxological data at presentation of puberty and response to GnRH agonist treatment. RESULTS: In adopted girls, age at onset of puberty was later and duration of treatment was shorter. At the start of treatment, height-standard deviation score (H-SDS) was +1.67 s.d. in group A. In group B, H-SDS was comparably increased (+0.04 s.d.) assuming that the mean H-SDS in their native country is lower than the mean on the Dutch curve. During treatment, H-SDS decreased in both groups. Group A reached a final height (FH) of 166.2 cm (-0.3 s.d.) and group B of 156.1 cm (-1.9 s.d.). Predicted adult height (PAH) at the start of treatment underestimated FH in group A and overestimated FH in group B. At the end of treatment, PAH overestimated FH in both groups. The SDS for weight was above the mean in both groups at the start of treatment and increased even more during treatment. The age of occurrence of menses after treatment was stopped was the same in both groups (12.7 and 12.8 Years respectively). CONCLUSION: Despite the difference in timing of puberty between girls with IPP and adopted girls with early puberty, their response to treatment was similar in many aspects.

Adoption↗
PubMed1994

Diagnosis and treatment of central precocious puberty--can final height be improved? German/Dutch Central Precocious Puberty Study Group.

Central precocious puberty is characterized by premature activation of the hypothalamic gonadotrophin-releasing hormone (GnRH) pulse generator, resulting in accelerated growth and bone maturation with clinical signs of gonadarche before the age of 8 years in girls and 9 years in boys. In rapidly progressing central precocious puberty, the plasma luteinizing hormone (LH) response to exogenous GnRH exceeds the reference range for sex and stage of puberty, and the ratio of LH:follicle-stimulating hormone after GnRH is usually above 1. Short adult stature, with unfavourable body proportions, i.e. an increased upper:lower segment ratio, is probably the only handicap of idiopathic central precocious puberty that persists into adulthood. This cannot be avoided by treatment with either medroxyprogesterone or cyproterone acetate. Following the first report of pituitary-gonadal suppression in a 2-year-old girl with central precocious puberty using daily injections of the gonadotrophin-releasing hormone (GnRH) agonist deslorelin, various short-acting GnRH agonists have been studied in children with central precocious puberty. Some of the older patients treated for shorter periods have now reached adult or near-final height. By 1985, slow-release (depot) GnRH agonists, such as triptorelin and later leuprorelin, were available. These are injected only once every 4 weeks instead of daily or given by nasal spray six times daily, making long-term treatment much more acceptable to patients and their parents. Moreover, suppression of gonadarche is more complete with long-acting (e.g. triptorelin) compared with short-acting (e.g. buserelin) agonists, resulting in significantly slower bone age progression and, thus, greater improvement in predicted, and probably also in achieved, final height.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1978

The effect of LH-RH infusion on serum LH, FSH and testosterone in boys with advanced puberty, delayed puberty and hypogonadotrophic hypogonadism.

LH-RH injection and infusion studies were performed in advanced puberty, delayed puberty and hypogonadotrophic hypogonadism. No differential diagnosis could be made between delayed puberty and hypogonadotrophic hypogonadism using LH-RH injection. In the LH-RH infusion studies evidence was obtained that stimulation of the pituitary during 4 h results in continuously rising LH levels in advanced puberty and in delayed puberty while in hypogonadotrophic hypogonadism the secretory capacity of the pituitary is gradually exhausted. This phenomenon can be used in the differential diagnosis between delayed puberty and hypogonadotrophic hypogonadism. Though the FSH data point in the same direction they are not useful in this connection as the overlap between the different categories was considerable.

Adolescent↗
PubMed2000

Circulating concentrations of nocturnal leptin, growth hormone, and insulin-like growth factor-I increase before the onset of puberty in agonadal male monkeys: potential signals for the initiation of puberty.

The factor(s) responsible for initiating the developmental increase in nocturnal gonadotropin-releasing hormone secretion, defining the onset of puberty, are not known. Although signals regulating prepubertal growth seem to be obvious candidates to control such a process, it is unclear whether prepubertal alterations occur in these growth-related factors such that they might provide the brain information on changing body size. Using samples analyzed previously describing the initiation of nocturnal pulsatile LH secretion in agonadal male monkeys (Endocrinology 139: 2774-2783, 1998), developmental changes in plasma concentrations of leptin, GH, and insulin-like growth factor I (IGF-I) were determined to test the hypothesis that an increase in circulating levels of one or all of these growth-derived signals precedes the onset of puberty. Hormone concentrations were determined in five juvenile males at 10-day intervals from approximately 60 days before and 50 days after the initiation of pulsatile nocturnal LH secretion. Leptin concentrations were determined in samples obtained at 1000 and 2200 h, 36 and 48 h before the nocturnal assessment of pulsatile LH. Mean nocturnal GH concentrations were determined from the sequential samples collected at night. IGF-I was determined in the 1000- or 2200-h presequential samples. Although daytime leptin concentrations did not increase developmentally, nocturnal leptin levels increased significantly during the 30 days before the onset of puberty. Furthermore, both nocturnal GH and IGF-I concentrations showed a significant sustained increase from the early prepubertal period to the 30 days preceding the onset of puberty. These data are the first to demonstrate an increase in nocturnal leptin and GH-induced IGF-I secretion prior to the onset of puberty in the agonadal male monkey and that these developmental changes occur independent of the gonadal influences. These findings provide justification for empirical investigation of the role of leptin and the GH axis, in particular IGF-I, in regulating developmental increases in pulsatile nocturnal gonadotropin-releasing hormone secretion initiating puberty in primates.

