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PubMed1985

Pulsatile gonadotropin-releasing hormone therapy in male patients with Kallmann's syndrome or constitutional delay of puberty.

The response to low-dose pulsatile gonadotropin-releasing hormone (GnRH) therapy was tested in three hypogonadotropic hypogonadal male patients and a boy with delayed puberty showing different luteinizing hormone responses (delta LH) to test doses of 25 micrograms GnRH intravenously before treatment. Four male patients, 16 to 20 years of age, three with Kallmann's syndrome and one with idiopathic delay of puberty, received 2 micrograms GnRH subcutaneously every 2 1/2 hours for 3 months by the use of the Zyklomat pump (Ferring GmbH, Kiel, FRG). In two patients with Kallmann's syndrome and decreased delta LH, serum testosterone did not increase during treatment, even after increasing the dosage and changing the route of administration (4 micrograms subcutaneously or 8 micrograms intravenously every 2 1/2 hours for 4 weeks with every dosage). The third patient with Kallmann's syndrome and the boy with delayed puberty, both with normal delta LH, presented normal serum testosterone after 3 months of subcutaneous low-dose treatment. The different responses to a GnRH test dose corresponding to the response to pulsatile GnRH therapy probably reflect different degrees of maturation of the pituitary gonadotrophs.

Eunuchism↗

PubMed2001

Treatment of delayed male puberty: efficacy of aromatase inhibition.

We hypothesized that inhibition of estrogen synthesis would delay maturation of the growth plates and ultimately result in increased adult height in boys with delayed puberty. We conducted a randomized, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone plus placebo (testosterone-placebo) or with testosterone plus letrozole (testosterone-letrozole). Letrozole effectively inhibited estrogen synthesis: 17beta-estradiol concentrations increased in the testosterone-placebo group, but in the testosterone-letrozole group, no such increase was observed until letrozole treatment was discontinued. After 1.5 years, bone age had advanced by 1.7 +/- 0.3 years in the testosterone-placebo group, but by only 0.9 +/- 0.2 years in the testosterone-letrozole group (p = 0.02). Predicted adult height did not change significantly in the testosterone-placebo group, whereas in the testosterone-letrozole group the increase was 5.1 +/- 1.2 cm (p = 0.004). Our findings suggest that, if estrogen action is inhibited in growing adolescents, adult height will increase. This observation provides a rationale for studies aimed at delaying bone maturation in several growth disorders.

Adolescent↗

PubMed1990

LH measurements by in vitro bioassay and a highly sensitive immunofluorometric assay improve the distinction between boys with constitutional delay of puberty and hypogonadotropic hypogonadism.

The basal and gonadotropin-releasing hormone (GnRH) stimulated levels of LH were measured in 21 boys with delayed puberty using conventional RIA, mouse interstitial cell in vitro bioassay (B-LH), and a highly sensitive immunofluorometric method (F-LH). On the basis of subsequent clinical follow-up, the subjects were diagnosed as idiopathic constitutional delay of puberty (CD, n = 13) or hypogonadotropic hypogonadism (HH, n = 8). The basal RIA LH levels were similar in the two diagnostic groups (HH, 2.92 +/- 0.76, CD 3.53 +/- 1.37 IU/L). In contrast, the mean basal B-LH was significantly lower in boys with HH than with CD (1.10 +/- 0.45 versus 2.91 +/- 1.23 IU/L; p less than 0.01). A similar finding was made by F-LH measurements which were clearly lower in the HH than the CD group (0.073 +/- 0.04 versus 1.71 +/- 0.97 IU/L, p less than 0.01). Also upon GnRH stimulation (3.5 micrograms/kg i.v.), the distinction between the CD and HH groups was better with the B-LH and F-LH measurements. The basal B/I ratio of the CD group (0.90 +/- 0.43) was more than that of the HH group (0.42 +/- 0.25, p less than 0.01) and this ratio increased significantly (more than 2-fold, p less than 0.01) during GnRH stimulation in the CD group, but not in the HH patients. Such differences were not found between the B/F ratios of the CD and HH groups. Measurements of basal and GnRH stimulated B- and F-LH levels clearly improved the distinction between CD and HH in comparison to the conventional RIA method, due to the low sensitivity and likely cross-reactions with some non-LH constituents of serum in the latter assay. This problem is, to a great extent, eliminated by better sensitivity and specificity of B-LH and F-LH measurements. For the same reasons, the difference in B/I ratios between the CD and HH samples, and the increased B/I ratio after GnRH stimulation in the CD group, were not observed in B/F ratios. In conclusion, the measurements of basal and GnRH-stimulated concentrations of serum B-LH and F-LH clearly improve the differential diagnostics between CD and HH. The discrepancies measured between the B/I and B/F ratios in these samples call for reevaluation of the bio/immuno ratios of circulating LH.

