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PubMed1989

[The significance and characteristics of the LHRH test in diagnosing precocious puberty development in girls: the stimulated LH/FSH quotient differentiates between central precocious puberty and premature thelarche].

LHRH tests (100 micrograms i.v.) were performed in 31 girls with central precocious puberty (PP); the girls were participating in an international multicentre trial for the treatment of PP with the LHRH agonist decapeptyl in microspheres, together with 18 girls with premature thelarche (PT). Assignment to these two groups was made after 6 months to 5 years of clinical follow-up. LH and FSH were determined centrally using a polyclonal RIA. Basal LH and FSH levels and stimulated LH levels were significantly higher in PP patients (p less than 0.001), but the stimulated FSH levels were not significantly different between the two groups. In the PP group, all stimulated LH levels were above the prepubertal range, whereas in the PT patients all stimulated LH levels were within the prepubertal reference limits. In PP and PT patients 52% and 56%, respectively, of the stimulated FSH levels were increased above the range for prepubertal girls. In 55% of the PP patients, stimulated LH levels were also above the reference range for the corresponding Tanner breast stage. In contrast, all stimulated LH levels of the PT group were within the reference limits for their breast stage. For FSH, 45% and 56% of the stimulated levels were above the normal ranges for the corresponding breast stages in the PP and PT groups, respectively. The LH-to-FSH ratio after LHRH stimulation was significantly higher in the PP than in the PT group (p less than 0.001). All but one of these ratios were above 1 in the PP patients and all ratios in the PT patients were below 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Determination by Skeleton↗
PubMed1999

Final height after long-term treatment with triptorelin slow release for central precocious puberty: importance of statural growth after interruption of treatment. French study group of Decapeptyl in Precocious Puberty.

The impact of treatment of central precocious puberty (CPP) with GnRH agonists on final statural height (FH) remains controversial, and guidelines on the optimal time point for interruption of these treatments have not been established. We analyzed the long term results of 58 girls and 8 boys uniformly treated with triptorelin slow release formulation (Decapeptyl, triptorelin-SR) for CPP and compared their FH with predicted height before treatment and with the FH of a historical group of patients not treated with GnRH agonist. The FH SD score was close to 0 and was not different from the genetic target height. In girls, FH was improved by 4.8 +/- 5.8 cm compared with predicted height before treatment and by 8.3 cm by comparison with a historical group. In boys, comparison with a historical group revealed a 13.7-cm improvement, whereas predicted height before treatment was similar to FH. Three variables were independently associated with FH in girls: the bone age/statural age ratio at the onset of treatment (negatively), the height SD score at the end of treatment, and the posttreatment growth spurt (delta FH - height at the end of treatment). The influence of the posttreatment growth spurt, itself dependent on age and bone age at the interruption of treatment, suggests that continuing treatment beyond the age of 11 yr in girls does not improve and could actually decrease FH. This point should be evaluated in a formal controlled trial.

Age of Onset↗
PubMed2001

Case study: sexual hyperactivity treated with psychostimulants in familial male precocious puberty.

Familial male precocious puberty is a form of precocious puberty resulting from an activating mutation of the luteinizing hormone receptor. Behavior problems are associated with the early onset of puberty. In this case, sexual hyperactivity was treated with psychostimulants. Implications for the effectiveness of methylphenidate in reducing sexual hyperactivity with and without familial male precocious puberty are discussed, and testable hypotheses are proposed for the effects of stimulants on sexual behavior in adolescents.

Central Nervous System Stimulants↗
PubMed2006

Precocious puberty.

The term precocious puberty encompasses a group of heterogeneous conditions that range from variants of normal to slowly progressive and rapidly progressive maturation of both sexes. It is defined as the appearance of secondary sex characteristics before the age of 8 in girls and 9 in boys. The clinician who is evaluating a child with precocious puberty should be aware of the normal events of puberty, the ages at which pubertal milestones are achieved and the tempo of pubertal progression. The mechanisms involved in the onset and progression of normal puberty are briefly discussed in this article. The diverse etiology of precocious puberty, the diagnostic evaluation of the patient including clinical, laboratory and radiological investigation as well as problems associated with precocious puberty and indications for treatment and treatment modalities are further discussed in the article.

Animals↗
PubMedDate not supplied

Precocious puberty and statural growth.

