Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PUBERTY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed1976

[Urocytogram and precocious puberty].

After a review of the technique of urocytogram the authors report the results obtained in 39 children between the ages of 3 and 12 years. Before the appearance of the first signs of puberty, urocytograms are similar in both girls and boys. Differences were seen in seven cases of male or female precocious puberty. Urocytograms are also different in patients with incomplete precocious puberty but less marked than in those with true precocious puberty. The authors consider the possibility of repeat urocytograms during the supervision or treatment of incomplete and complete precocious puberty.

Brain Neoplasms↗
PubMed2002

[Biophysical parameters of early puberty in girls].

OBJECTIVE: The appearance of breast development in girls characterizes an early period of puberty. Ultrasonographic examinations of the uterus and ovaries make possible the estimation of first pubertal changes in sexual organs. DESIGN: The aim of this work was to study the clinical and ultrasonographical features of early puberty in girls. MATERIAL AND METHODS: 33 healthy girls were observed quarterly in the course of prepuberty. Body mass, height, body mass index (BMI), quantity of adipose tissue were investigated. Stage of puberty was established according to Tanner. The uterus and ovaries were studied ultrasonographically, and the volume of the uterine body, length of the cervix and ovarian volume and size of ovarian follicles were scrutinised. RESULTS: Statistical differences were observed in weight, height, quantity of adipose tissue and the volume of body and that of the uterus, in length of the cervix between prepuberty and early puberty periods. Luminastity of mucus in the cervical canal in half of girls in the breast stage M1 was obtained. CONCLUSION: Ultrasonographic investigations of internal sexual organs with estimation of clinical sexual features are helpful in examination of early stage of puberty.

Adolescent↗
PubMed2003

The CYP3A4*1B variant is related to the onset of puberty, a known risk factor for the development of breast cancer.

Breast development, one of the first signs of puberty, is closely associated with age at menarche; and early menarche is in turn a well-established risk factor for female breast cancer. We examined the relationships between the onset of puberty and gene variants for certain enzymes that regulate hormone metabolism among 137 healthy nine-year-old girls from two pediatric clinics. High-activity CYP17 alleles, involved in estrogen formation, and high-activity CYP1A2 and CYP1B1 alleles, whose gene products metabolize estradiol, were not associated with pubertal stage. High activity CYP3A4, but not CYP3A5, which primarily metabolizes testosterone, showed a striking association with the onset of puberty (adjusted odds ratio, 3.21; 95% confidence interval, 1.62-6.89 for the genotype 0-1-2 rapid alleles). Of the homozygous CYP3A4*1B/1B girls, 90% had reached puberty; whereas, for the low-activity homozygous CYP3A4*1A/1A individuals, only 40% had done so. In heterozygotes, 56% had reached puberty. CYP1B1, CYP3A4, and CYP3A5 rapid variants were more common in African-American than in Hispanic or Caucasian girls.

Alleles↗
PubMed2003

Basal luteinizing hormone/follicle stimulating hormone ratio in diagnosis of central precocious puberty.

BACKGROUND: Precocious puberty is characterized by breast development in girls prior to 8 years old and may have acne, adult odor, growth spurt and menstruation. Conventionally, gonadotropin releasing hormone (GnRH) stimulation test is a gold standard for diagnosis of central precocious puberty but it is a time-comsuming procedure that is not practical on an out patient basis. OBJECTIVE: To evaluate the basal luteinizing hormone (LH)/follicle stimulating hormone (FSH) ratio in diagnosis of central precocious puberty in order to save time and cost. SUBJECTS AND METHOD: The GnRH stimulation tests were performed on 51 girls with breast development before 8 years old. The 51 girls were divided into 2 groups, 24 girls with central precocious puberty (CPP) and 27 girls with premature thelarche (PT), and the clinical data and GnRH stimulation tests data were compared between the 2 groups. The authors also compared the clinical data and GnRH stimulation tests data between 13 girls with PT and 12 girls with thelarche variants (TV) who developed puberty approximately 1 year later as confirmed by GnRH stimulation test. RESULTS: Girls with CPP had a large bone age and chronological age ratio and advancement of breast staging. Girls with TV had a greater level of basal luteinizing hormone (LH), peak LH and 120 min estradiol than girls with PT. Basal luteinizing hormone and follicle stimulating hormone (FSH) ratio greater than 0.2 can be used to diagnose CPP with 75 per cent sensitivity, 85 per cent specificity, 82 per cent positive predictive value (PPV) and 82 per cent negative predictive value (NPV). CONCLUSION: Girls with CPP have a basal LH/FSH ratio greater than 0.2 and this can be used as a cut-off point for the diagnosis CPP.