Adolescent↗

PubMed2006

The effect of a short-term delay of puberty on trabecular bone mass and structure in female rats: a texture-based and histomorphometric analysis.

Accrual of bone mass and strength during development is imperative in order to reduce the risk of fracture later in life. Although delayed pubertal onset is associated with an increased incidence of stress fracture, evidence supports the concept of "catch up" growth. It remains unclear if deficits in bone mass associated with delayed puberty have long-term effects on trabecular bone structure and strength. The purpose of this study was to use texture-based analysis and histomorphometry to investigate the effect of a delay in puberty on trabecular bone mass and structure immediately post-puberty and at maturity in female rats. Forty-eight female Sprague-Dawley rats (25 days) were randomly assigned to one of four groups; (1) short-term control (C-ST), (2) long-term control (C-LT), (3) short-term GnRH antagonist (G-ST) and (4) long-term GnRH antagonist (G-LT). Injections of either saline or gonadotropin-releasing hormone antagonist (GnRH-a) (100 microg/day) (Cetrotide, Serono, Inc.) were given intraperitoneally for 18 days (day 25-42) to both ST and LT. The ST groups were sacrificed after the last injection (day 43) and the LT groups at 6 months of age. Pubertal and gonadal development was retarded by the GnRA antagonist injections as indicated by a delay in vaginal opening, lower ovarian and uterine weights and suppressed estradiol levels in the short-term experimental animals (G-ST). Delayed puberty caused a transient reduction in trabecular bone area as assessed by histomorphometry. Specifically, the significant deficit in bone area resulted from a decreased trabecula number and an increase in trabecular separation. Texture analysis, a new method to assess bone density and structural anisotropy, correlated well with the standard histomorphometry and measured significant deficits in the density measure (M(Density)) in the G-ST group that remained at maturity (6 months). The texture energy deficit in the G-ST group was primarily in the 0 degrees orientation (-13.2%), which measures the longitudinal trabeculae in the proximal tibia. However, the deficit in the G-LT group was in the 45 degrees and 135 degrees orientations. These results suggest that any "catch-up" growth following the cessation of the GnRH-antagonist injection protocol may be directed in trabeculae oriented perpendicular to 0 degrees at the expense of trabeculae in other orientations.

Animals↗

PubMed2004

Serum androgen bioactivity in adolescence: a longitudinal study of boys with constitutional delay of puberty.

We have examined the relationship between serum androgen bioactivity, as measured with a recombinant cell bioassay, and progression of puberty in 14 boys with constitutional delay of puberty. Six boys were followed up without treatment (control group), and eight boys received low-dose (1 mg/kg) testosterone enanthate im for 0-6 months together with an aromatase inhibitor, letrozole, 2.5 mg orally once a day for 0-12 months (treatment group). In the control group, serum androgen bioactivity increased during the course of puberty (P < 0.001). During 0-12 months of the study, the boys in the treatment group had higher androgen bioactivity levels (P < 0.05) and faster rate of pubic hair growth than the control boys (P < 0.05). Overall, the average serum androgen bioactivity during 12 months of follow-up correlated strongly with the concomitant changes in Tanner genital (r(S) = 0.89; n = 13; P < 0.005) and pubic hair stages (r(S) = 0.79; n = 13; P < 0.01). In conclusion, our results suggest that circulating androgen bioactivity mediates the tempo of pubertal maturation and that the combination of testosterone and letrozole given to boys with constitutional delay of puberty accelerates puberty.

