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PubMedDate not supplied

[Endocrinological problems in male adolescents].

The male adolescent may present several endocrinological problems, the most frequent of which is the retardation or absence of puberty due to constitutional delay of growth and development. This form does not require therapy and must be distinguished from other forms of hypogonadism (primitive or secondary) by endocrine tests (LHRH test, nightly pulses LH secretion, plasmatic basal level of testosterone and after HCG, cerebral NMR). Hypogonadism treatment consists of replacement therapy with testosterone or testes stimulation with HCG or LHRH. Another frequent disease is gynecomastia, usually due to physiological enlargement of mammary gland during pubertal development, sometimes it may be secondary to hypogonadism, tumors, liver function abnormalities. Severe or psychologically disturbing gynecomastia can be corrected by reductive mammoplasty. Very often, adolescents may present diseases related to incorrect food habits. Obesity is common and anorexia is becoming an important problem also in males.

Adolescent↗

PubMed2006

Gonadal hormone effects on entrained and free-running circadian activity rhythms in the developing diurnal rodent Octodon degus.

The slowly maturing, long-lived rodent Octodon degus (degu) provides a unique opportunity to examine the development of the circadian system during adolescence. These studies characterize entrained and free-running activity rhythms in gonadally intact and prepubertally gonadectomized male and female degus across the first year of life to clarify the impact of sex and gonadal hormones on the circadian system during adolescence. Gonadally intact degus exhibited a delay in the phase angle of activity onset (Psi(on)) during puberty, which reversed as animals became reproductively competent. Gonadectomy before puberty prevented this phase delay. However, the effect of gonadal hormones during puberty on Psi(on) does not result from changes in the period of the underlying circadian pacemaker. A sex difference in Psi(on) and free-running period (tau) emerged several months after puberty; these developmental changes are not likely to be related, since the sex difference in Psi(on) emerged before the sex difference in tau. Changes in the levels of circulating hormones cannot explain the emergence of these sex differences, since there is a rather lengthy delay between the age at which degus reach sexual maturity and the age at which Psi(on) and tau become sexually dimorphic. However, postnatal exposure to gonadal hormones is required for sexual differentiation of Psi(on) and tau, since these sex differences were absent in prepubertally gonadectomized degus. These data suggest that gonadal hormones modulate the circadian system during adolescent development and provide a new model for postpubertal sexual differentiation of a central nervous system structure.

Animals↗

PubMed2002

Colony-stimulating factor 1 regulation of neuroendocrine pathways that control gonadal function in mice.

Colony stimulating factor 1 (CSF-1) is the primary regulator of cells of the mononuclear phagocytic lineage. Consequently mice lacking CSF-1 (Csf1(op)/Csf1(op)) have depleted populations of macrophages in many tissues. In addition, both sexes have reduced fertility with females having extended estrus cycles and poor ovulation rates, whereas males have low circulating LH and T. In this study, we show that puberty was significantly delayed in Csf1(op)/Csf1(op) females compared with control littermates. Restoration of circulating CSF-1 over the first 2 wk of life accelerated puberty, and this treatment until puberty completely corrected the extended estrous cycles. In a standard LH surge induction protocol, Csf1(op)/Csf1(op) females showed diminutive negative and no positive feedback response to E2. These data, together with that from male Csf1(op)/Csf1(op) mice that showed normal release of LH with a GnRH agonist, indicate that the hypothalamus is the site of the primary defect causing fertility problems in CSF-1-deficient mice. In the hypothalamus, microglia are the only CSF-1 receptor-bearing cells, and the recruitment of a full complement these cells is slightly delayed in Csf1(op)/Csf1(op) mice. These data suggest a role for CSF-1 and its target cells, microglia, in establishing the feedback sensitivity to circulating steroid hormones in the hypothalamus of mice.

Animals↗

PubMed1989

Persistently low immunoreactive and normally bioactive plasma LH during male puberty.

