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PubMedDate not supplied

Precocious puberty in children after traumatic brain injury.

True precocious puberty frequently occurs secondary to central nervous system pathology and is a rare sequelae of severe head injury in early childhood. It is a clinical entity consisting of accelerated somatic development, thelarche and pubarche. We describe two female children, 3 and 5 years of age, who, following head trauma, displayed early pubertal changes including breast enlargement, pubic hair and vaginal secretions. Subsequent laboratory tests, which included hormone assays and luteinizing hormone response after injection of luteinizing hormone releasing hormone, established the diagnosis of precocious puberty of central origin. Long-term sequelae of this condition include accelerated skeletal growth and advanced bone age eventually resulting in short stature. The most effective form of treatment is long-acting luteinizing-hormone-releasing-hormone agonists, which result in temporary reversible chemical castration.

Brain Concussion↗

PubMed1997

A comparison of patients with premature thelarche and idiopathic true precocious puberty in the initial stage of illness.

A comparative study of patients with premature thelarche and patients with idiopathic true precocious puberty was conducted. The age at the first visit tended to be lower for those with precocious puberty. In comparison with normative data for children, the frequency of low birthweight and small for date (SFD) status was greater in the 55 patients with premature thelarche, but SFD was also frequent in the 18 patients with precocious puberty. The height, weight and Kaup's index were all within the normal range for these two groups. The ratios for bone age/chronologic age and bone age/height age tended to be high in both groups. In the patients with premature thelarche, the blood luteinizing hormone (LH) level showed a normal response, and the blood follicle stimulating hormone (FSH) level a hyper-response, to stimulation with luteinizing hormone-releasing hormone (LH-RH). In contrast, both the blood LH and FSH levels showed a normal response to LH-RH stimulation in most of the patients with precocious puberty, and a hyper-response was rare among them. Although the blood estradiol (E2) level was higher in patients with precocious puberty than in those with premature thelarche, about 50% and 90% of the patients in the respective groups had normal levels. These results suggest that normal responses of blood LH and excessive responses of blood FSH to LH-RH loading may be useful in some patients for diagnosing premature thelarche at an early stage.

Age Determination by Skeleton↗

PubMed1981

Therapeutic use of pituitary desensitization with a long-acting lhrh agonist: a potential new treatment for idiopathic precocious puberty.

A two year girl with idiopathic true precocious puberty was treated with a long-acting LHRH agonist, D-Trp6-Pro9-NEt-LHRH (LHRHa). Prior to therapy, the patient demonstrated pulsatile gonadotropin secretion during both night and day, a pubertal response to exogenous LHRH, and an elevated plasma estradiol level. After eight weeks of therapy (4 microgram/kg daily), a mean gonadotropin levels fell to the prepubertal range, there was no evidence of pulsatile discharge of gonadotropins nor any response to exogenous LHRH, and plasma estradiol levels became undetectable. No adverse drug reactions were encountered and all effects of therapy were reversed following cessation of treatment for two months. LHRH analogs may offer a new approach to the therapy of idiopathic precocious puberty and merit further study.

Child, Preschool↗

PubMed1991

[Exploring the substantial basis of the features yinxu huowang in girls with precocious puberty].

Differential diagnosis to 75 girls with true precocious puberty was made using method of TCM. It was observed that each girl had Yinxu Huowang (intense internal heat due to deficiency of vital essence) to a certain extent, these features were very remarkable in most of them. To explore the substantial basis of the features, the functions of hypothalamic-pituitary-ovarian axis were determined. The results showed that the levels of serum FSH, LH, E2 in the girls rise significantly than those in normal girls of the same age, and LHRH stimulating test displays characteristic changes of excessive activity. Treated with TCM of Ziyin Xiehuo, (nourish vital essence reducing intense internal heat) and remitted, the levels of serum FSH, LH, E2 descend significantly, the volume of uterus and ovary reduce markedly, secondary sexual characteristics retrogress evidently, while the features of intense internal heat due to deficiency of vital essence mitigate obviously. According to the above mentioned, the authors consider that the hypothalamic-pituitary-ovarian axis starting beforehand and being hyperfunction are likely to be the substantial basis of the features--that deficiency of Shen Yin, (vital essence) accompanied with intense Fire of the Vital Gate--of the girls with true precocious puberty.