Child↗
PubMed2005

A novel mutation of estrogen receptor gene detected in girls with precocious puberty.

Female precocious puberty is caused by premature activation of the hypothalamic-pituitary-gonadal axis, exposure to exogenous sex steroid hormones, and the presence of endogenous sex steroids caused by various factors. Estrogen is the final key factor to start onset of puberty. However,in some cases of precocious puberty in girls estrogen elevation could not be detected. The raised sensitivity of estrogen receptor, which may caused by ESR1 mutation or polymorphism, has been frequently mentioned for interpreting the etiology of sporadic low estrogen type cases. But no case evidence has been found in clinical practice. For the purpose of screening possible mutations in estrogen receptor gene, leukocyte genomic DNA were collected from 16 girls with precocious puberty of sporadic low estrogen,and exons of ESR1 were amplified and analysized using PCR-SSCP/silver staining method. A single strand conformation change in exon 8 was found in one of the patients (No. 14). The suspected fragment were cloned to a T vector and sequenced for analysis. Sequencing of these clones revealed that this conformation change is caused by a C to T transition. This mutation results in the replacement of arginine by cystine at position 548 of ESR1 protein. The mutation created an extra Btsl digest site and made it can be readily identified by PCR-PFLP method. Further detection using this method, and sequencing of cloned exon8 colonies from patients proved that the patient No. 14 is Arg548/Cys548 heterozagous in genotype. This mutation increased hydrophobility of the area dramatically. The position and the conservative of this residue in vertebrates suggested Arg548 may play an important role in ESR1 function. For study the role of this mutation in the onset of precocious puberty, a firefly luciferase reporter plasmid pGL3-promoter-ERE was constructed,and a pCR3. 1-hermut pisimid expressing Cys548 ER was constructed based on wild type pCR3. 1her. Co-transfection of reporter and pCR3. 1 -hermut in CMF-7 cell strain proved that Cys548 mutant can significantly increase the transcription activity over the Arg548 wild type.

Amino Acid Substitution↗
PubMed2006

[Precocious puberty and von Recklinghausen's disease].

Von Recklinghausen's disease belongs to a group of neurocutaneous syndromes and is characterised by skin, nerve and bone abnormalities. We present a case of von Recklinghausen's disease and precocious puberty in 7-year-old boy. At the age of three café au lait spots on the skin and an incranial tumour situated near the optic chiasm--qualified as inoperable--were discovered. At the age of 7 first signs of precocious puberty appeared (pubic hair P3 and enlargement of the testes (15 ml) and penis). Laboratory measurements included: LH 7.5 mIU/ml, FSH 1.1 mIU/ml, testosterone 183 ng/ml, assessment of bone age: 9 years. The response to LHRH stimulation was characteristic for true precocious puberty (LH 15.9 mIU/ml and FSH 1.5 mIU/ml after 30 minutes). The MRI of the brain showed a tumour of the suprasellar region with compression of pituitary stalk. True precocious puberty was diagnosed. Treatment with Diphereline was introduced. At present the boy is 9 years old and has been treated with Diphereline for 16 months. The volume of the testicles has decreased to 7 ml and loss of pubic hair was noted. The MRI does not show any progression in tumour growth. The authors would like to underline the need of close observation of children with von Reclinghausen disease with regard to possibility of uncovering true precocious puberty which is critical for rapid diagnosis and introduction of correct treatment.