Low basal and LRH-stimulated (50 mcg/m2 i.v.) levels of plasma immunoreactive (IR) LH were repeatedly found in 8 boys aged 13 to 16 years who had been referred because of delayed onset of puberty (basal IR-LH 0.19 +/- 0.1 and peak 0.48 +/- 0.2 vs. 0.24 +/- 0.09 and 1.71 +/- 0.9 mIU/ml in matched normal controls, respectively). Upon termination of puberty (no more than 3.5 years after referral) IR-LH levels were still low in all 8. Using a rat Leydig cell bioassay system with LER-907 (NPA) as standard, LH bioactivity in these patients was compared with that in 8 matched controls (basal LH was 0.32 +/- 0.33 and 0.11 +/- 0.07, and peak levels 0.8 +/- 0.47 and 1.22 +/- 0.44 mIU/ml respectively). The ratio of basal LH bioactivity to IR-LH was higher in the patients (1.24 +/- 0.95) than in controls (0.47 +/- 0.26, P less than .05) as was that of peak bioactivity (1.89 +/- 1.2 vs. 0.83 +/- 0.35, P less than .05). In the three patients tested during sleep IR-LH levels showed no significant change. Basal plasma testosterone levels were appropriate for pubertal stage (400 +/- 80 ng/dl) and in the four patients tested following prolonged LRH stimulation (500 mcg i.v. over 3 hours) increased to 530 +/- 60 ng/dl. It is concluded that in some boys there may be consistently low plasma levels of IR-LH in association with normal LH bioactivity.

Adolescent↗

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↗

PubMed1993

[Growth and endocrine function in major thalassemia].

BACKGROUND: The risk of secondary endocrine dysfunction in patients with thalassemia major remains high, despite improvements in the care of hematologic problems. POPULATION AND METHODS: 31 patients (15 males, 16 females) with thalassemia major were studied. 28 of them had been regularly given blood transfusions since the age of 3.7 +/- 3.6 years. Iron chelation therapy had started before the age of 10 years in 9 patients, after this age in 15 patients; it was not performed or the time not specified in the 7 others. The mean dosage of deferoxamine was 20 +/- 6 mg/kg/day (9.6-34 mg/kg/day). Endocrine functions were evaluated at a mean age of 11.8 +/- 4.9 years and were monitored for 6.1 +/- 4.6 years (0 to 19 years). The hormones assay were: growth hormone (GH), thyroid, adrenal cortex, parathyroid and gonadal functions. RESULTS: The GH peak after stimulation was normal, but plasma somatomedin CIGFI was low and did not increase at puberty. 6 patients had peripheral hypothyroidism. Plasma cortisol was normal in the 16 patients examined, but plasma dehydroepiandrosterone sulfate was low in 24; this might be partly responsible for the delayed development of pubic hair. 2 patients aged 20 and 27 years was suffered from diabetes mellitus. Hypoparathyroidism occurred in 7 patients and 12 of the 24 patients with impuberism had a gonadotropin deficiency. The mean final height was -1.3 +/- 1.0 SD in boys (n = 7, mean age: 20 +/- 1 yr) and -1.3 +/- 0.9 SD in girls (n = 7; mean age: 19 +/- 1 yr), whether puberty was spontaneous or induced. CONCLUSIONS: The most frequent endocrine complications in these patients are delayed puberty because of gonadotropin deficiency, hypoparathyroidism and peripheral hypothyroidism. Substitution therapy, using sex steroids at an appropriate age, can induce the pubertal growth spurt.

Adolescent↗

PubMed1991

Constitutional delay of growth: expected versus final adult height.

Constitutional delay of growth and puberty is believed to represent a variation of normal growth, and it is expected that children with this condition will grow for a longer duration than average and reach a height that is normal for their genetic potential. The records of children with constitutional delay of growth and puberty who were initially seen in the Pediatric Endocrine Clinic at the Oregon Health Sciences University between 1975 and 1983 were retrospectively reviewed. Criteria for study included a height more than 2 SD below the mean, a significantly delayed bone age, and a normal growth velocity on follow-up. Forty-two subjects were located and final adult height measurements were obtained. AT contact, the 29 male subjects (mean age = 23.9 years) were 169.5 +/- 4.5 cm tall (mean +/- SD), and the 13 female subjects (mean age = 20.5 years) were 156 +/- 3.8 cm tall. Adult height predictions during follow-up, using either the Bayley-Pinneau or Roche-Wainer-Thissen method, were close to final adult heights. The males were 1.2 SD and the females 1.3 SD below the 50th percentile as adults. This finding was not fully explained by genetic short stature; the males fell 5.1 cm and the females 5.3 cm below target heights based on midparental heights. It is concluded that this discrepancy is most likely explained by a selection bias of the shortest children referred to and observed in a subspecialty clinic, although a defect in human growth hormone secretion or function in children at the far end of the spectrum of constitutional delay of growth and puberty cannot be excluded.

