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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↗
PubMed2000

Recent advances in the diagnosis and treatment of precocious puberty.

In the last two decades, the diagnosis and treatment of precocious puberty has undergone important changes. The use of supersensitive assays to determine gonadotropins and gonadal hormones has increased the sensitivity and decreased the number of blood samples required to assess the diagnosis. The introduction of gonadotropin-releasing hormone (GnRH) agonists produced a revolution in the diagnosis and treatment of this disorder. Recently, the use of long acting GnRH agonists improved the adherence of patients to medical treatment and decreased the need for uncomfortable repeated doses. The medications in the treatment of the GnRH independent causes of precocious puberty, and the important revelations in the pathophysiology of these disorders, have advanced our knowledge and management of the affected children.

Adolescent↗
PubMed1987

Treatment of central precocious puberty with an LHRH agonist (Buserelin): effect on growth and bone maturation after three years of treatment.

The LHRH analog Buserelin was used to treat 27 children (21 girls, 6 boys) with central precocious puberty. Nineteen patients had idiopathic precocious puberty and 8 had organic lesions (hamartoma, hydrocephalus or suprasellar arachnoid cyst). All patients received 20 or 30 micrograms/kg/day s.c. of Buserelin, and we obtained plasma E2 less than 20 pg/ml, vaginal maturation index less than 30 in girls or plasma testosterone less than 0.3 ng/ml in boys. The mean growth rate decreased from 9.3 +/- 0.5 to 4.6 +/- 1.3 cm/year after 3 years. The velocity of skeletal maturation decreased so that the final height prediction improved by a mean value of 1.6 SD. As the follow-up increases, this study confirms that LHRHa therapy is effective and potentially improves the final height of children presenting active and severe central precocious puberty.

Aging↗
PubMed1986

Intranasal nafarelin: an LH-RH analogue treatment of gonadotropin-dependent precocious puberty.

The agonistic analogues of luteinizing hormone releasing hormone decrease biochemical findings and clinical signs of gonadotropin-dependent precocious puberty. We tested a new analogue, nafarelin acetate, in 15 girls with gonadotropin-dependent precocious puberty. The hydrophobic nature and potency of this compound allow it to be administered by intranasal inhalation. Laboratory assessment of vaginal cytology, estradiol and urinary gonadotropin levels, and growth velocity revealed that nafarelin acetate 800 to 1200 micrograms/day diminished these values during a 6-month treatment period. These results suggest gonadotropin-dependent precocious puberty in girls can be treated with intranasal administration of nafarelin acetate.

Administration, Intranasal↗
PubMed1998

Role of surgical resection in the treatment of hypothalamic hamartomas causing precocious puberty. Report of six cases.

Hypothalamic hamartomas (HHs) are benign tumors that are often associated with central precocious puberty. Resection of HHs has been recommended as a treatment option for selected cases of pedunculated lesions, especially in young children. The role of surgery has to be evaluated in the light of the availability of effective medical treatment with gonadotropin-releasing hormone analogs (GnRHas). The authors report the long-term results of total resection of HHs in two children with central precocious puberty and compare it with medical management in four children. The two surgically treated patients underwent total resection of pedunculated HHs at 1.75 (Case 1) and 3.25 years (Case 2) and have received follow-up care for 9 and 8 years, respectively. There were no postoperative complications and computerized tomography scanning confirmed complete tumor removal in both patients. Both patients subsequently experienced some regression of secondary sexual characteristics. The response of luteinizing hormone to GnRH became prepubertal in one patient and was diminished in the other. However, the growth velocity remained elevated (> 7 cm/year), bone age remained advanced (> +2 standard deviations) 5 years after surgery, decreasing adult height prediction. In one child, GnRHa therapy was initiated 7 years postsurgery. Four children were treated solely with GnRH agonists and have received follow-up care for 2.3, 6, 9, and 9 years, respectively. These patients have had a complete regression of endocrinological abnormalities, including a normalization of growth velocity and reduction in the rate of skeletal maturation. No side effects were noted with decapeptyl treatment, and one child developed sterile abscesses while receiving Lupron-Depot. The proven efficacy of GnRHa in suppressing puberty and reducing bone age advancement leads the authors to advise against surgery as the initial management of central precocious puberty caused by HHs.

Child↗
PubMed1985

Paraneoplasic precocious puberty. Report of a new case with hepatoblastoma and review of the literature.