Child↗
PubMed1980

Age at first conscious ejaculation: a milestone in male puberty.

The age of occurrence of the first conscious ejaculation was registered in 263 boys belonging to two categories: (1) 128 boys (70 normal controls, 22 boys with unilateral cryptorchidism with normal puberty, and 36 boys with delayed puberty) who had been under regular follow-up throughout puberty. All underwent a complete physical examination at intervals of 3 to 6 months, and in most a wrist X-ray was made within three months of the first ejaculation. (2) A group of 135 boys examined and questioned at their school served as additional controls. Eighty of these reported ejaculations. Despite a wide range in the chronological age at occurrence of the first conscious ejaculation, the mean bone age in all groups, including that with delayed puberty, was 13 1/2 +/- 1/2 years (SD), with a range between 12 1/2-15 1/2 years. There was no correlation between the age at first ejaculation and testicular volume, pubic hair or penis length. It is proposed that the age at the first conscious ejaculation be used as an index of maturation in male puberty.

Adolescent↗
PubMed1984

Intellectual function of girls with precocious puberty.

The IQ of 52 girls with precocious puberty (mean age 9.5 +/- 2.8 years) was compared with that of 51 normal matched control subjects (mean age 9.7 +/- 2.8 years) and with that of eight girls with fast puberty (onset at normal age but accelerated advancement). Girls with precocious puberty had a significantly higher verbal IQ score than the control subjects but no difference was found in the performance score. The distribution of the verbal IQ score in the girls with precocious puberty was skewed toward the upper side of the theoretical distribution curve. The distribution was two or more times the expected theoretical percentile in the above average area (greater than 110, 56.9% v 25%), and five times more in the very superior area (greater than 130, 10.1% v 2.2%). The girls with fast puberty had the same behavior as the population with normal development. The results are interpreted as possible evidence of an effect of sex hormones on brain development, especially on the left hemisphere, during the prepubertal period.

Adolescent↗
PubMed1982

[Precocious puberty. Comment on the diagnostic conditions and etiological aspects].

The present review is based on the retrospective study of 124 children with precocious puberty, 92 girls and 32 boys. In girls, the analysis of the clinical initial presentation has shown that premature pubarche (n = 18), premature adrenarche (n = 2) or isolated menstruations (n = 3) must be ruled out, as these symptoms can remain isolated for more than a year. However, in most cases the presence of growth acceleration and vaginal estrogenisation was of major diagnostic value. Bone maturation, although generally accelerated, can be normal in recently developed puberty. Precocious puberty may proceed by steps, with complete disappearance of physical signs in the intervals. Organic causes were found in 31% of the girls, and 44% of the boys with some characteristic features as rapid progression, and elevated LH response to LRF stimulation. Main causes were glioma of the optic chiasma (n = 11), 3rd ventricule invasive tumors, hamartoma (n = 8). The latter should be looked for by a non invasive procedure as the CT scan. In girls, precocious puberty with very high circulating estrogen levels was observed as part of a McCune-Albright syndrome. As the effect of precocious puberty on the final adult height is variable, the evaluation of therapeutic results remains uncertain. Medroxyprogesterone as well cyproterone acetate have not been fully efficient in controlling bone maturation. More recently, and still controversial, the treatment with long acting LRF analogues might provide a more satisfactory statural prognosis.

Bone Development↗
PubMed1980

[Puberty in congenital hypothyroidism (author's transl)].

Puberty was studied in 95 patients with congenital hypothyroidism treated between 1953 and 1977 from the first months or first year of life. Pubertal abnormalities were observed in 13 cases: 1. Delayed puberty in 11 cases (late diagnosis in 6 cases, insufficient treatment in 2 cases, delayed puberty in the family in 1 case). 2. An amenorrhea-galactorrhea syndrome was observed in two cases with insufficient treatment. In the other cases, the outcome of puberty seemed within the normal range. However a careful study showed: 1st. A delay of every stage of puberty, 2nd. The absence of the peak of high velocity in some cases. 3rd. The age of menarche was 13 years 8 months (9 years 1 month-16 years 6 months) (normal girls: 13 years). Final height was dependent upon an early and efficient treatment, and upon a fast catch up of growth and bone maturation.

