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PubMed2006

[Primary amenorrhea: constitutional delayed puberty or hormonal disturbance].

Investigations were carried out in 2 women of 17 and 18 years with primary amenorrhea, normal external female genitalia and delayed secondary sexual characteristics, for the reasons for delayed puberty. The 17-year-old patient had reduced values of FSH, LH and oestradiol. This disturbance in the hypothalamo-hypophysary axis was caused by hydrocephalus. Menarche occurred following drainage of the fluid. The 18-year-old patient had raised values ofFSH and LH and a lowered oestradiol value. There was therefore a disfunction existing at ovarian level, which appeared to be caused by an XX-gonadal dysgenesis. The patient was treated with hormones which led to breast development and menarche taking place. The cause ofprimary amenorrhea can mainly be divided into three categories: constitutional delayed puberty, delayed puberty due to hypogonadotropic hypogonadism, or delayed puberty due to hypergonadotropic hypogonadism. A carefully taken medical history, together with determination of the serum levels of FSH and LH, is helpful in differentiating between these categories. Subsequently, structured clinical management must be performed in order to approach the differential diagnosis of each of these categories, which will then be followed by the final diagnosis.

Adolescent↗
PubMed2006

Munc18 plays an important role in the regulation of glutamate release during female puberty onset.

Munc18, a mammalian homolog of C. elegans Unc, is essential for neurotransmitter release. The aim of this study was to identify estrogen-dependent expression of Munc18-1 and its role in the regulation of glutamate release for puberty onset. Hypothalamic munc18-1 mRNA levels were significantly increased by estrogen treatment in ovariectomized, immature female rats. During pubertal development, the munc18-1 mRNA levels dramatically increased between the juvenile period and the anestrous phase of puberty. Intracerebroventricular administration of an antisense oligodeoxynucleotide against munc18-1 mRNA significantly decreased glutamate release and delayed the day of puberty onset. These results suggest that Munc18-1, expressed in an estrogen-dependent manner, plays an important role in the onset of female puberty via the regulation of glutamate release.

Animals↗
PubMed1978

[Animal experiment studies on the neurohumoral control of female puberty].

To study the mode of action of oestrogen in female sexual maturation, prepubertal female rats were treated in different ways with oestradiol benzoate (OB). Using an improved implantation method, former findings on a hypophysial site of oestrogen action in the positive feedback (Hohlweg effect) were confirmed. A single s.c. injection or intrahypophysial implantation of OB at 25 or 26 days of age induced precocious vaginal opening (VO) and one ovulation, but the subsequent ovarian cycle was significantly prolonged, so that the first spontaneous ovulation occurred only at the normal time of the onset of puberty. Further studies demonstrated that the sensitivity to the ovulation-inducing effect of oestrogen increases as the rats approach the age of puberty, and that the first pubertal ovulation can be suppressed by intrahypophysial, but not by intrahypothalamic implantation of progestereone. The conclusion is drawn that the precocious induction of one ovulation via the Hohlweg effect is not tantamount to an advancement of puberty. The results furthermore suggest that the positive oestrogen feedback forms the basis for the first pubertal ovulation as it does with regard to later cyclic ovulations. True acceleration of sexual maturation was achieved by daily injections of 0,05 microgram OB/100 g b.w. from 5 days of age to VO. In contrast to findings obtained by other authors in Sprague-Dawley rats, a shortened OB treatment from 26 days of age to VO was not effective in advancing the onset of puberty unless the rats had additionally been injected with OB from 5 to 10 days of age. A final experiment demonstrated that the first ovarian cycle was not prolonged after neonatal ovariectomy and implantation of ovaries at 24, 28 or 32 days of age. Thus, maturation of the neurohormonal mechanisms that are responsible for the cyclic ovarian function continues during the prepubertal development in the absence of ovarian steroids.

Age Factors↗
PubMed1988

Male-induced puberty acceleration in young female wild mice: hormonal regulation and source of pheromonal cue.