Adolescent↗

PubMed2005

Short-term delay of puberty causes a transient reduction in bone strength in growing female rats.

Multiple factors affect the structural development of the skeleton; in particular, estrogen levels during growth are an important factor in the pathogenesis of bone fragility. The delay of menarche and infrequent menstrual cycles decrease estrogen levels during adolescence and decrease peak bone mass. The aim of this study was to determine if delayed puberty through administration of a GnRH antagonist initiated prior to the onset of the first estrus cycle would delay the increase in estrogen levels and impede bone strength development in female rats. Twenty-three-day-old female Sprague-Dawley rats were randomly assigned to one of four groups; 1) short-term control group (C-ST) (n = 12), 2) long-term control (C-LT) (n = 12), 3) short-term GnRH antagonist group (G-ST) (n = 12) and 4) long-term GnRH antagonist group (G-LT) (n = 12). Injections (0.2 ml) of either saline or GnRH antagonist (100 microg/day) (Cetrotide, Serono, Inc) were given intraperitoneally for a duration of 18 days. Pubertal and gonadal development was retarded as indicated by a delay in vaginal opening (an indicator of pubertal onset), lower ovarian and uterine weights and lower estradiol levels in the short-term experimental animals (G-ST). However, at maturity (G-LT), there were no significant differences found in these measures. A delay in the timing of puberty significantly attenuated the development of femoral bone strength at 6 weeks of age. Peak moment, yield moment and stiffness in the G-ST group were all significantly less than the C-ST group. Cortical width was significantly attenuated due to the increased percentage of marrow area per total bone area in the G-ST group. However, femoral bone strength was recovered at maturity (G-LT). In summary, a transient delay in pubertal timing has short-term effects on bone strength development. In the current animal model of delaying puberty through GnRH antagonist injections, there appears to be no long-term effects on bone strength.

Animals↗

PubMed1998

Predictive value of serum follicle-stimulating hormone levels in the differentiation between hypogonadotropic hypogonadism and constitutional delay of puberty.

OBJECTIVE: Gonadotropin secretion was evaluated to predict hypogonadotropic hypogonadism (HH) in 36 children suspected of having HH. METHODS: LH was measured for 24 h at 10-min intervals, and FSH and estradiol or testosterone at 1-hour intervals. Twenty boys (age 15.7, range 13.2-19.3 years) and 16 girls (age 16.1, range 13.0-20.6 years) were studied. RESULTS: LH pulses were detected in 9 boys and 5 girls. HH was confirmed in all 11 LH apulsatile boys and in 8 of 11 LH apulsatile girls. Random FSH values of < or =1.11 and < or =2.86 IU/l in boys and girls, respectively, discriminated patients with LH pulses from patients without (sensitivity for lack of LH pulses 97 and 100%, respectively). In boys testicular volume was not discriminatory. In 1 girl LH pulses were observed without estradiol production, suggesting LH neurosecretory dysfunction. CONCLUSIONS: Low FSH levels in adolescence are strongly related to a lack of LH pulses. Lack of LH pulses is highly suspect for HH. FSH may be a tool in the differentiation between HH and delayed puberty.

Adolescent↗

PubMed1993

Serum levels of mullerian inhibiting substance in boys throughout puberty and in the first two years of life.