Adult↗

PubMed1981

The pattern of age-specific tuberculin hypersensitivity in two groups of South African schoolchildren.

In epidemiological studies on tuberculosis we have observed a decrease in the prevalence of positive tuberculin reactions around the age of 13. This decrease was apparent in a variety of populations studied. Statistical analysis of the tuberculin testing data demonstrates the significance of the decrease in the proportion of positive reactors at age 13 and also of a reduction in size of reactions. The possibility of suppression of the delayed hypersensitivity reaction at about puberty is considered.

Adolescent↗

PubMed1984

Seasonal variation in acceleration and delay of sexual maturation in female mice by urinary chemosignals.

Data were compiled and analysed from experiments done over a 10-year period on the acceleration and delay of sexual maturation of female house mice by urinary chemosignals from conspecific males and females. Distinct seasonal patterns emerged for control mice treated with water and for both the acceleration of maturation due to a chemosignal in male mouse urine and the delay of maturation which results from treatment with urine from grouped females. Urine from males accelerated puberty during the period March to September, but not during the months of October through February. Urine from grouped females delayed puberty for the months of September to April, but not for the period May through August.

Animals↗

PubMed2005

Role of prophet of Pit1 (PROP1) in gonadotrope differentiation and puberty.

The prophet of Pit1 (PROP1) gene is essential for normal gonadotropin production in both humans and mice. Transgenic mice that overexpress PROP1 in gonadotropes and thyrotropes have transient hypogonadotropic hypogonadism and increased risk of pituitary adenomas. Here we report a temporal study of pituitary gonadotrope terminal differentiation and hypogonadism, delayed onset of puberty, and transient growth insufficiency in the transgenic males. The Prop1 transgenic mice recover from their abnormalities and exhibit normal size and fertility at 3 months. The relatively normal expression pattern of GnRH receptor (Gnrhr) suggests that the pituitary gonadotrope cell lineage is appropriately specified, but the ability to synthesize LH and FSH is impaired by excess PROP1. We report no obvious abnormalities in expression of the transcription factors early growth response 1, NR5A1, GATA2, TBX19, and NR0B1, or the TGFbeta pathway members including activin, inhibin, and activin receptors. Thus, overexpression of PROP1 may influence gonadotrope development by a novel mechanism. Microarray analysis identified the inhibitory transmembrane receptor gene Klrg1 and the protease gene Prss28 as candidates for involvement in this process. We hypothesize that variation in PROP1 expression could affect the growth spurt and the onset of puberty in humans.

Animals↗

PubMed1975

Altered sexual development in male rats after oestrogen administration during the neonatal period.

Male rats given 250 mug oestradiol benzoate by subcutaneous injection on Day 4 of postnatal life showed a marked delay in the onset of the pubertal increase in the weight of the testes and seminal vesicles and in spermatogenesis but not a complete failure of sexual development. The increase in plasma testosterone concentration at puberty was also delayed in oestrogen-treated males but the eventual increase in seminal vesicle weight was closely related in time to the delayed increase in plasma testosterone concentration. Both plasma LH and FSH concentrations were reduced for about 10 days after oestrogen administration as compared to control values. After 22 days of age, plasma LH concentration did not differ significantly from the control values. The plasma FSH concentration of the oestrogen-treated males showed a delayed rise to values equal to or higher than those of controls of the same age. The delayed rise in plasma FSH concentration in the oestrogen treated males preceded the delayed rise in plasma testosterone in these animals. The decrease in plasma FSH concentration from the high prepubertal values to the lower values in adults occurred at different ages in the control and in oestrogen-treated rats but in both groups the decrease occurred as plasma testosterone levels were increasing and the first wave of spermatogenesis was reaching completion. The increase in plasma FSH concentration after castration was reduced in oestrogen-treated males during the period throughout which FSH levels in the intact animals were subnormal but the levels in oestrogen-treated males castrated after the delayed rise in FSH had occurred did not differ from control values. It is suggested that the delayed sexual maturation of male rats treated with high doses of oestrogen in the neonatal period is related principally to abnormalities in the secretion of FSH.

Animals↗

PubMedDate not supplied

Prenatal ethanol exposure and opiatergic influence on puberty in the female rat.

