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PubMedDate not supplied

Association study of six activity SNPS in adrenal steroid hormone metabolism and IBM related genes with precocious puberty in Chinese girls.

OBJECTIVES: In order to investigate whether the variances in the candidate genes (Insulin receptor substrate IRS-1, beta3-adrenergic receptor ADRB3, 3 beta-hydro-xysteroid dehydrogenase HSD3B2, glucocorticoid receptor GRL and 21-hydroxylase CYP21) which affect the metabolism of adrenal steroids hormone and body composition, are associated with precocious puberty in Chinese girls. METHODS: PCR-RFLP analysis method was applied in the typing of six activity SNPs in five genes in two groups: 176 precocious puberty girls as case and 192 healthy girls as control. RESULTS: The typing results showed that the frequencies of the allele CYP21 L282 polymorphism were 32.7% and 32.6% in case and control groups (P=0.518), respectively. For IRS-1 R972, they were 0.6% in cases and 2.3% in controls (P=0.043), for ADRB3 R64, 13.6% in cases and 12% in controls (P=0. 378), and for GRL S363, 7.4% in cases and 5.73% in controls (P=0.335). No sample in the two groups carries the variation of CYP21 I172N and HSD3B2 L236S. CONCLUSION: Among these six activity SNPs in five candidate genes, IRS-1 972R was statistically associated with the onset time of puberty in Chinese girls. In order to confirm whether the candidate genes have any other activity SNPs that are associated with the onset time of puberty in Chinese girls, resequencing of these candidate genes is needed in following time.

3-Hydroxysteroid Dehydrogenases↗
PubMed2006

How do environmental estrogen disruptors induce precocious puberty?

Puberty is regulated by the endocrine system. Disruption of that system by exposure to environmental hormone-mimicking substances (i.e. endocrine disruptors) may, therefore, affect this development profoundly. There has been a great secular trend in the earlier timing of puberty such as both puberty onset and menarche age. This is apparently caused by environmental factors such as improved socioeconomic status, better healthcare and improved nutrition. However, part of the phenomenon could be associated with exposure to endocrine disruptors that have intrinsic estrogen activity or increase endogenous sex hormone levels. These estrogen pollutants tend to degrade slowly in the environment, to bioaccumulate in the food chain and to have long half-lives in humans. Because most of environmental chemicals, called estrogen disruptors or xenoestrogens, are toxic and estrogen/antiandrogen active, they can disregulate hypothalamic-pituitary-gonadal axis potentially inducing reproductive disorders. There are several case reports of accidental exposure to estrogenic compounds in cosmetic products, food and pharmaceuticals. The outbreak of epidemics of premature thelarche in some geographical areas has also been suggested to be linked to exposure to estrogen disrupters such as dioxins, furans and organohalogens. We review data on adverse health and reproductive outcomes have been attributed to estrogen disruptors in laboratory animals and in wildlife as well as in humans, specially focusing on the puberty timing.

Age Factors↗
PubMed2006

[Precocious puberty].

Precocious puberty is usually defined as the appearance of secondary sexual development before the age of 8 years in girls and 9 years in boys. Precocious puberty is a heterogenous condition generally divided into central and peripheral forms driven respectively by hypothalamic-pituitary axis or by excessive production of sex steroids. Taking into account the risk associated with the underlying disorder as well as the impact of precocious puberty on stature growth and development of reproductive and mental functions, this condition has important consequences for affected children and their families. In this paper, the pathophysiology, clinical presentation, laboratory and radiological features, and treatment of the disorders leading to precocious puberty are reviewed. Particular attention is devoted to the results of the recently published studies.

Child↗
PubMed1989

[Study on cases of precocious puberty].

Two boys and one girl with idiopathic precocious puberty were treated with medroxyprogesterone acetate (MPA) for 2 years and 2 months to 9 years and 5 months, and its efficiency was evaluated. Treatment with MPA suppressed the gonadotropin levels, the signs and symptoms of patients with precocious puberty, and also had a suppressive effect on bone-age advance, so these patients showed almost normal growth in height. There has been controversy about the age when treatment for idiopathic precocious puberty should be finished. Our data suggested that the treatment should be stopped at 11-13 years when patients reach the age of puberty.