Serum levels of Mullerian inhibiting substance (MIS) have been measured in 91 boys throughout normal pubertal development. MIS levels fell sharply after pubertal stage 1 and were mostly undetectable at pubertal stage 6. The relationship between MIS concentration and pubertal stage was similar when compared with age. Seven patients with precocious puberty and 12 with delayed puberty were also investigated and found to have MIS levels consistent with their degree of pubertal development. Precocious puberty was associated with MIS levels that were abnormally low for age, while delayed puberty resulted in persistence of high MIS levels. Serum MIS levels were also measured in 29 boys less than 2 yr of age undergoing minor surgery. High levels were found throughout this time period, which is consistent with previous reports. MIS levels appear to be inversely related to levels of gonadotropins, steroids, and inhibin, which fall in the first 2 yr of life and rise throughout puberty.

Adolescent↗

PubMed1985

LH and FSH responses to GnRH in health and disease.

LH and FSH responses to intravenous bolus GnRH were evaluated in healthy men and women and in patients with various hypothalmo-pituitary disorders. Higher LH FSH responses to GnRH were recorded. In prepubertal girls FSH responses were higher than those of LH; however, while FSH responses remained unaltered through pubertal development stages 2-5, there was a progressive increase in LH response during that period. GnRH test was marginally useful in diagnosis of delayed puberty but more so in hypogonadotropic hypogonadism and true precocious puberty. In experimental hyperprolactinemia, GnRH induced a near normal LH response but caused an exaggerated FSH response, which was normalized after clomiphene treatment. GnRH test was found to be useful to assess pituitary reserve of gonadotropins in a variety of clinical situations involving hypothalamo-pituitary gonadal axis.

Acromegaly↗

PubMed2000

Molecular defects causing ovarian dysfunction.

The functions of the hypothalamic-pituitary-ovarian and -adrenal axes are intertwined, and molecular defects in either axis may cause ovarian dysfunction. Advances in molecular genetics have allowed new insights into the pathophysiology of ovarian disorders. Specific gene mutations causing delayed puberty and/or ovarian failure, and heterosexual or isosexual precocious puberty have recently been described. The molecular insights gained into ovarian dysfunction have already led to rational therapies for some of these conditions.

Aromatase↗

PubMed1986

Growth hormone response to thyrotropin-releasing hormone in children and adolescents: a reappraisal.

In normal subjects, thyrotropin-releasing hormone (TRH) is not involved in the control of growth hormone secretion. Paradoxical growth hormone (GH) responses to TRH have been described in acromegalic subjects and, recently, in some constitutionally tall children. To confirm this finding, we have examined the GH response to combined LHRH-TRH tests performed to assess the pituitary function of children with GH deficiency, tall stature before and during bromocriptine therapy, precocious or delayed puberty as well as in a group of patients of average height and normal bone age. Unlike prolactin, the GH "response" to TRH, in children followed longitudinally, is particularly heterogeneous with an unpredictable pattern of secretion in repeated tests. Over 90% of children display peaks of GH (greater than or equal to 5 ng/ml), of which 38% occur twice during the test period. Amplitude and frequency of GH peaks appear to be independent of height, chronological age or bromocriptine therapy. Secretory rate estimated by integrated surface area increases in parallel to sex steroids impregnation. The pattern of GH secretory episodes, the increase in mean GH secretion in parallel to the production of gonadal sex steroids and the failure of bromocriptine to affect GH secretion in constitutionally tall children allow to speculate that what is measured after TRH injection is normal spontaneous GH rhythm rather than a direct effect of TRH on GH secretion.

Adolescent↗

PubMed2006

Development and biological function of the female gonads and genitalia in IGF-I deficiency -- Laron syndrome as a model.

Laron syndrome (LS) or primary GH insensitivity is a unique human model to study the effects of congenital IGF-I deficiency. Within our cohort of 63 patients with LS, 15 female patients were regularly followed since birth or infancy, throughout puberty. We observed that they were short at birth, with small genitalia and gonads -- during puberty, developed delayed puberty but eventually reached between 16 and 19 1/2 years full sexual development. Reproduction is unaffected at a young adult age. It is concluded that IGF-I in concert with the sex hormones has a modulatory but not essential function on female sexual development and maturation.