Adolescent↗
PubMed1976

Clinical use of the LH-RH in assessing gonadotropic reserve in children with idiopathic precocious puberty, premature thelarche and premature adrenarche.

Serum LH and FSH were assayed in 31 girls with normal pre puberty, precocious puberty, premature thelarche, and premature adrenarche, aged 2 to 9 years. The effect of synthetic luteinizing hormone-releasing hormone (LH-RH) on serum gonadotropins was evaluated in eleven of them. In all girls with precocious puberty, serum LH was increased up to high levels. The mean releasable LH in two girls with idiopathic precocious puberty was significantly greater than in normal prepubertal or pubertal children. Basal FSH in children with precocious puberty was within the limits of normal prepuberal children, and FSH secretion in response to LH-RH was not significantly greater than in the group of normal prepubertal and pubertal girls. In children with premature thelarche and premature adrenarche, basal levels of LH and FSH, as well as gonadotropin response to LH-RH were in the prepubertal range. These preliminary results show that the LH-RH test might be of clinical value in differenitating abnormal puberal development.

Age Factors↗
PubMed1994

Update on therapy for precocious puberty.

The onset of pubertal development before age 8 years in girls or 9 years in boys indicates precocious puberty. The numerous causes of precocious puberty can be classified as central or peripheral. CPP arises from premature activation of the hypothalamic-pituitary axis; therefore, it has hormonal and physical characteristics similar to normal puberty. PPP results from production of sex steroids independent of the hypothalamic-pituitary axis. All types of precocious puberty are characterized by rapid growth and skeletal advancement, leading to the paradox of the tall child becoming a short adult secondary to early epiphyseal fusion. The choice of therapy for precocious puberty is dependent on the underlying etiology with differing strategies employed for central and peripheral causes (Table 3). Long-acting GnRH-a provide effective, selective, and reversible therapy for CPP. GnRH-agonists are not effective in PPP; however, other agents such as testolactone, spironolactone, and ketoconazole can be used to manage the premature sexual maturation associated with these conditions.

Adolescent↗
PubMed1994

[Long-term therapy of true precocious puberty in girls using Decapetyl-Depot, a superactive gonadoliberin agonist in depot microcapsulated form].

Within the framework of an international prospective multicentre study 93 girls with gonadotropin-dependent precocious puberty were treated with Decapeptyl-Depot LHRH agonist (75 micrograms/kg, once a month by the i.m. route). This treatment led to prompt, immediate and long-term suppression of the pituitary-ovarian axis with subsequent regression of premature onset of secondary sex signs, to the arrest of premature menstruation, to normalization of the pathologically accelerated growth and inhibition of the accelerated bone maturation. This improved the mean expected growth during the first four years of treatment from 159 to 165 cm (p < or = 0.01). Concurrently in the majority complete normalization of the severely impaired mental condition of the affected girls due to the premature onset of puberty occurred (mean onset of puberty -4.5 years). Selective suppression of the pubertally increased gonadotropin secretion was even after prolonged treatment fully reversible after termination of treatment with a subsequent onset of normal puberty and cyclic ovarian activity. Undesirable side-effects and antibodies against Decapeptyl were not detected, the local tolerance of the injected microcapsules was satisfactory. GnRH agonists in depot form are becoming, due to their superior suppressive action incl. that on bone maturation, the drug of choice in long-term treatment of central precocious puberty as they are the first which mitigate or can prevent, if treatment is started in time, a final small stature which frequently is the greatest handicap for a life-time (frequently associated with adverse bodily disproportions).

Child↗
PubMed1996

The GH/IGF-I axis in puberty.