Fetal alcohol exposure (FAE) is associated with a variety of physiological and behavioral dysfunctions, including deficits to reproductive function. FAE has also been shown to increase brain beta-endorphin levels. This study sought to determine whether the common delay of the onset of puberty in fetal alcohol-exposed animals could be due to increased opiate inhibition of LH release. Prepubertal female rats were injected with an opiate antagonist, naltrexone, over days 26-29. This naltrexone treatment led to an acceleration of vaginal opening and first estrus in FAE animals; had no effect on chow-fed or pair-fed controls. The vaginal opening and first estrus advancement in FAE animals occurred at a lower body weight indicating independence from growth-promoting effects of the drug treatment. It is concluded that delays in puberty in FAE animals are not directly due to pituitary pathology, but are related, at least in part, to increased inhibition of the LHRH neuron and functional impairment of gonadotrophin secretion.

Animals↗

PubMed2003

Longitudinal studies of inhibin B levels in boys and young adults with Klinefelter syndrome.

The aim of the study was to investigate the longitudinal changes of inhibin B in a group of patients with Klinefelter syndrome (KS; karyotype 47,XXY) progressing through puberty and to compare them to a group of age- and puberty-matched controls. Seven boys with nonmosaic KS (karyotype 47,XXY) and 11 controls were followed with longitudinal serum inhibin B measurements every 3-12 months as they approached and entered puberty. None of the boys had significant bone age delay, and all entered puberty at the normal time and progressed through it at the expected time. In addition, 15 young adults with KS, aged 16.7-29.5 yr, were studied. We found normal levels of inhibin B in prepubertal boys with KS and controls. In patients with KS as well as controls, inhibin B increased progressively before clinical pubertal onset. However, during late puberty inhibin B levels decreased gradually to the low/unmeasurable levels observed later in adult KS, while remaining unchanged in the controls.

Adolescent↗

PubMed1988

Cessation of long day melatonin rhythms time puberty in a short day breeder.

This study tested the hypothesis that in the female sheep, a short day (SD) breeder, puberty can occur normally in the absence of ambient short days. More specifically, the photoperiod cue timing the transition into adulthood is exposure to and then termination of a long day melatonin rhythm. Control lambs born in the spring were exposed to 5 weeks of long days (LD; 16 h of light, 8 h of darkness; 18-23 weeks of age) and were raised in SD (8 h of light, 16 h of darkness) at other times. As expected from previous studies, this alternating photoperiod sequence (SD-LD-SD) induced puberty at the normal age in autumn [33 +/- 2 weeks (mean +/- SEM); n = 6]. The other three groups were exposed only to LD from birth; the superior cervical ganglia were removed bilaterally at different ages to denervate the pineal gland in order to block transduction of subsequent LD cues. Puberty occurred normally (31 +/- 1 weeks; n = 7) after ganglionectomy at 23 weeks of age, indicating that ambient short days are not required to initiate reproductive cycles. LD are necessary, as evidenced by the results for the other two groups ganglionectomized neonatally at 4 weeks of age. With no further treatment, puberty was either delayed (n = 1) or did not occur during the first year of life (n = 5), after which the study ended. This delay was prevented in the other group of ganglionectomized lambs by a 5-week (18-23 weeks of age) exposure to LD melatonin patterns by means of 8-h melatonin infusions nightly; 12 weeks after melatonin replacement therapy, puberty occurred at the normal time (34 +/- 1 weeks; n = 6). The inference is that for puberty to occur in the female lamb the animal must be exposed to relatively limited periods of LD, followed by the blockade or absence of further LD cues (pineal denervation, termination of LD melatonin infusion, or presence of SD). This supports the concept that the LD of summer, followed by their disappearance in autumn, time puberty in the female sheep.

Animals↗

PubMed1984

Adult height in Turner syndrome with and without androgen therapy.

Adult heights of 66 individuals with karyotype documentation of Turner syndrome were analyzed. The mean adult height of 29 individuals given growth-promoting hormones, oxandrolone or fluoxymesterone, did not differ significantly from that of 37 untreated subjects (148.1 +/- 4.7 vs 146.3 +/- 5.5 cm, respectively). The type of X chromosome abnormality did not influence the mean adult height. No significant deleterious effect on height was seen with earlier induction of puberty with estrogens. Parental heights did not appear to influence final adult height. Based on this study, the use of androgens to increase adult height in Turner syndrome cannot be recommended and there appears to be no benefit in delaying induction of puberty with exogenous hormones beyond the mid-teens (14 to 16 years).