Child↗

PubMed1994

A sporadic case of male-limited precocious puberty has the same constitutively activating point mutation in luteinizing hormone/choriogonadotropin receptor gene as familial cases.

Familial male-limited precocious puberty (FMPP) is an autosomal dominant disorder characterized by marked elevation of serum testosterone despite low levels of gonadotropin. Recently, a single point mutation in the LH/hCG receptor (LH/CGR) gene was found in FMPP families that constitutively activates the LH/CGR, causing Leydig cell activation and precocious puberty. Among the Japanese population, only four sporadic cases of male-limited precocious puberty have been reported. In the current study, we examined one of the four reported Japanese patients with sporadic male-limited precocious puberty and found the same mutation as that in the FMPP families. Genomic DNA was isolated, and the polymerase chain reaction (PCR) was performed to amplify a fragment of LH/CGR DNA encoding amino acid residues that include transmembrane helixes 5 and 6. Sequencing of the PCR products revealed a heterozygous adenosine-guanine transition at nucleotide 1733 in codon 578. The mutation encodes an aspartic acid578-glycine substitution in transmembrane helix 6. The mutant LH/CGR, created by site-directed mutagenesis in vitro, exhibited constitutively higher cAMP levels in transfected COS-7 cells than the wild-type LH/CGR, as described previously; however, basal inositol phosphate levels were not increased by transfection with complementary DNA for the mutant receptor. The concentration and affinity of [125I]hCG-binding sites were similar in cells transfected with the mutant and wild-type LH/CGR complementary DNAs, indicating that the mutant did not alter the production of receptor or its ability to bind human LH/CG. The sporadic occurrence of this case was confirmed by further studies. The mutation creates a recognition site for the restriction endonuclease MspI. Restriction digestion was positive for the mutant not digested by MspI, indicating that the patient's mutant allele was not inherited from his parents. DNA analysis of the patient and the parents, using microsatellite repeat markers, was compatible with biological paternity and maternity. We conclude that the aspartic acid578-->glycine mutation in the LH/CGR has arisen in the Japanese population and is the cause of a sporadic case of male-limited precocious puberty.

Aspartic Acid↗

PubMedDate not supplied

Leptin changes in Taiwanese girls with central precocious puberty before and during the GnRH agonist treatment.

To examine the relationship between leptin serum levels and pubertal development in girls with progressive central precocious puberty. We longitudinally investigated the leptin levels of 37 girls with central precocious puberty before and during treatment with the gonadotropin-releasing hormone agonist depot (leuprorelin acetate). Leptin and other hormone levels were determined by radioimmunoassay. Girls with central precocious puberty before treatment showed no significant difference in leptin levels as compared to the puberty stage at diagnosis of disease. In addition, the changes in leptin concentrations of girls with central precocious puberty during treatment were not statistically significant. In the Spearman correlation analysis of leptin levels with body mass index, bone age, chronological age, clinical pubertal signs along with luteinizing, follicle-stimulating, and estradiol hormone levels, we found that body mass index, weight, and chronological age were significantly correlated with leptin levels (p < 0.05) at both 3 and 6 months of leuprorelin treatment. Leptin levels increased with body mass index; however, this trend did not reach statistical significance at all follow-up time points. These data demonstrated that treatment with depot gonadotropin-releasing hormone agonist does not influence leptin concentrations. Serum leptin levels in patients with central precocious puberty are associated with body weight and body mass index.

Body Mass Index↗

PubMedDate not supplied

[Surgical treatment of GnRH secretory hypothalamic hamartomas causing precocious puberty].