A new case of precocious puberty secondary to production of human chorionic gonadotropin (HCG) by an hepatoblastoma was studied in an 8-month-old infant. A review was made of the 35 cases of paraneoplasic precocious puberty previously reported in the literature. The most frequent cause is hepatoblastoma, which was responsible for 18 cases. There are nine reports of mediastinal teratoma, six of which were observed in patients with Klinefelter Syndrome. In another six cases, the paraneoplasic syndrome was attributed to intracranial tumoration, and two of these patients showed teratoma with areas of choriocarcinoma, whereas germinoma was suspected for clinical reasons in another three. Lastly, one case of presacral teratoma and one of retroperitoneal carcinoma were reported. The differential characteristics of paraneoplasic precocious puberty are: almost exclusive occurrence in males, because of tumoral production of HCG, moderate or absent increase of testicle size, hyperplasia of Leydig's cells without spermatogenesis, and rapidly progressive signs of puberty.

Carcinoma, Hepatocellular↗
PubMed1975

The LH response to LH releasing hormone in children with true isosexual precocious puberty treated with cyproterone acetate.

Fourteen girls and one boy with isosexual precocious puberty were submitted to LHRH stimulation tests, during and without therapy with cyproterone acetate. In addition, fourteen girls with isosexual precocious puberty not receiving any therapy were tested and served as controls. It was found that cyproterone acetate induces suppression of the responsiveness of the pituitary gland to secrete LH on LHRH stimulation. Daily oral therapy was found to be more effective than the regimen of intramuscular depot injections. These findings demonstrate that cyproterone acetate has an antigonadotrophic effect.

Administration, Oral↗
PubMed1995

A potential novel mechanism for precocious puberty in juvenile hypothyroidism.

Some children with juvenile hypothyroidism exhibit unexplained precocious puberty. Interaction of TSH with the human FSH receptor (hFSH-R) is a possible pathophysiological mechanism for this syndrome that has not been explored due to the lack of hFSH-free TSH preparations and the scarcity of a suitable hFSH-R-based assay system. To devise an in vitro FSH bioassay suitable for exploring this mechanism, we expressed hFSH-R complementary DNA in COS-7 cells and stimulated them with recombinant hTSH (rec-hTSH). Rec-hTSH elicited a dose-dependent cAMP response in the in vitro hFSH-R bioassay; however, the concentration of rec-hTSH required for half-maximal stimulation was several logs greater than that of hFSH. Rec-hTSH acted as a competitive inhibitor of hFSH at the hFSH-R, indicating that hTSH and hFSH are acting through the same receptor, namely the hFSH-R. This provides a potential novel mechanism for the precocious puberty of juvenile hypothyroidism.

Biological Assay↗
PubMed2000

Serum levels of growth hormone binding protein in children with normal and precocious puberty: relation to age, gender, body composition and gonadal steroids.

AIM: To study the regulation of GHBP serum levels by gonadal steroids in normal and precocious puberty. STUDY PROTOCOL: We studied GHBP levels in relation to age, sex, pubertal maturation, body composition as well as to circulating IGF-I and gonadal steroid levels in 320 healthy children. Furthermore, we studied the regulation of circulating GHBP in 33 girls with central precocious puberty before and during gonadal suppression with GnRH agonist. METHODS: GHBP was determined by a time-resolved fluoroimmunoassay (GHBP TR-FIA) based on a commercially available immunoassay for GH, the DELFIA GH assay. RESULTS: In healthy children GHBP levels were significantly higher in normal girls compared with boys, and there was no significant increase in GHBP in puberty in both sexes. GHBP levels did not correlate with height (SDS), age, pubertal stage, IGF-I or testosterone/oestradiol levels in boys and girls, respectively. There were significant correlations between BMI and GHBP in boys and girls (R 2 = 0.14 and R 2 = 0.12, both P < 0.0001). Furthermore, GHBP correlated highly significantly with the percentage body fat, determined by BIA in 43 healthy girls (R 2 = 0. 40, P < 0.0001). GHBP levels were significantly higher in girls with central precocious puberty (CPP) (1.31 SDS (1.26), mean (SD)) compared to prepubertal controls (P < 0.0001), and above + 2 SD in 10 out of 33 patients. In girls with CPP, GHBP correlated inversely with oestradiol before treatment (R 2 = 0.26, P < 0.01) and there was a tendency towards a positive correlation with BMI (R 2 = 0.13, P = 0.078). By contrast, there were no signficant correlations between GHBP and IGF-I or height SDS. Gonadal suppression with GnRH agonist treatment caused a transient significant increase of 0.57 SD after 2 months of treatment (P < 0.001), but decreased to baseline levels hereafter. CONCLUSION: We conclude that in children, as in adults, body fat is the primary determinant for the circulating level of GHBP, and that the difference in body fat is probably the main factor for the higher levels of serum GHBP in girls compared with boys, as well as for the negative influence of testosterone levels in boys and of oestrogen levels in girls. The elevation in GHBP levels observed in girls with central precocious puberty is probably due their higher body fat content.