Puberty, either spontaneous, precocious or pharmacologically induced has profound effects on the physiology of the GH/IGF-I axis. Both spontaneous and stimulated GH secretion increase with puberty. The increase in spontaneous GH secretion is the result of increased GH pulse amplitude rather than frequency, and is probably an oestrogen-dependent effect. Parallel to the increase in GH secretion at puberty, circulating IGF-I and IGF binding protein-3 also increase. The pubertal increase in IGF-I correlates with stages of puberty as well as sex steroid levels. Circulating immunoreactive GHRH also increases with puberty, while circulating GH-binding protein levels are not affected by sexual maturation. Several data suggest an important role for the GH/IGF-I axis in the pubertal growth spurt. More recent data, however, have provided evidence of an important role for gonadal hormones in promoting adolescent growth independent of GH.

Adolescent↗
PubMed1997

[Endocrinological mechanism of puberty in men].

Puberty is a developmental stage during which endocrinological, physical and psycho-social changes proceed. During prepubertal period, hypothalamic-pituitary-gonadal axis is maintained in an inactive state by negative feedback regulation or inhibitory function of central nervous system. The onset of puberty and sexual maturation are gained by the alternation of these inhibitory system. In recent years, highly sensitive techniques for evaluating the hormones of hypothalamic-pituitary-gonadal system have been developed. And many explorations of the hormonal mechanisms of puberty have been achieved. In this chapter, hormonal changes in puberty is reviewed, and mechanism of puberty in men is discussed.

Adolescent↗
PubMed1997

[Constitutional delay of growth and puberty in male].

Constitutional delay of growth and puberty (CDGP), featuring short stature, delayed puberty and delayed bone age, is the most common condition in pediatric endocrine clinic and becomes an important differential diagnosis in boys with short stature. The conventional management is to assure eventual development of puberty and normal final stature. Treatment with androgens to induce secondary sex characteristics is given only when the boy is under psychosocial stress. Recent reports revealed poor final height outcomes. The results of growth hormone treatment in idiopathic short stature, including CDGP, has not been successful. New findings showed that adults with a history of delay puberty had significant osteopenia and may have a risk of fracture, and that suppression of spinal growth was closely related to pubertal delay, leading to short stature. These two facts suggest the necessity of induction of puberty in normal timing.

Adolescent↗
PubMed1986

Endogenous opioid inhibitory tone on LH secretion in normal puberty and in several pubertal disturbances.

To further evaluate the role exerted by endogenous opioids on LH secretion a naloxone challenge (0.08 mg/Kg b.w. i.v.) was performed in 23 healthy children at different stages of puberty, in 5 adolescents in different period of menstrual cycle, in 3 case of idiopathic precocious puberty (PP), in 7 cases of delayed puberty (DP), in 4 females affected by hypogonadotropic hypogonadism (HH) and in 6 patients affected by polycystic ovary disease (PCOD). Naloxone does not induce any significant change on LH plasma levels in prepubertal healthy children and in all the cases of PP and DP. Similarly there was no LH response in healthy adolescents neither in HH nor in PCOD, the response to naloxone appears only in preovulatory and luteal phases. These data indicate that the central opioid system regulating LH secretion in humans is active only at more advanced stages of puberty and it does not seem to play a role in the beginning of sexual maturation. Moreover gonadal steroids seem to play a fundamental modulatory role on opioid-controlled LH secretion.

Adolescent↗
PubMed1999

Disorders of puberty.

Normal puberty begins between eight and 14 years of age in girls and between nine and 14 years of age in boys. Pubic hair distribution is used to stage puberty, along with breast size and contour in girls and testicular volume in boys. Some children experience constitutional sexual precocity, but precocity is likely to be pathologic if it occurs in very young children, if there is contrasexual development or if the sequence of normal pubertal milestones is disrupted. Delayed puberty may be constitutional, but pathologic causes should be considered. The etiology of a pubertal disorder can often be determined with the use of a focused medical history, a directed physical examination and appropriate diagnostic tests. Treatment for disorders of puberty is determined by the underlying cause.

Adolescent↗