Precocious puberty results mostly from the precocious activation of the gonadotropic axis. Although the age limits have recently been discussed, most physicians consider that onset of pubertal development before the age of 8 years in a girl or 9 years in a boy warrants at least a clinical and bone age evaluation by a paediatric endocrinologist. The major concern in precocious puberty is the underlying condition, and central nervous system or gonadal neoplasm have to be formally excluded as a first step in the diagnosis. A secondary concern is height, since precocious puberty leads to accelerated growth, accelerated bone maturation and ultimately reduced stature. Precocious puberty is heterogeneous and strict criteria should be used to define it, both in terms of age and in terms of potential for progression. Depot forms of GnRH agonists are now the standard treatment for progressive central precocious puberty and aim at alleviating the clinical symptoms of early pubertal development, their psychological consequences and the effects on growth. Here, we review the consequences of both central and gonadotropin-independent precocious puberty on adult stature and the information available on outcomes using the therapeutic regimens currently available. In girls with progressive precocious puberty, all published evidence indicates a gain of adult height over height predicted before treatment or over untreated historical controls. However, the apparent height gain (derived from the comparison of predicted and actual heights) is very variable, in large part due to the inaccuracy of height prediction methods. In girls with onset of puberty at the lower half of the normal age (8-10 years) distribution, trials using GnRH agonists have given negative results (no benefit of treatment). In boys, precocious puberty is rare and fewer results are available but point in the same direction. The most appropriate time for interrupting the treatment is still controversial. In conclusion, GnRH agonists restore adult height in children when it is compromised by precocious puberty.

Adolescent↗
PubMed2005

Clinical suppression of precocious puberty with cetrorelix after failed treatment with GnRH agonist in a girl with gonadotrophin-independent precocious puberty.

This report presents the case of a 7-year-old girl with gonadotrophin-independent precocious puberty treated with cetrorelix [gonadotrophin-releasing hormone (GnRH) antagonist] after poor response to GnRH agonist therapy was observed in the endocrinology outpatient clinic. Uterine and ovarian morphology returned to within the normal prepubertal range after GnRH antagonist was injected subcutaneously. Vaginal bleeding stopped completely. The effects of GnRH antagonist treatment were comparable to those of GnRH agonist. The potential advantage of GnRH antagonists would be a clinically significant direct effect on the ovary, if it exists, and GnRH antagonists should be available for use in such children.

Child↗
PubMed1991

A novel testis-stimulating factor in familial male precocious puberty.

BACKGROUND: Familial male precocious puberty is a gonadotropin-independent form of precocious puberty that occurs only in males. The cause of the disorder is unknown. To examine the hypothesis that the plasma of boys with familial male precocious puberty contains a novel stimulator of testicular testosterone production, we developed a bioassay using adult male cynomolgus monkeys. METHODS: We collected plasma from 12 boys with familial male precocious puberty, 7 normal prepubertal boys of similar ages and with similar plasma gonadotropin levels, and 1 boy with hypogonadotropic hypogonadism and infused it into the testicular artery of adult male cynomolgus monkeys that had been pretreated with gonadotropin-releasing-hormone antagonist to inhibit the endogenous secretion of gonadotropins. Testicular venous effluent was collected at 15-minute intervals for 3 or 5 hours for the measurement of testosterone. RESULTS: The mean (+/- SE) peak testosterone response, as compared with base line, was significantly greater in the monkeys infused with plasma from the 12 boys with familial male precocious puberty than in the monkeys infused with plasma from the 7 normal prepubertal boys and the boy with hypogonadotropic hypogonadism (385 +/- 51 vs. 184 +/- 25 percent, P less than 0.005) in the three-hour studies. Plasma from 92 percent of the boys with familial male precocious puberty and 12.5 percent of the normal prepubertal boys stimulated a response greater than 195 percent of base-line values. In the animals studied for five hours after receiving a second dose of antagonist, the mean peak testosterone response, as compared with base line, was significantly greater in the monkeys infused with plasma from three boys with familial male precocious puberty than in the monkeys infused with plasma from three normal prepubertal boys (363 +/- 81 vs. 115 +/- 6 percent, P less than 0.01). The mean area under the testosterone-response curve was significantly larger in the monkeys infused with plasma from the boys with familial male precocious puberty in the five-hour studies (154 +/- 34 vs. -58 +/- 10 percent, P less than 0.005), but not in the three-hour studies. CONCLUSIONS: These findings support the presence of a circulating testis-stimulating factor in the plasma of boys with familial male precocious puberty. The production of such a factor would explain the biologic nature of the disorder.