Adult↗

PubMed1989

The metoclopramide test: a useful tool with the luteinizing hormone-releasing hormone test in distinguishing between constitutional delay of puberty and hypogonadotropic hypogonadism.

To evaluate the effectiveness of intravenous metoclopramide, alone or in combination with luteinizing hormone-releasing hormone (LH-RH), in distinguishing between constitutional delay of puberty and hypogonadotropic hypogonadism, 12 patients with constitutional delay of puberty and 10 patients with hypogonadotropic hypogonadism were studied. All patients received 10 mg/m2 of intravenous metoclopramide and 100 micrograms of intravenous LH-RH on separate days. The mean prolactin (PRL) response following metoclopramide was significantly higher in the constitutional delay of puberty group when compared with the hypogonadotropic hypogonadism patients (P less than 0.01 at 15, 30, 45, and 60 minutes); all patients with constitutional delay of puberty increased their PRL level to greater than or equal to 60 ng/ml, except one who had a peak PRL level of 38 ng/ml. While only 2 of the hypogonadotropic hypogonadism subjects reached a peak PRL concentration of greater than or equal to 60 ng/ml, 4 had peak PRL levels greater than 38 ng/ml. The mean LH and follicle-stimulating hormone (FSH) responses after LH-RH were significantly higher in the constitutional delay of puberty group (P less than 0.01 at 30, 45, and 60 minutes for LH and P less than 0.01 at 45 and 60 minutes for FSH). All constitutional delay of puberty subjects responded to both the metoclopramide and LH-RH tests, while patients with hypogonadotropic hypogonadism responded only to one or to neither of these tests. Therefore, while metoclopramide alone did not allow us to clearly distinguish constitutional delay of puberty from hypogonadotropic hypogonadism, the combined use of both of these stimuli permitted us to detect all subjects with constitutional delay of puberty.

Adolescent↗

PubMed1989

Seizure-induced delay of puberty in female rats: effects of age, stress and opioid antagonists.

We have shown that pre- and post-pubertal female rats are sensitive to seizures. For example, daily convulsions commencing at 24 days of age delay puberty. Here we examine the effect of seizures at various ages. In addition, because opioid peptides are implicated in regulating the onset of puberty and are activated by convulsions, we also investigate the effect of opioid antagonists in the seizure-induced delay of puberty. A single daily electroconvulsive shock (ECS) was given for 10 days to neonatal (days 2-11), infantile (days 15-24) and juvenile (days 22-31) rats. The treatment delayed vaginal opening (VO) in juvenile rats. Neonatal and infantile rats were unaffected. VO was also delayed by daily ECS for only 5 days in the late juvenile (days 27-31) period. The opioid receptor antagonists naloxone, naltrexone and nalmefene injected before and after single daily ECS were unable to block this effect of ECS on VO. To examine whether the effect of ECS is related to stress, we examined several stressors known to induce opioid-mediated alterations in gonadotrophin secretion. Footshock, immobilization and ether stress administered in the juvenile period (days 27-31) did not affect the timing of VO. In addition, rats anaesthetized with halothane, and then given ECS, still showed a delay of VO. These data demonstrate that rats in the late juvenile stage of development are most sensitive to convulsions. We also suggest that opioids are not critical to the mechanism by which the ECS disturbs puberty, and that ECS elicits its effect seemingly independently of the convulsive stress.

Aging↗

PubMed1999

[Algorithms for the initial management of precocious or delayed female puberty].

An algorithmic approach is proposed for the initial management of disorders of female puberty: premature pubarche and precocious or delayed breast development.

Adolescent↗

PubMedDate not supplied

[The characteristics of the sexual development of boys suffering from obesity].