Adolescent↗
PubMed1989

Calcium homeostasis and mineralization in puberty.

Calcium homoeostasis and bone mineralization have been the subject of many studies, but few have dealt with these aspects specifically in puberty. The main observations in our own studies - together with those in other recent reports - are summarized below. According to the aims of the present survey (Chapter 1) the results are grouped as follows: BLOOD MINERAL HOMOEOSTASIS AND ALKALINE PHOSPHATASE. The serum concentrations of calcium, total or ionized, remain remarkably constant throughout puberty, which probably reflects the important functions of the calcium ion. Serum phosphate, however, remain high in childhood, increase slightly with acceleration of growth and pubertal development and the levels then decrease toward adult values. Consequently, the pattern of the product of serum calcium and phosphate, essential for mineralization, follows that of phosphate. Serum magnesium does not change during puberty. The serum concentrations of alkaline phosphatase increase with acceleration in linear growth and pubertal development which has to be taken into consideration, in evaluation of changes in serum AP. Changes in osteoblastic activity, as expressed by AP (and BGP), are closely associated with changes in testosterone secretion with almost simultaneous increases in serum levels of both variables. It is further concluded that longitudinal study designs may add to the understanding of the growth process and rate of changes, whereas cross-sectional data are relevant to establish proper reference ranges. BONE MINERAL CONTENT. The use of photon absorptiometry in determining BMC is a precise, easy, atraumatic and reproducible method. It is shown that forearm BMC has a highly significant correlation to total body bone mineral also in the pubertal period of rapid growth. It should be noted that single measurements of BMC are of little diagnostic value in the presence of wide biological variation. A spurt in mineralization corresponding to that of height in puberty has been known since the development of the BMC technique. It is evident from our data that BMC and indices of body size are only significantly related after the start of the growth spurt. Significant increases of 25% in the BMC have been found in the year prior to PHV progressing with each PH stage. The mean time of maximal increase in forearm BMC occurred some 5 months later than that of testosterone and AP, and changes in these three variables are closely interrelated. The change in the serum concentrations of the two major adrenal androgens did not appear to be related to BMC.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1988

Somatomedin-C/IGF-I measured by radioimmunoassay and somatomedin bioactivity in adolescents with insulin dependent diabetes compared with puberty matched controls.

Plasma concentrations of insulin like growth factor-I in the adolescent diabetic remain controversial. IGF-I levels were determined by radioimmunoassay in 81 insulin dependent adolescent diabetics (49 boys and 32 girls) and compared with 75 puberty stage matched normal controls. Plasma somatomedin bioactivity was determined by cartilage bioassay in a smaller group of 10 normal and 25 diabetic subjects. IGF-I concentrations increased in the normals during puberty and there were no observed differences between the sexes. (P1, 0.77 +/- 0.08; P2, 1.33 +/- 0.2; P3, 1.59 +/- 0.16; P4, 1.76 +/- 0.16; P5, 2.24 +/- 0.09). IGF-I also increased in the diabetics reaching a peak level at stage three in both girls and boys. Combining the data from both sexes the diabetics had significantly lower levels of IGF-I compared to controls at stages; (P1, 0.67 +/- 0.05, ns. P2, 0.92 +/- 0.1, p less than 0.05; P3, 1.16 +/- 0.09, p less than 0.01; P4, 0.73 +/- 0.11, p less than 0.001; P5, 1.13 +/- 0.11, p less than 0.001). Plasma somatomedin bioactivity was elevated in the normals but inhibitory responses were observed in all but two of the diabetic subjects, highlighting the presence of inhibitory factors in diabetic plasma. HbA1C levels rose in the diabetics during puberty, however using covariance analysis there was no relationship between IGF-I and HbA1C when changes relating to puberty were excluded. The importance of controlling for pubertal stage as opposed to age is noted when assessing IGF-I status in the diabetic adolescent.

Adolescent↗
PubMedDate not supplied

[True precocious puberty in non-tumor hydrocephalus. An analysis of 16 cases].