Animals↗
PubMed2004

Results of long-term follow-up after treatment of central precocious puberty with leuprorelin acetate: evaluation of effectiveness of treatment and recovery of gonadal function. The TAP-144-SR Japanese Study Group on Central Precocious Puberty.

We evaluated the effect of leuprorelin treatment on adult height (AH) and followed recovery of reproductive function in 63 girls and 13 boys with central precocious puberty (CPP). Mean treatment durations were 3.8 +/- 2.0 and 4.1 +/- 2.5 yr, and posttreatment follow-up durations were 3.5 +/- 1.3 and 2.6 +/- 1.1 yr for girls and boys, respectively. AH was 154.5 +/- 5.7 cm for girls, and 89.5% of girls reached AH within their target height range. For boys, AH was 163.2 +/- 13.0 cm, and 90.9% reached target height range. It appeared that the Bayley-Pinneau method, modified for Japanese children, using a table for advanced bone age (BA), overestimated AH in CPP; and this method, using a table for average BA and projected height for BA, was suitable for prediction of AH in CPP. Menarche or remenarche occurred in 96.8% of girls at the age of 13.1 +/- 1.5 yr. Of 11 girls who contributed urine samples, all seven idiopathic and two organic cases were considered to have ovulation. Serum testosterone levels reached normal adult level in all boys. In conclusion, long-term leuprorelin treatment for children with CPP improved AH and had no adverse effects on recovery of reproductive function.

Adolescent↗
PubMed2006

[Effects of Chinese herbal medicine on modulating the course of puberty development in children with precocious puberty].

OBJECTIVE: To explore the therapeutic effects of Ziyin Xiehuo Recipe (ZYXHR) for nourishing yin and lowering fire and Yishen Tianjing Recipe (YSTJR) for nourishing kidney and replenishing essence on regulating the gonadotrophic and somatotrophic functions of hypothalamic-pituitary axis, and to reveal the mechanisms of ZYXHR and YSTJR in modulating the course of pubertal development of children with precocious puberty. METHODS: The pubertal rats were fed with ZYXHR or YSTJR for 30 days, and the parameters of rats were monitored as the followings: The content of gonadotropin-releasing hormone (GnRH), the frequency and amplitude of GnRH impulse releasing, the releasing amounts of aminoacid neurotransmitters, and neuropeptide Y (NPY) and beta-endorphin (beta-END) in the gonadotrophic area of the hypothalamus were detected with neurobiological methods (push-pull perfusion, homogenate, incubation of brain slices, and immunohistochemical staining). The levels of gene and protein expressions of GnRH, growth hormone releasing hormone (GHRH) and somatostatin (SS) in hypothalamus, and follicular stimulating hormone (FSH), luteinizing hormone (LH) and growth hormone (GH) in adenohypophysis as well as insulin-like growth factor I (IGF-I) in metaphysis were determined with real time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The ZYXHR could reduce the activity of GnRH neurons in hypothalamus through inhibiting the release of central exciting aminoacid neurotransmitters, whereas promoting the release of central inhibiting aminoacid neurotransmitters, NPY and beta-END in gonadotrophic area of hypothalamus. The expression levels of GnRH, FSH and LH mRNAs were down-regulated while the expression level of SS mRNA in hypothalamus was up-regulated in the ZYXHR-treated group. The GH mRNA in hypophysis and the IGF-I mRNA in metaphysis were both down-regulated by ZYXHR. The YSTJR could promote the activity of GnRH neurons in hypothalamus through inhibiting the release of NPY in gonadotrophic area of hypothalamus, up-regulating the expression levels of GnRH, FSH, LH and GH mRNAs in hypophysis, and IGF-I mRNA in metaphysis, while down-regulating the expression level of SS mRNA in hypothalamus. CONCLUSION: The ZYXHR and YSTJR could both regulate the gonadotrophic and somatotrophic functions of hypothalamic-pituitary axis through modulating the neuroendocrine regulation and the gene expressions of GnRH and SS in hypothalamus, GH, FSH and LH in hypophysis, and IGF-I in metaphysis. These may be the chief mechanisms of ZYXHR and YSTJR in modulating the course of pubertal development and ameliorating the skeletal development in children with precocious puberty.