RIA tests to determine the blood levels of gonadotropins, prolactin and different fractions of androgens have shown that the time course of the endogenous level of gonadotropins and androgens in boys aged 9 to 16 with Il-III degree of obesity without clinical signs of disturbed puberty is of the same type as that in healthy boys. However much lower concentrations of testosterone and FSH with a high level of LH and dehydroepiandrosterone were noted in the former. A single administration of chorionic gonadotropin has shown that in normal puberty first develops a mechanism of rapid excretion of testosterone into blood with its maximum concentration in 24-48 h, followed by the development of a mechanism of long-term activation of androgenesis at later stages of puberty. Obese boys with delayed puberty after the type of adiposogenital dystrophy or the syndrome of wrong puberty, demonstrate a more marked blood level of testosterone and FSH than in normal puberty. The clinical level of delayed puberty is determined by the peculiarities of the hypothalamohypophyseal system: the syndrome of wrong puberty is characterized by a sharp rise of adrenal androgenesis leading to premature pubarche, a decrease in the sensitivity of gonads to LH with a simultaneous rise of its blood concentration. Moderate activation of androgenesis in the adrenal glands was observed in false adiposogenital dystrophy, the prepubertal level of LH secretion being preserved.

Adolescent↗

PubMed2002

Leuteinizing hormone responses to leuprolide acetate discriminate between hypogonadotropic hypogonadism and constitutional delay of puberty.

OBJECTIVE: To assess if leuprolide acetate stimulation discriminates between hypogonadotropic hypogonadism (HH) and constitutional delay of puberty (CDP) in males. DESIGN: Case-control study. SETTING: Patients attending an academic research environment. PATIENTS: Only male patients were studied: 10 with HH (group 1, age 16.5 +/- 6.0 years), 8 prepubertal with CDP (group 2, age 14.3 +/- 1.2 years), 6 healthy prepubertal (group 3, age 9.5 +/- 3.3 years), and 8 healthy late-pubertal (group 4, age 15.1 +/- 3.1 years). INTERVENTION(S): Blood samples were obtained after an overnight fast. Leuprolide acetate was then administered SC, and blood samples were drawn at 0, 30, 60, 120, 180 minutes, and 6 and 24 hours after stimulation. MAIN OUTCOME MEASURE(S): Clinical follow-up evaluations of data and serum levels of LH, FSH, 17-hydroxyprogesterone, and testosterone. RESULT(S): Basal LH levels were similar in groups 1 through 3 and differed significantly from those in group 4. Peak serum LH levels were significantly higher in CDP compared with HH (8.9 +/- 1.4 vs. 1.4 +/- 0.2 IU/L). Baseline FSH levels were significantly higher only in pubertal boys (versus the HH group); peak levels did not differ among the groups. Basal and peak testosterone levels were significantly higher only in the control pubertal group when compared to the other groups; peak 17-hydroxyprogesterone concentrations were significantly higher in pubertal controls compared with HH and CDP. CONCLUSION(S): Peak LH responses clearly discriminate HH from CDP. Timing for blood sampling should be fixed at 0, 60, 120, 180 minutes after stimulation.

17-alpha-Hydroxyprogesterone↗

PubMed2002

Putative effects of endocrine disrupters on pubertal development in the human.

Pubertal development is regulated by gonadotrophins and sex hormones. There has been a clear secular trend in the timing of puberty during the last century, puberty becoming earlier. Although improved nutrition is assumed to be the cause, this could partly be associated with exposure to so-called endocrine disrupters. Precocious puberty has been described in several case reports of accidental exposure to oestrogenic compounds in cosmetic products, food and pharmaceuticals. Local epidemics of premature thelarche have also been suggested to be linked to endocrine disrupters. Children adopted from developing countries to industrialized countries often develop precocious puberty. Not only precocious puberty, but also delayed puberty can, theoretically, be associated with exposure to endocrine disrupters. While it is very plausible that endocrine disrupters may disturb pubertal development, there is very little research on this and, therefore, we do not yet have any clear cause-effect relationships in humans.

Adolescent↗