True precocious puberty occurred in 16 children (15 girls and 1 boy) with non tumoral shunted hydrocephalus at a mean age of 6.8 years. They had mild clinical manifestations of precocious puberty, and the other pituitary functions were found to be normal. Except for one child, precocious puberty did not correlate with raised intracranial pressure or lack of cerebral drainage by the shunt. Growth was the main concern in this group as the predicted height fell at a mean value of 1.7 SD below the parental target height, and even more in children with myelomeningocele. This growth retardation is due to an early progression of bone age observed even prior to the appearance of breast or pubic hair. Therefore we suggest that these children might benefit from early treatment by an LHRH analogue as soon as precocious puberty occurs.

Age Factors↗
PubMedDate not supplied

[Precocious puberty caused by a suprasellar arachnoid cyst. Analysis of 6 cases].

The authors report 6 cases (4 girls and 2 boys) with central precocious puberty associated with a suprasellar arachnoid cyst. Precocious puberty is rarely the presenting sign of arachnoid cysts. It was characterized by early onset, patent symptoms and frequent association (3 of 6 cases) with growth hormone deficiency. The latter represents a further risk of short stature. Evolution of precocious puberty varied from one case to another, without any relation with the quality of control of the arachnoid cyst and associated hydrocephalus. Half-yearly follow-up of height and bone age allowed for deciding a suppressive treatment of precocious puberty and a substitutive growth hormone therapy when needed.

Body Height↗
PubMed1979

[Retardation of puberty and growth].

The disturbed puberty is most frequently manifested by a retardation of sexual maturation and growth. For a correct classification of a developmental disturbance the knowledge of the endocrine processes, of the stages of puberty, tables of height and methods of the assessment of the skeletal maturity is necessary, the use of which for the population of the GDR is discussed. The large differential diagnosis of the delayed puberty and of the short stature must be above all concentrated to the causal-therapeutically influencible endocrinopathies, even though the proportion of the constitutional delayed puberty as an extreme variant of the norm with a good spontaneous prognosis prevails. In order to prevent serious psychosocial conflicts, after transgression of a critical age limit of about 16 years in sexual immaturity an adequate hormone treatment should be introduced even then, when the etiopathogenesis of the disturbance could not be completely clarified.

Adolescent↗
PubMed1977

[A case of HCG-producing ectopic pinealoma in a girl with precocious puberty (author's transl)].

HCG-producing ectopic pinealoma of two cell pattern type was demonstrated in a 5-year old girl who presented precocious puberty and bilateral choked discs. The tumor was localized at the anterior third ventricle and suprasellar region. Endocrinological findings are as following: Plasma basal LH was markedly elevated to 306 mIU/ml and HCG was elevated to 1,192 ng/ml. Provocative test of hypophyseal function revealed low response. Plasma estrogen was not detectable. HCG content of resected tumor tissue was elevated to 400 ng/mg. FSH, however, was not detectable. Histological findings of this tumor showed atypical teratoma, so-called two cell pattern pinealoma. Electron microscopic findings revealed two types of cells, dark and clear cells. Many secreting granules were found in the dark cells. In this case, HCG in plasma, CSF and tumor tissue was remarkably elevated. In addition, plasma FSH was also elevated to 8.9 mIU/ml. Precocious puberty associated with tumor in the pineal-suprasellar region has been seen only in boys. There has been no case report of precocious puberty in girls. This case is the first female case is which HCG-producing ectopic penealoma is caused in precocious puberty.

Brain Neoplasms↗
PubMedDate not supplied

[Onset of puberty in boys: comparison between clinical indicators and the changes in the plasma levels of gonadotropic hormones and testosterone].