Adolescent↗
PubMed2006

Early growth acceleration in girls with idiopathic precocious puberty.

OBJECTIVE: To determine the growth pattern of girls with idiopathic precocious puberty (IPP) from birth until diagnosis. STUDY DESIGN: We studied 47 girls with IPP and 35 control girls. In each subject, height and weight were measured at diagnosis, whereas data on height from birth until diagnosis were taken from the personal health book of the patient. Height standard deviation score (HSDS) and body mass index SDS were calculated. RESULTS: Mean age (+/-SD) of the girls with IPP was 7.6 (1.1) years and of control girls was 7.5 (0.9) years. At birth, HSDS of the patients with IPP was -0.01 (0.8); at the age of 2 years, 0.42 (1.2); at the age of 4 years, 0.64 (1.1); and at diagnosis, 1.23 (1.7) (P < .001). HSDS of control girls was 0.02 (0.8) at birth, 0.25 (0.8) at 2 years, 0.12 (0.9) at 4 years, and 0.19 (1.1) at assessment (P > .05). There was no statistical difference between body mass index SDS of the patients 0.6 (1.1) versus that of control girls 0.5 (1.0). CONCLUSIONS: The early growth acceleration pattern may be used as an additional clue to the diagnosis of idiopathic precocious puberty.

Birth Weight↗
PubMed1995

Genetic heterogeneity of constitutively activating mutations of the human luteinizing hormone receptor in familial male-limited precocious puberty.

Genomic DNA from 32 unrelated families with male-limited precocious puberty was examined for the previously described Asp-578-->Gly, Met-571-->Ile, and Thr-577-->Ile mutations in transmembrane helix 6 of the human luteinizing hormone receptor (hLHR). Twenty-eight families had the inherited form of the disorder, and of these, 24 were found to have the Asp-578-->Gly mutation. Four additional mutations were found among the remaining four families with the inherited form and in four sporadic cases of the disorder: an A-->C transversion resulting in substitution of leucine for Ile-542 in the fifth transmembrane helix, an A-->G transition resulting in substitution of glycine for Asp-564 in the third cytoplasmic loop, a G-->T transversion resulting in substitution of tyrosine for Asp-578 in the sixth transmembrane helix, and a T-->C transition resulting in substitution of arginine for Cys-581 in the sixth transmembrane helix. Human embryonic kidney cells transfected with cDNAs for each of the mutant hLHRs, created by PCR-based mutagenesis of the wild-type hLHR cDNA, exhibited increased levels of basal cAMP production in the absence of agonist, indicating constitutive activation of the mutation hLHRs. Three of the additional mutations had specific features: Ile-542-->Leu and Cys-581-->Arg appeared ligand-unresponsive, whereas Asp-578-->Tyr appeared to correlate genotype with phenotype. We conclude that the region spanning nt 1624-1741 of exon 11 is a hotspot for heterogeneous point mutations that constitutively activate the hLHR and cause male-limited precocious puberty.

Amino Acid Sequence↗
PubMed1996

An association between precocious puberty and fragile X syndrome?