Experiments were designed to examine the influence of adult males on the rate of sexual maturation in young female wild mice. In one experiment, young females were raised in presence of adult males, adult females and in absence of any individual, while in another, they were exposed to urines of: (1) castrated males, (2) spayed females, (3) castrated and TP-treated males, (4) castrated and placebo-injected males. Female maturation as measured by age at vaginal opening and first vaginal oestrus was accelerated by presence of adult males, whereas presence of adult females considerably delayed the vaginal opening and the appearance of first oestrus in young females. In the other set of the experiments, urine from castrated or castrated and placebo-injected males was ineffective in inducing early puberty while urine from spayed females highly delayed the sexual maturation. By contrast, urine from castrated and TP-treated males accelerated the puberty more or less like normal males. The results indicate that male's chemosignal accelerating puberty in young females is present in urine and its production is under the control of androgens. However, the female-originating urinary pheromone which delays the puberty in young females is not regulated by ovarian hormones.

Animals↗
PubMed1981

Failure to demonstrate a significant influence of ovarian maturity on the onset of puberty in female rats.

Ovaries of 23- and 35-day-old rats were transplanted under the kidney capsules of 31- and 23-day-old females, respectively. The recipient rats were ovariectomized on the fourth day after transplantation, and the onset of puberty was recorded. Neither the age and body weight at vaginal opening and first ovulation nor the length of the first ovarian cycle differed significantly between the experimental rats and sham-transplanted or untreated controls. Estimation of the serum FSH an LH concentrations before and after ovariectomy provided no evidence that different gonadotropic responses had masked puberty-delaying or puberty-advancing effects of the implanted immature and prepuberal ovaries, respectively. The results suggest that the developmental stage of the ovaries is not a decisive factor in the control of the onset of female puberty.

Animals↗
PubMed1982

Influence of photoperiod on puberty in the female pony.

Thirteen 6-8 month-old fillies were assigned to 3 treatment groups: Group 1 had a 16-h fixed daily photoperiod (16L:8D, N = 4), Group 2 a daily photoperiod equivalent to ambient daylength (control, N = 5), and Group 3 a 9-h fixed daily photoperiod (9L:15D, N = 4). The light treatments extended from 17 December to 9 August. Hair shedding occurred first in Group 1 followed by Group 2, then Group 3. The proportions of fillies with 1 or more ovulations (puberty) by the end of the project were 2/4, 5/5, 2/4 in Groups 1, 2 and 3, respectively. The hypothesis that a fixed daily photoperiod which corresponded to maximum daylength at the summer solstice in temperate zones (16 h) would hasten puberty was not supported. Instead, the 16-h light treatment interfered with the attainment of puberty, as indicated by the reduced proportion of fillies ovulating, reduced numbers of ovulations, luteal bodies, and oestrous periods/filly, the extended intervals from the beginning of the project to the first ovulatory oestrus and the shorter period of oestrus. Hair coat changes were dissociated from changes in reproductive activity in Group 1. Puberty also appeared to be retarded in Group 3, but the results were less pronounced than those for Group 1.

Animals↗
PubMed1981

[Selection of laboratory rats for fertility components under conditions of estrus synchronization with Suisynchron-Praemix. 3. Results of puberty parameters].

The following results, in the context of puberty parameters, were recorded from laboratory rats, eight generations after Suisynchron-Prämix was begun to be used for synchronisation of oestrus, in studies on selection for fertility: -- Correlated success of selection in terms of earlier onset of puberty were found to exist in both oestrussynchronised and unsynchronised populations selected for fertility. The timing of both vaginal opening and first oestrus as well as weight parameters were affected. -- Earlier onset of puberty was interpreted as a consequence of elevated oestrogen level resulting from selection for fertility. -- Puberty characteristics were not influenced by synchronisation of oestrus.

Aging↗
PubMed1978

[Ovulation in gilts following biotechnical puberty induction and followed by ovulation stimulation].