The blood plasma LH, FSH and testosterone concentrations were determined in 155 boys aged, 10 to 17 years, by radioimmunoassay. The growth, body weight and puberty degree were detected according to Tanner and the testicular volume by Prader's orchidometer. It was found that hormonal changes in the hypothalamic-hypophyseal-testicular system proceed not parallelly to physical transformations, characteristic of puberty, i.e. hormone concentration rise is seen before the first phenotypical alterations and becomes maximum prior to puberty completion. FSH concentration is 1.67 times as high, reaching the maximum values by the pilar period of the 4th stage and the testicular volume of 8 to 12 ml. LH level is 1.47 times as high, reaching the maximum by the pilar period of the 3d stage and the testicular volume of 8 to 12 ml. Testosterone concentration is 10.47 times as high, reaching the maximum values by the pilar period of the 3d to 6th stage and the testicular volume of 12 to 16 ml. A decrease in the hypothalamic sensitivity to the blood circulating steroids plays a leading role in the puberty pathogenesis.

Adolescent↗
PubMed1984

[Prognostic values of the determination of sleep-related gonadotropin rhythm in delayed puberty].

Sleep-related gonadotropin rhythms are specific for puberty. Sleep-dependent increases of prolactin, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were studied in 6 boys and 1 girl with constitutional delay of growth and puberty. The purpose of this study was to determine whether gonadotropin rhythms occur in the same hormonal sequence in children with constitutional delay of puberty as in normal children. At the onset of puberty a sleep-related FSH increase was detectable, followed by LH-rhythms 1 to 2 years later. The findings of a sleep-dependent FSH increase excludes a hypogonadotropic hypogonadism and triggers the development of secondary sex characteristics.

Adolescent↗
PubMed1981

[Premature thelarche and precocious puberty. Clinical findings and endocrinological data useful for differential diagnosis].

Clinical features, urocytogram and gonadotropin response to LHRH (100 microgram/1,73 m2 i.v.) were evaluated in 10 girls with premature thelarche and 4 girls with precocious puberty to purpose to describe the differences between the two diseases. The subjects with Premature Thelarche showed peculiar clinical and endocrinological characteristics which allowed their discrimination from patients with Precocious Puberty: 1) breast development of mild degree without any modification of nipples and areolae and not accompanied by pubic hair or morphologic changes of genitalia; 2) spontaneous regression of thelarche more or less complete (6/10 cases); 3) not anticipation of puberal maturation; 4) growth rate not accelerate (only a mild advancement of statural age was observed); 5) LH/FSH ratio at prepuberal levels; 6) mean LH peak values overlapping to those obtained in normal infants under 1 year of age. Our findings confirm that: 1) the girls with Premature Thelarche showed different growth pattern and clinical features than those observed in the girls with Precocious Puberty; 2) LHRH test and urocytogram are further valuable parameters for the differential diagnosis between Premature Thelarche and Precocious Puberty; 3) the isolated breast enlargement in girls under 8 years of age is likely to originate from a protracted gonadotropin hyperstimulation as in early life; 4) it is a variant of the normal, not difficult to asses, which merits, however further follow-up.

Adolescent↗
PubMed1984

[Effect of hematologic treatment on the growth and puberty of children with thalassemia major].

This study reports on the endocrine abnormalities associated with delayed growth and puberty, observed in 10 children presenting with thalassemia major. Hormonal changes were followed up during treatment with regular transfusions and efficient chelating agents. Recovery of growth and onset of puberty were observed in most cases. When puberty was delayed, an associated substitutive treatment with sexual hormones was useful. In one case only, an isolated gonadotropic deficiency could be proven. In all cases STH, TSH and PRL secretions were normal. Without efficient and early treatment, the main consequence of the disease with respects to growth seems to be the risk of delayed puberty, mainly functional, or rarely hypogonadotropic due to definite LH and FSH deficiency.

Adolescent↗
PubMed1981

Precocious puberty and hypothalamic hamartoma.