Adolescent↗

PubMed2005

Kisspeptin and its receptor: new gatekeepers of puberty.

The recent finding that the hormone kisspeptin plays a pivotal role in the onset of puberty is one of the biggest discoveries in human reproductive biology in 30 years. Mutations in the receptor for kisspeptin cause humans and mice to fail to reach puberty and to be sterile. It is the first time since the identification of gonadotrophin-releasing hormone that a single gene is found to have such a dramatic effect on reproduction. This discovery opens new possibilities in the treatment of reproductive disorders such as delayed or advanced puberty, infertility and sex hormone-dependent cancers.

Animals↗

PubMed2004

Randomized, crossover comparison study of the short-term effect of oral testosterone undecanoate and intramuscular testosterone depot on linear growth and serum bone alkaline phosphatase.

AIM: To compare the effects of oral testosterone undecanoate (TU) 40 mg daily and intramuscular depot sustanon 50 (SUS), 4 weekly, on short-term growth and bone turnover. METHOD: Prospective, randomised, cross-over study over 26 weeks with 4 weeks of run-in, 8 weeks of treatment I (TU/SUS), 4 weeks of wash-out, 8 weeks of treatment II (SUS/TU) and 4 weeks of final wash-out. MAIN OUTCOME MEASURES: Weekly change in lower leg length (LLL) as measured by knemometry, i.e. LLL velocity (LLLV) and absolute bone alkaline phosphatase levels (bALP), as well as percentage change in bALP (%bALP). PATIENTS: Fourteen boys with delayed growth and puberty; two declined and one boy with sickle cell trait dropped out with priapism a week after SUS. The remainder had a median age of 14.3 years (range 12.5-17.4), testicular volume of 2 ml each (2-6), HtSDS of -2.1 (-3.3 to -1.0) and BA delay of 2.4 years (0.7-4.4). RESULTS: Median LLLV in the treatment blocks was 0.7 mm/wk (-0.27 to 2.2) and LLLV during the run-in and wash-out periods was 0.27 mm/wk (-0.3 to 0.6) (p <0.005). LLLV during treatment with TU and SUS was 0.51 mm/wk (-0.22 to 2.17) and 0.67 mm/wk (-0.27 to 2.2), respectively (NS). Median LLLV during the washout phases that followed the TU block and the SUS block was similar at 0.28 mm/wk (-0.1 to 0.6) and 0.3 mm/wk (-0.2 to 0.6), respectively. LLLV peaks and troughs that were related to the timing of the injection were more evident during SUS therapy. Median bALP during the run-in period was 94.2 U/l (16-282) and the median %bALP during this period was 1.2% (-57, 16). The main rise in bALP occurred during the treatment blocks with a %bALP of 19.3% (-28.8, 121.7) (p <0.005). Median bALP at the beginning and end of the SUS block was 99.7 U/l (51.7, 225) and 170 U/l (64.8, 273), respectively (p <0.05). Median bALP at the beginning and end of the TU block was 111 U/l (51, 287) and 127.6 U/l (66.4, 298) (NS). Median %bALP during SUS was higher than during TU at 28.1% (4.4, 121.7) and 11.8% (-28.8, 83.6) (p = 0.07). CONCLUSION: At the doses studied, testosterone undecanoate was as effective as sustanon at promoting short-term growth but changes in bone alkaline phosphatase were more marked during sustanon therapy.

Administration, Oral↗

PubMed1978

Preadolescent and adolescent endocrinology: physiology and physiopathology. II. Hormonal changes during abnormal pubertal development.

Based on the knowledge of the physiology of regulation of gonadotropins and gonadal steroids, basal levels of these hormones might be indicative of the etiologic factors of abnormal pubertal development. In addition, stimulatory tests may help in the diagnosis of such conditions. It is interesting that the pubertal maturation of the adrenal cortex is independent of the hypothalamic-pituitary-gonadal axis. The role of the adrenal cortex for the pubertal development remains questionable: adrenal androgens are low in isosexual precocious puberty, low in delayed adolescence, and normal in hyper- or hypogonadotropic hypogonadism. The importance of this role is doubled in congenital virilizing adrenal hyperplasia. When the disease is untreated, although adrenal androgens in excess advance bone age and hypothalamic maturation, girls remain prepubertal. When the therapeutic control is good, normal puberty occurs. The action of the adrenal androgens on growth and puberty remains to be determined.

Adolescent↗