STUDY OBJECTIVE: To determine the FMR1 gene status in a 10-year, 10-month-old girl with a history of precocious puberty and a family history of fragile X syndrome. DESIGN: Case report. SETTING: The outpatient facility of the Division of Adolescent Medicine and the Division of Genetic and Metabolic Disorders at Children's Hospital of Michigan and the Medical Genetics and Birth Defects Center of Henry Ford Hospital, Detroit, Michigan. PARTICIPANT: A 10-year, 10-month-old girl with a history of precocious puberty. INTERVENTION: Evaluation for menorraghia, DNA extraction, and fragile X gene analysis of blood samples from the patient and her mother. MAIN OUTCOME MEASURES: Identification of a full mutation in the FMR1 gene. RESULTS: Southern blot analysis of the FMR1 gene identified a full mutation in the daughter with approximately 750 repeats of the CGG sequence. Methylation studies showed that the full mutation was completely methylated. FMR1 DNA studies on her mother identified a premutation of approximately 100 repeats. CONCLUSIONS: This report identifies a young girl with a history of precocious puberty and fragile X syndrome. It is also the first report of molecular genetic FMR1 studies in a female with precocious puberty. A possible association between the two conditions is suggested and warrants further investigation.

Blotting, Southern↗
PubMed2002

Long-term suppression of pituitary-gonadal function with three-month depot of leuprorelin acetate in a girl with central precocious puberty.

OBJECTIVE: The efficacy of a 3-month depot preparation of the GnRH agonist leuprorelin acetate in central precocious puberty was studied. METHODS: Treatment with a 3-month depot of leuprorelin acetate was performed subcutaneously in a 7.3-year-old girl with central precocious puberty. RESULTS: During treatment the hormonal suppression was constant and complete as demonstrated by suppressed GnRH stimulation tests and prepubertal estradiol plasma levels. The size and volume of the uterus and ovaries returned to the normal range. The rate of bone maturation was significantly reduced with a ratio deltaBA/deltaCA of 0.58 for 3 treatment years. Thus, the effects of treatment were comparable to those reported for treatment with 1-month depot of GnRH agonists. CONCLUSION: Three-month depots have the advantage of a prolonged injection interval which is more convenient for the patients and reduces costs by necessitating fewer visits to the physician and being approximately 10% cheaper than the 1-month depot. We suggest that comparative and randomized studies be performed to make 3-month depots of GnRH agonists available for routine use in children with central precocious puberty.

Body Height↗
PubMed1997

Long-term outcome of male-limited gonadotropin-independent precocious puberty.

Long-term outcome of five new cases of male-limited precocious puberty (MPP) is reported. Three patients had positive family history. One patient was untreated; 2 boys received cyproterone acetate (2.0-3.6 mg/kg/daily) without clinical effects. Two patients were treated with ketoconazole (600 mg/daily); in 1, GnRH analogue therapy (Buserelin, 1,600 microg/day) was added after 6 months of effective ketoconazole treatment for development of central precocious puberty. The other patient did not develop central puberty under ketoconazole treatment and improved his predicted adult height from 172.4 to 181.1 cm. Four patients reached final height [B.A. (therapy cyproterone acetate): age 22.0 years, -2.0 SDS; B.G. (untreated): age 15.5 years, -1.7 SDS; M.M. (therapy cyproterone acetate): age 19.5 years, -1.6 SDS; M.F. (therapy ketoconazole plus GnRH analogue): age 21.3 years, -2.2 SDS]; three had reduced testicular volume (B.A.: -1.6/-1.6 SDS; B.G.: -2.1/-2.1 SDS; M.F.: -2.4/-1.9 SDS); one (M.F.) showed oligospermia. We concluded that in MPP cyproterone acetate treatment did not improve final height; ketoconazole was effective in reducing testosterone secretion, but its real effect on final height cannot be determined; the timing of central puberty may be precocious, suggesting that an adjunctive GnRH analogue treatment may be needed. In some patients, testicular impairment may be present in young adulthood.

Androgen Antagonists↗
PubMed1992

Psychological aspects of precocious puberty. An overview.

During the last three decades the psychological consequences of precocious puberty have received considerable attention. The nature and shortcomings of relevant studies are described. It is emphasized that specialized counselling and guidance of families with children who have to cope with precocious puberty is important, since it often contributes to an appropriate behaviour adjustment without the development of psychiatric symptomatology. Guidelines for medical service and psychological management are provided.

Child↗
PubMed1993

Hypomelanosis of Ito and precocious puberty.

We describe two girls with hypomelanosis of Ito, one of whom was demonstrated to have diploid-triploid mixoploidy in skin fibroblasts. Both had precocious puberty which was probably gonadotrophin-independent. The association of precocious puberty and hypomelanosis of Ito has not been previously reported. We have speculated on the possible mechanism of gonadotrophin-independent precocious puberty.

Child↗