A 3-year-old boy with true precocious puberty and hamartoma of the hypothalamus is described. Preliminary diagnosis was established by the presence of unusually advanced puberty and skeletal age without other evidence of central nervous system dysfunction, elevated blood gonadotropin and testosterone concentrations, and positive computed tomography scans. Pneumoencephalography further delineated the tumor. Hypothalamic-pituitary-gonadal and adrenal functions were studied. Release of gonadotropins after the injection of synthetic luteinizing hormone-releasing hormone and the suppression of luteinizing hormone and of testosterone by oral fluoxymesterone were comparable to maximal responses of normal men. The diagnosis was confirmed by histologic and electron microscopic study of an excised portion of the tumor. Immunofluorescence studies indicated the presence of luteinizing hormone-releasing hormone in the hamartoma and radioimmunoassays detected thyroid-stimulating hormone-releasing hormone and somatostatin. The hamartoma resembles an autonomously functioning accessory hypothalamus. The ectopic neuroendocrine pathways, however, are responsive to hormonal stimulation and feedback. The clinical, endocrinologic, and pathologic features of published cases of precocious puberty and hypothalamic hamartoma are reviewed. Advanced or rapidly progressive true precocious puberty in the very young with elevated concentrations of blood gonadotropins and gonadal steroids and positive pneumoencephalography appear to be characteristic.

Child, Preschool↗
PubMed1995

[Delayed constitutional puberty or hypogonadotrophic hypogonadism?].

This review is focused on the diagnosis, clinical and general therapeutic approach of constitutional growth and puberty delay and hypogonadotrophic hypogonadism in males, two entities that are difficult to distinguish. Clinical history and physical examination must be carefully performed. Delayed puberty is due to constitutional growth and puberty delay in the vast majority of children. These must be distinguished from a small fraction of boys with hypogonadism, a pathological condition. A number of laboratory test allow the prediction of puberty onset and progression. Nevertheless, the advent of highly sensitive immunoassay and radiometric immunoassay systems for LH, FSH and testosterone has not entirely solved the problems, since their values may overlap between normal and pathological conditions.

Adolescent↗
PubMed1993

[Follow up results of treatment for premature puberty (central origin)].

Distant treatment results of premature central origin puberty with chlormadinone (Polfa) were described. Premature central origin puberty was diagnosed at 19% (38/202) of patients examined with premature puberty as a initial diagnosis. Annual medium height intake 5.5 cm +/- 1.2 cm and puberty inhibition testify to proper drug doses. Hormonal treatment should be employed till patients height is 150 cm, what is usually obtained at the age 9 at half. It makes possible to obtain final height of 162 cm +/- 4.2 cm. The average menarche age of treated girls was 10- and 11 months, and the first menstruation approximately 15 months after hormonal treatment.

Body Height↗
PubMed1993

[Comparison between complete and incomplete suppression of the hypophyseal-gonadal axis in girls with central precocious puberty: effect on growth and prospective final height].

BACKGROUND: Whether short-acting or slow-release gonadotropin-releasing hormone agonists have different effects on growth and bone maturation in children with central precocious puberty is still unknown. METHODS: In a meta-analysis, we studied 21 previously untreated girls with central precocious puberty treated with Buserelin and 22 previously untreated girls with central precocious puberty treated with Decapeptyl Depot. Duration of treatment was at least 18 months in both groups. RESULTS: At start of therapy, chronological age, bone age, height velocity and pubertal stage were well comparable between the groups. During the first 6 months of treatment, clinical and biochemical escapes from suppression were more frequent in the Buserelin group; height velocity and bone maturation (delta bone age/delta chronological age) remained significantly higher (p < 0.0001 and p < 0.01, resp.) in Buserelin than in Decapeptyl Depot patients. In contrast to the Decapeptyl Depot group, in the Buserelin patients height standard deviation score for bone age did not change and predicted adult height decreased. From 6 to 18 months of therapy, the development of height velocity, delta bone age/delta chronological age, standard deviation score for bone age and predicted adult height showed an almost parallel course in both groups. Height velocity and bone maturation tended to be faster in the Buserelin group. Mean predicted adult height rose significantly in the Decapeptyl Depot group, but not in the Buserelin-treated girls. CONCLUSIONS: A slow-release gonadotropin-releasing hormone agonist appears to be superior to short-acting drugs not only in terms of long-term tolerance but also for achieving the auxological objectives in central precocious puberty therapy. This is mainly due to their faster and more complete suppression of gonadotropins during the first 6 months of treatment.

Age Determination by Skeleton↗