Animals↗
PubMed2004

Decreased hypothalamic aromatization in female rats of true precocious puberty.

The true precocious puberty animal model induced by the single dose of danazol was used for investigating the expressions of hypothalamic aromatase in the advanced onset of puberty in rats. The day of vaginal opening and first estrus showed significant advancement in the model rats compared with the normal and vehicle rats (P < 0.01, respectively). The hypothalamic gonadotropin-releasing hormone (GnRH) mRNA expression increased significantly in the model rats compared with that in the normal and vehicle ones (P < 0.01). The levels of aromatase mRNA and protein expressions detected by RT-PCR and Western blot both decreased in the model rats compared with those in the normal and vehicle groups (P < 0.05). The results suggested that the hypothalamic aromatization might diminish in the onset of true precocious puberty of female rats.

Animals↗
PubMed1993

A constitutively activating mutation of the luteinizing hormone receptor in familial male precocious puberty.

Familial male precocious puberty (FMPP) is a gonadotropin-independent disorder that is inherited in an autosomal dominant, male-limited pattern. Affected males generally exhibit signs of puberty by age 4. Testosterone production and Leydig cell hyperplasia occur in the context of prepubertal levels of luteinizing hormone (LH). The LH receptor is a member of the family of G-protein-coupled receptors, and we hypothesized that FMPP might be due to a mutant receptor that is activated in the presence of little or no agonist. A single A-->G base change that results in substitution of glycine for aspartate at position 578 in the sixth transmembrane helix of the LH receptor was found in affected individuals from eight different families. Linkage of the mutation to FMPP was supported by restriction-digest analysis. COS-7 cells expressing the mutant LH receptor exhibited markedly increased cyclic AMP production in the absence of agonist, suggesting that autonomous Leydig cell activity in FMPP is caused by a constitutively activated LH receptor.

Adenine↗
PubMed1995

Characterization of heterogeneous mutations causing constitutive activation of the luteinizing hormone receptor in familial male precocious puberty.

Familial male precocious puberty (FMPP) is a gonadotropin-independent disorder that is inherited in an autosomal dominant, male-limited pattern. A heterozygous mutation encoding substitution of Asp578 with Gly in transmembrane helix 6 of the G protein-coupled receptor for luteinizing hormone (LHR) has been found in affected males from nine American FMPP families. Cells expressing the mutant LHR exhibit markedly increased cyclic adenosine monophosphate (cAMP) production in the absence of agonist, suggesting that autonomous Leydig cell activity in FMPP is caused by a constitutively activated LHR. We have now analyzed genomic DNA from affected males from six additional FMPP families. PCR was used to amplify a fragment of the LHR gene encoding amino acid residues 441-594. None of the six new samples contained the Asp578-->Gly mutation, as indicated by absence of digestion with MspI. PCR products were then screened for heterozygous mutations using temperature-gradient gel electrophoresis. DNA fragments from two of the patients migrated abnormally. Direct sequencing of PCR product from one affected German male revealed a heterozygous mutation (ATG-->ATA) encoding Met571-->Ile at the cytoplasmic end of helix 6, the same mutation that has been reported in another European FMPP kindred. Affected males in the second family had a novel Thr577-->Ile mutation (ACC-->ATC). Mutations in different portions of the LHR or in a different gene may be responsible for disease in the other FMPP kindreds. Agonist binding and functional coupling of the mutant receptors to the cAMP and inositol phosphate pathways were studied by transiently expressing them in COS-7 cells. Agonist affinity was unaffected by the mutations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Ovarian follicle cysts and precocious puberty].

A "transient" precocious puberty with ovarian follicular cysts was observed in four girls. Each girl presented with several successive and transient episodes of development of secondary sex characters: breast development, areolar pigmentation, brown abdominal median line were the clinical signs of oestrogen secretion. At the time of referral, plasma and urinary gonadotropins levels were low in the prepubertal range while plasma oestradiol concentrations were elevated, in the pubertal range. At this time, as well as during each episode of "pubertal" development, the gonadotropins response to GnRH stimulation was blunted. In contrast, a prepubertal or pubertal response was observed when the clinical symptoms of estrogenization had resumed. Ultrasonography showed one or several ovarian follicular cysts. In two cases, the treatment with the GnRH agonist, D-TRP 6 GnRH [Decapeptyl (R)], was successful, suggesting a central dysfunction

Child↗
PubMed1988

Growth and precocious puberty.