Animals↗
PubMed1986

Is heterozygosity for the steroid 21-hydroxylase deficiency responsible for hirsutism, premature pubarche, early puberty, and precocious puberty in children?

We applied the ACTH-stimulation test developed in our laboratory for the detection of heterozygous carriers of the 21-hydroxylase deficiency gene to patients suffering from hirsutism (n = 89), premature pubarche (n = 75), early puberty (n = 37), and precocious puberty (n = 22). While, in the general population, this test is positive in less than 2%, we found in 33% of hirsute patients, in 41% of patients with premature pubarche, and in 33% of patients with early puberty a hormonal response similar to the one seen in heterozygous carriers for the 21-hydroxylase defect. In contrast, only 18% of patients with precocious puberty responded abnormally. Thus we speculate that, at least in some patients with hirsutism, premature pubarche, and early puberty, heterozygosity for the 21-hydroxylase defect plays a major role in the pathogenesis of these disorders.

17-alpha-Hydroxyprogesterone↗
PubMed2003

Inhibin B, follicle stimulating hormone, luteinizing hormone and testosterone during childhood and puberty in males: changes in serum concentrations in relation to age and stage of puberty.

Inhibin B is a gonadal dimeric polypeptide hormone that regulates synthesis and secretion of follicle stimulating hormone (FSH) in a negative feedback loop. The aim of the present study was to determine changes in serum inhibin B, gonadotropins and testosterone concentrations during childhood and puberty in males. We studied the relationship between circulating inhibin B, gonadotropins and testosterone in serum of healthy boys during the first two years of life and then in pubertal development. Using a recently developed two-side enzyme-linked immunosorbent assay (ELISA), inhibin B levels were measured in the serum of 78 healthy boys divided into eleven age groups from birth to the end of pubertal development. In addition, serum levels of gonadotropins and testosterone were measured. Serum inhibin B, gonadotropins and testosterone increased during the first months of postnatal life. A peak in serum inhibin B and gonadotropins concentrations was observed around 3-4 months of age. There was a significant positive correlation between serum inhibin B and gonadotropins and testosterone levels during the first 2 years of life. After this early increase, serum inhibin B, gonadotropins and testosterone levels decreased significantly and remained low until puberty followed by an increase beginning with the onset of puberty. Serum levels of inhibin B reached a peak at stage G3 of puberty. Around midpuberty, inhibin B lost its positive correlation with luteinizing hormone (LH) and testosterone from early puberty, and developed a strong negative correlation with FSH, which persisted into adulthood. We conclude that inhibin B plays a key role in the regulation of the hypothalamic-pituitary-gonadal hormonal axis during male childhood and pubertal development. Inhibin B is a direct marker of the presence and function of Sertoli cells and appears to reflect testicular function in boys.

Aging↗
PubMed1986

[Controlling precocious puberty--surgical excision of hypothalamic hamartoma causing precocious puberty].

Among the causes of precocious puberty, hypothalamic hamartoma comprises a small percentage. However, the frequency of precocious puberty in the presence of hypothalamic hamartoma is quite high. Recently, results of surgery in 14 cases of hypothalamic hamartoma were reported. Precocious puberty completely subsided in three cases and slight improvement was achieved in another three cases. We performed surgery in four patients with hypothalamic hamartomas, with the goal of decreasing the symptoms of precocious puberty. The patients were two females (aged 1 yr, 3 mo and 6 mo) and two males (aged 3 yr, 7 mo and 1 yr, 9 mo). The main symptoms were precocious puberty and mental retardation of varying degrees. The males had excessive growth of body and external genitalia, while the females had genital bleeding and premature breast development. In each case, computed tomographic scans disclosed a round, isodense mass in the interpeduncular cistern, attached to the base of the hypothalamus. Contrast enhancement was negative. Endocrinologically, in case 1, testosterone was 92.6 ng/ml, FSH was 16 mIU/ml, and LH was 2.2 mIU/ml. Although LH was within normal limits, it overresponded to LH-RH stimulation. In case 2, estrogen was 13.5 ng/day, LH was 5.2 mIU/ml, FSH was 5.3 mIU/ml, and LH showed an exaggerated response to LH-RH stimulation. In case 3, testosterone was 362 ng/ml, LH was 8.8 mIU/ml, FSH was 4.8 mIU/ml, and LH showed an abnormally high response to LH-RH stimulation. In case 4, LH was 18.4 mIU/ml, FSH was 12.0 mIU/ml, and both hormones were stimulated abnormally strongly by LH-RH.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗
PubMed1994

Prostaglandin F2 alpha immunization of prepubertal beef heifers: effects of conjugate dose and timing of immunization relative to puberty on the onset of puberty and subsequent ovarian function.