Eighty gilts were slaughtered following different time intervals from biotechnical puberty induction, using 500 IU or PMS and 250 IU of HCG, and stimulation of ovulation, using 500 IU of HCG, 72 hours after puberty had been induced. The majority of those animals was found to have ovulated between 96 and 120 hours from puberty induction. Only 3.2 per cent of the follicles formed had undergone ovulation after 96 hours but as much as 94,0 per cent after 120. Not only had sexual maturity been reached by all animals, following the above treatment, but genuine superovulation was recordable from the first oestrus, with the average of formed follicles being 23.9. Stimulation of ovulation following puberty induction, therefore, is considered to be useful in providing favourable conditions for effective time-oriented insemination.

Animals↗
PubMed2025

Polycystic ovary syndrome and idiopathic central precocious puberty: two sides of the same coin?

PURPOSE: Several studies have reported an association between central precocious puberty (CPP) and a higher prevalence of polycystic ovary syndrome (PCOS), raising the hypothesis that CPP may act as an early-life indicator of increased PCOS risk. This review investigates the shared genetic, epigenetic, and environmental factors potentially underlying CPP and PCOS, with the aim of clarifying their connection and supporting advances in early detection and management. METHODS: A comprehensive literature review was conducted using the PubMed/MEDLINE database, prioritizing research from the past two decades, supplemented by key studies from earlier years. This research included studies on genetic and epigenetic factors, endocrine-disrupting chemicals (EDCs), and metabolic influences related to CPP and PCOS. Both original research and review articles were selected, focusing on the identification of pathophysiological mechanisms and risk factors linking these disorders. RESULTS: Genome-wide association studies (GWAS) have linked genetic variants in the kisspeptin and neurokinin B signaling pathways to increased gonadotropin-releasing hormone (GnRH) secretion, triggering early puberty. Moreover, increased GnRH pulsatility contributes to elevated luteinizing hormone (LH) levels, altered LH/follicle-stimulating hormone (FSH) ratios, and ovarian hyperandrogenism—key pathophysiological features of PCOS. Additionally, epigenetic modifications, particularly changes in DNA methylation at CpG sites, have been observed in both CPP and PCOS. A hyperandrogenic intrauterine environment and inadequate fetal growth contribute to prenatal epigenetic alterations, while postnatal factors such as obesity, insulin resistance, and exposure to EDCs further influence epigenetic modifications. Although insulin resistance and hyperandrogenism are central features linking CPP to PCOS, the precise mechanisms underlying these associations remain complex and not yet fully elucidated. CONCLUSIONS: Identifying shared genetic and environmental factors influencing early puberty onset and PCOS highlights the importance of close clinical monitoring in early life, though preventive interventions remain unproven. Further research is needed to clarify these mechanisms, which will support the development of more precise prevention and treatment strategies in clinical practice.

Humans↗
PubMed1997

Congenital adrenal hyperplasia complicated by central precocious puberty: linear growth during infancy and treatment with gonadotropin-releasing hormone analog.

Some children with congenital adrenal hyperplasia (CAH) develop true precocious puberty with early maturation of the hypothalamic-pituitary-gonadal axis. We have seen six such children who had the diagnosis of CAH with late initiation of corticosteroid treatment and/or poor compliance who developed central precocious puberty (CPP). These patients were treated with standard-dose hydrocortisone and fludrocortisone. Administration of depot leuprorelin (3.75 mg subcutaneously every 28 days) for 2 years or longer was effective in arresting the manifestations of puberty, decelerating the pretreatment growth velocity ([GV] 10.8 +/- 1.5 v3.65 +/- 0.95 cm/yr), increasing the predicted adult height ([PAHT] 147.5 +/- 7.8 v 153.4 +/- 8.3 cm), and decreasing the bone age to statural age ratio (1.26 +/- 0.13 v 1.16 +/- 0.09). Analysis of auxanological data during the first 2 years of life showed that linear growth was significantly accelerated and bone age was advanced in patients who developed CPP compared with 11 age-matched patients. It appears that proper glucocorticoid replacement to achieve adequate control of hyperandrogenemia during early life might prevent development of CPP in these patients. Gonadotropin-releasing hormone agonist (GnRHa) therapy can improve the final adult height, bringing it closer to that expected from the genetic potential.

Adrenal Hyperplasia, Congenital↗
PubMed1982

Studies on the gonadotropin secretion during sleep in patients with abnormal sexual development--the role of the CNS in the onset of puberty.