Treatment of precocious puberty of central origin is aimed at controlling the development of sexual characteristics and improving final height. Increased growth rate is one of the major clinical symptoms, accompanied by an even more marked advance in bone age. Medroxyprogesterone acetate and cyproterone acetate have provided almost satisfactory control of pubertal characteristics, but with accompanying adrenal insufficiency. The data with regard to growth and bone maturation are contradictory. LHRH analogues have recently become available, and provide good control of gonadotrophin secretion. In a series of 21 cases (13 girls, 8 boys), a significant decrease in growth rate was achieved in both sexes with an LHRH analogue, with a significant increase in the height age/bone age ratio; control of gonadal secretions was also obtained. These results are only preliminary, but provide hope that the final height of these children will be improved.

Age Determination by Skeleton↗
PubMed1986

Sonographic monitoring of LHRH analogue therapy in idiopathic precocious puberty in young girls.

Precocious puberty in young girls is defined as the development of secondary sexual characteristics and gonadal growth before 8 years of age. Approximately 60% of isosexual precocious development in girls has no organic cause and is termed idiopathic precocious puberty. Thirteen young girls with idiopathic precocious puberty were treated with LHRH analogue under a well-established protocol. Pelvic ultrasound was added to the protocol to examine ultrasound's role in supplying a morphologic parameter of suppression of the pubertal process. Initially, 11 patients had ovarian volumes greater than normal, and ovarian cysts measuring 0.5 cm to 4 cm in diameter were identified in seven patients. All 13 patients had enlarged pretreatment uteri greater than 3 cm in length. Eleven of these patients had a pubertal or adult uterine configuration. After 1 year of therapy, 11 patients had normal prepubertal ovarian volumes, and 12 of 13 patients had a decrease in ovarian volume. No demonstrable cysts were present at 1 year. Eleven had a reduction in uterine length. Nine of the 11 patients with a pubertal uterine configuration reverted to a more prepubertal-like morphology. The sonographic morphologic changes correlated well with laboratory and clinical data indicating suppression of the hypothalamic-pituitary-gonadal axis.

Child↗
PubMedDate not supplied

Pathogenesis and epidemiology of precocious puberty. Effects of exogenous oestrogens.

Precocious puberty is generally defined as the appearance of secondary sex characteristics before age 8 years in girls (or menarche before age 9 years) and before 9 years in boys. The overall incidence of sexual precocity is estimated to be 1:5,000 to 1:10,000 children. The female-to-male ratio is approximately 10:1. In addition to the psychosocial disturbances associated with precocious puberty, the premature pubertal growth spurt (with less time for prepubertal growth) and the accelerated bone maturation result in reduced adult height. Precocious puberty may be gonadotrophin-dependent [i.e. of central origin with premature activation of the gonadotrophin-releasing hormone (GnRH) pulse generator] or gonadotrophin-independent (i.e. peripheral where the GnRH pulse generator is suppressed). This can be determined by GnRH testing. The pathophysiology is the basis for different diagnostic and therapeutic strategies, i.e. in the first case a stimulated LH/FSH ratio >1 and suppressive treatment with GnRH agonists (e.g. in hypothalamic hamartoma), and in the second decreased gonadotrophins and removal or suppression of the endogenous or exogenous sex steroid source (e.g. congenital adrenal hyperplasia). While several cases of gonadotrophin-independent precocious puberty due to oestrogen exposure via the transdermal, oral, or inhalative route have been reported, no case is known with the development of subsequent secondary central precocious puberty. Food contamination with oestrogens is theoretically possible, but would most probably be sporadic and, thus, would not lead to precocious puberty. As steroid hormones in meat production are banned in the European Union, no data on the impact of environmental oestrogenic substances on human maturation are currently available. In conclusion, the risk for children to develop precocious puberty through exposure to oestrogens (or androgens) in the environment or in food is very low. Nevertheless, studies of the effects of defined environmental oestrogenic substances on the human reproductive system and on pubertal development are warranted.

Estrogens↗