Fifty-six prepubertal Hereford cross Friesian heifers were assigned to seven treatment groups: (1) primary (day 0) and booster (day 41) using 10 mg human serum albumin (HSA) (control); (2) primary and booster (day 41) immunizations using 3.3 mg prostaglandin F2 alpha PGF-HSA conjugate; (3) primary and booster (day 83) using 3.3 mg PGF-HSA; (4) primary and booster (day 210) using 3.3 mg PGF-HSA; (5-7) as in treatments 2-4 except 10 mg PGF-HSA were used. Plasma progesterone concentrations were used to determine the onset of puberty and the presence of a corpus luteum (CL); plasma PGF antibody titres were determined at 28-day intervals. There was no effect (P > 0.05) of conjugate dose or booster interval on mean antibody titres and there was no interaction between them. However, heifers in the 83- and 210-day booster treatments had higher (P < 0.05) peak antibody titres than heifers in the 42-day booster treatments. Puberty was delayed in 40% (16/40) of PGF-immunized heifers and 40% (16/40) of heifers formed persistent CL after puberty. Overall, eight of the heifers with delayed puberty also formed a persistent CL. There was a positive correlation between mean titre and onset of puberty but not with duration of persistent CL.

Animals↗
PubMed1988

Resumption of puberty after long term luteinizing hormone-releasing hormone agonist treatment of central precocious puberty.

To determine whether puberty resumes normally after long term LHRH agonist (LHRHa) treatment, we studied 16 children with central precocious puberty treated with LHRHa (D-Trp6,Pro9,NEt-LHRH) for 1-4 yr (mean, 3.3 yr). Treatment was discontinued at a mean age of 11.6 +/- 1.3 (+/- SD) yr. Plasma hormone levels, growth velocity, rate of bone maturation, and pubertal stage were assessed at the end of treatment and 3 and 12 months later. Basal plasma sex steroid and basal and LHRH-stimulated gonadotropin levels returned to near-pretreatment levels 3 months after discontinuation of therapy and were fully restored to pretreatment levels at 12 months. Growth velocity, which had been 7.8 cm/yr before treatment, was stable after discontinuation of treatment at approximately 2.6 cm/yr. The predicted height, which had increased during treatment (P less than 0.01), remained stable at approximately 5 cm above the pretreatment predicted height. The rate of bone age advancement (delta bone age/delta chronological age) increased gradually from 0.4 at the end of treatment to the normal value of 0.9 12 months posttreatment. Breast and pubic hair pubertal stages, which were stable throughout treatment and were 4.0 +/- 0.8 (+/- SD) and 3.6 +/- 1.0 at the end of treatment, increased to 4.9 +/- 0.2 and 4.5 +/- 1.0. This approximated the normal rate of 1 stage/yr. Menses occurred in 8 of 12 girls within 1 yr after treatment and in an additional 3 by 20 months after treatment. Six of the girls had menstruated before treatment, and all of these menstruated within 14 months after discontinuing therapy. We conclude that gonadotropin and sex steroid secretion and the clinical progression through puberty appear to resume normally after discontinuation of long term LHRHa treatment of central precocious puberty. Long term follow-up will be required, however, to determine whether the improvement in predicted height of these patients will be achieved, and whether adult reproductive function will be normal.

Body Height↗
PubMed1998

Delayed puberty in obese boys: comparison with constitutional delayed puberty and response to testosterone therapy.

OBJECTIVE: To evaluate the results of a brief course of testosterone therapy in boys with delayed puberty and to compare the responses seen in boys with constitutional delayed puberty (CDP), boys with obesity, and boys with possible gonadotropin deficiency. DESIGN AND SETTING: A retrospective chart review was done for 36 boys aged 14 years or older, seen between 1983 and 1996 because of delayed puberty, who were given 4 monthly injections of testosterone, 100 mg/mo, and had adequate follow-up. RESULTS: There were 23 boys whose findings before and after treatment were consistent with a diagnosis of CDP. Testosterone treatment increased the growth rate from 4.3 cm/y to 11.2 cm/y (P <.00001), and mean testis length increased 0.6 to 0.8 cm in all (from a mean of 2.9 to 3.6 cm, P <.00001) in the 4 months after testosterone treatment. Serum testosterone 4 months after therapy was higher than that before therapy (P =.00003). Of 5 boys with growth hormone deficiency but unknown gonadotropin status, 2 had lack of progression after testosterone therapy and were believed to have permanent gonadotropin deficiency. Seven of the 36 boys were obese (body mass index, >25), and 6 had a response to testosterone similar to boys with CDP with clear pubertal progression. One obese boy and one nonobese boy were diagnosed as having isolated gonadotropin deficiency. CONCLUSIONS: Monitoring the growth and genital responses to a 4-month course of testosterone injections helps to differentiate CDP from gonadotropin deficiency in boys with delayed puberty. Obese boys constitute a distinct category of boys with pubertal delay in terms of their growth, but their response to testosterone is similar to that observed in boys with classic CDP.

Adolescent↗