In order to evaluate the secretory patterns of luteinizing and follicle-stimulating hormones in various forms of abnormal sexual development, plasma levels of these hormones were measured every 20-30 minutes during sleep in 9 patients with true precocious puberty and 2 patients with primary hypogonadism. Seven patients with idiopathic precocious puberty and 2 patients with organic CNS lesion-related precocious puberty exhibited fluctuating plasma concentrations of these hormones that resembled findings in normal pubertal subjects who had significantly increased concentrations of plasma luteinizing hormone during sleep. Two patients with primary hypogonadism also showed episodic fluctuation of both hormones and augmented luteinizing hormone concentrations during sleep. These results suggest that the pubertal sleep-related gonadotropin secretion is dependent on the sleep-entrained CNS mechanism, and that the central nervous system plays an important role in sexual maturation.

Adolescent↗
PubMed2002

Delayed puberty.

Puberty is the acquisition of secondary sexual characteristics associated with a growth spurt and resulting in the attainment of reproductive function. Delayed puberty is diagnosed when there is no breast development by 13.4 years of age in a girl and no testicular enlargement by 14.0 years in a boy. The aetiologies are: (i) pubertal delay, either with constitutional delay of growth and puberty or secondary to chronic illness, and (ii) pubertal failure, with hypogonadotrophic (defect in the hypothalamo-pituitary region) or hypergonadotrophic (secondary to gonadal failure) hypogonadism, or both (secondary to radio/chemotherapy). The investigation includes: history, auxological data and pubertal development examination. Boys usually require treatment and, if they do not respond, investigation. In girls it is appropriate to measure the thyroid function and karyotype first and, if necessary, to offer treatment. If they present with dysmorphic features, or positive familial history, an assessment is required before treatment.

Adolescent↗
PubMed2002

Androgens and puberty.

Puberty is associated with an increasing production of androgenic steroids. Adrenal androgen formation, termed adrenarche, may precede gonadal testosterone synthesis. Both adrenal and gonadal androgens exert their biological effects via the androgen receptor, a nuclear transcription factor modulating a specific transcription regulation of largely unknown genes. During puberty, virilizing actions such as genital enlargement and sexual hair growth can be distinguished from anabolic action such as the gain in muscle strength and general changes in body composition. Furthermore, androgens play a major role in the initiation and maintenance of spermatogenesis. Thus, different androgenic steroids play an important role in the process of puberty. The control of their biosynthesis, their possible differential action on the molecular level, as well as the different target organs in males and females are discussed.

Androgens↗
PubMed1988

Effect of increased haemoglobin levels on growth hormone (GH) secretion in beta-thalassaemia major: differences between prepubertal subjects and patients with delayed puberty.

Basal and L-dopa-stimulated secretion of growth hormone (GH) was investigated in 10 patients with beta-thalassaemia major. Five patients were prepubertal (chronological age 8 to 12 years), whereas 5 patients had delayed puberty (chronological age 15 to 19 years). Ten normal prepubertal subjects (chronological age 8 to 11 years) served as the control group. Each thalassaemic patient was subjected to two L-dopa tests (0.5 g L-dopa plus 0.7 mg/Kg body weight propranolol, orally): one was performed under conditions of low haemoglobin (Hb) levels (30 days after the last blood transfusion), and the second in the presence of increased Hb concentrations (10 days after the transfusion of packed red blood cells). Before the transfusion of packed red blood cells, basal GH concentrations were significantly higher in the patients with delayed puberty (4.3 +/- 1.6 ng/ml), than in prepubertal thalassaemic (1.8 +/- 0.9 ng/ml, p less than 0.05) and control (1.9 +/- 1.0 ng/ml, p less than 0.02) subjects. In contrast, the pituitary responsiveness to L-dopa, expressed as the relative maximum response for GH (GH delta %), was significantly higher in the latter two groups (8.5-fold, p less than 0.05, and 10.9-fold, p less than 0.02, respectively). The transfusion of packed red blood cells increased significantly Hb concentrations in both groups of thalassaemic patients (prepubertal +27%, p less than 0.05, delayed puberty +33%, p less than 0.025, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2004

Final height after combined growth hormone and GnRH analogue treatment in adopted girls with early puberty.

BACKGROUND: Girls adopted from developing countries often have early or precocious puberty, requiring treatment with gonadotrophin-releasing hormone (GnRH) analogues. During such treatment, decreased growth velocity is frequent. AIM: To study whether the addition of growth hormone (GH) to GnRH analogue treatment improves final height in girls with early or precocious puberty. METHODS: Forty-six girls with early or precocious puberty (age < or =9.5 y) adopted from developing countries were randomized for treatment for 2-4 y with GnRH analogue, or with a combination of GH and GnRH analogue. RESULTS: During treatment, the mean growth velocity in the GH/GnRH analogue group was significantly higher compared to the control group. Combined GH/GnRH analogue treatment resulted in a higher final height: 158.9 cm compared to 155.8 cm in the GnRH analogue-treated group. Three out of 24 girls (13%) in the combined group and nine of the 22 girls (41%) treated with GnRH analogue alone attained a final height below -2 standard deviation scores (SDS). CONCLUSION: The difference between the two groups is statistically significant, and possibly of clinical importance. A future challenge is to identify a subgroup with clinically significant advantage of GH addition to GnRH analogue treatment. Being very short on arrival in Sweden and being short and young at start of treatment are possible indicators.

Adoption↗
PubMed1999

Effect of low-dose testosterone treatment on craniofacial growth in boys with delayed puberty.

Craniofacial growth was investigated in boys treated with low-dose testosterone for delayed puberty (> 14 years old; testicular volume < 4 ml; n = 7) and compared with controls (12-14 years; n = 37). Cephalometric radiographs, statural height and pubertal stage were recorded at the start of the study and after 1 year. Craniofacial growth was assessed by nine linear measurements. At the beginning of the study, statural height, mandibular ramus length, upper anterior face height, and total cranial base length were significantly shorter in the delayed puberty boys than in the controls. After 1 year, the growth rate of the statural height, total mandibular length, ramus length, and upper and total anterior face height was significantly higher in the treated boys than in the untreated height-matched controls (n = 7). The craniofacial measurements were similar in the treated boys as compared with the controls. These results show that statural height and craniofacial dimensions are low in boys with delayed puberty. Low doses of testosterone accelerate statural and craniofacial growth, particularly in the delayed components, thus leading towards a normalization of facial dimensions.

Adolescent↗
PubMed1986

Autonomous ovarian hyperfunction followed by gonadotrophin-dependent puberty in McCune-Albright syndrome.

A 5-year-old girl with the McCune-Albright syndrome presented with precocious puberty secondary to autonomously functioning ovarian cysts, followed by true central puberty. Progression from gonadotrophin-independent to gonadotrophin-dependent precocious puberty may occur from elevated sex steroid levels leading to the early maturation of the hypothalamic-pituitary axis.

Child, Preschool↗
PubMed2000

Progressive deceleration in growth as an early sign of delayed puberty in boys.

OBJECTIVE: To describe the prepubertal growth pattern in boys with delayed puberty. METHODS: Growth curves for height and height velocity covering the age range 4-14 years were constructed on the basis of retrospectively obtained data in 85 boys with delayed puberty, who attained a normal final height. RESULTS: Between the age of 4 and 14 years the height in this cohort progressively deviated from the normal reference. At the age of 4 years, the height SDS was already significantly lower (median -0.8; p < 0.001) and progressively diminished during childhood, resulting in a median height SDS of -1.1 at the age of 12 years (p < 0.001). The median final height of this cohort (-0.4) was not different from their target height (-0.2). The degree of deceleration in growth during childhood was not determined by birth weight or birth height and did not influence final height. The decline of the height velocity with age in this group of boys with delayed puberty was significantly smaller (p < 0.001) than predicted by the model of Rikken and Wit. CONCLUSION: Late-maturing boys often show a prepubertal deceleration in growth that starts at an early age but that does not affect final height.

Adolescent↗