Hypothalamic hamartomas (HHs) are benign lesions often associated with central precocious puberty. Resection of HHs has been recommended as a treatment option for selected cases, however recent reports stressed the role of effective medical management with a long-acting GnRH agonist. This paper describes incomplete response to the initial GnRH therapy and results of total resection of HHs. Five children two boys and three girls with physical signs of puberty at a mean age of 20.2 months (range 5-36 months) have been treated at our institution. All children had a pedunculated mass below the tuber cinereum. Two children were initially treated with GnRH agonist and had received follow-up care for 11 and 12 months respectively. These patients had incomplete regression of endocrinological disturbances to prepubertal level. Both patients were subsequently operated on. All five children underwent total surgical removal of HHs. The hamartomas were excised through pterional approach. Postoperatively two children showed transient third nerve palsy and one diabetes incipidus. There was no permanent disability due to surgical intervention. The clinical and biochemical symptoms and signs of precocious puberty completely regressed postoperatively including two cases treated initially with GnRH analog. The children have been followed for 1 to 6 years and no recurrence of puberty was observed. Surgical excision of pedunculated HHs is still a valuable option in the treatment of precocious puberty in small children. This alternative should be considered if the initial GnRH therapy failed to suppress++ puberty and reduce bone age advancement.

Brain Diseases↗

PubMed1999

Diagnostic value of fluorometric assays in the evaluation of precocious puberty.

To establish normative data and determine the value of fluorometric AutoDELFIA assays (Wallac Oy) in the investigation of precocious puberty, we determined serum levels of LH, FSH, testosterone, and estradiol under basal and GnRH-stimulated conditions in 277 normal subjects at various pubertal stages and in 77 patients with precocious puberty. A substantial overlap was observed in basal and GnRH-stimulated gonadotropin levels in normal individuals of both sexes with pubertal Tanner stages 1 and 2. The 95th percentile of the normal prepubertal population was the cut-off limit between prepubertal and pubertal levels. These limits were 0.6 IU/L in both sexes for basal LH, 9.6 IU/L in boys and 6.9 IU/L in girls for peak LH after GnRH stimulation, 19 ng/dL in boys for basal testosterone, and 13.6 pg/mL in girls for basal estradiol. Basal and peak LH exceeding these limits were considered positive tests for the diagnosis of gonadotropin-dependent precocious puberty. According to these criteria, the sensitivities of basal and peak LH for the latter diagnosis were 71.4% and 100% in boys, and 62.7% and 92.2% in girls. The specificity and positive predicted value were 100% in both sexes for basal and peak LH levels. The negative predicted values for basal and peak LH were 62.5% and 100% in boys, and 40.6% and 76.5% in girls. Basal and GnRH-stimulated FSH levels overlapped among the various pubertal stages in normal subjects and were, in general, not helpful in the differential diagnosis of precocious puberty. In conclusion, basal LH levels were sufficient to establish the diagnosis of gonadotropin-dependent precocious puberty in 71.4% of boys and 62.7% of girls. In the remaining patients, a GnRH stimulation test was still necessary to confirm this diagnosis. Finally, suppressed LH and FSH levels after GnRH stimulation indicate gonadotropin-independent sexual steroid production.

Adolescent↗

PubMed2000

Successful treatment of hypothalamic seizures and precocious puberty with GnRH analogue.

Patients with hypothalamic hamartomas and precocious puberty may develop gelastic seizures that are resistant to conventional antiepileptic drug therapies. While treating precocious puberty in two such patients with long-acting GnRH analogue, the authors observed cessation of gelastic seizures. Although the mechanism is unclear, long-acting GnRH analogue should be considered as a possible therapy for gelastic seizures in patients with hypothalamic hamartomas.

Adolescent↗

PubMed1991

Low growth hormone levels are related to increased body mass index and do not reflect impaired growth in luteinizing hormone-releasing hormone agonist-treated children with precocious puberty.

To test the hypothesis that GH deficiency might explain the low growth velocity of some LHRH agonist (LHRHa)-treated children with central precocious puberty, we measured stimulated (n = 81) and spontaneous (n = 32) GH levels during or after LHRHa treatment. GH stimulation tests in the children who were receiving LHRHa treatment were performed after 2 days of ethinyl estradiol administration. Thirty-one of 81 children (38%) who underwent GH stimulation tests had subnormal responses (less than or equal to 7 micrograms/L) to all tests administered (at least 2 stimuli), including 22 of 67 (33%) who had precocious puberty that was idiopathic or associated with hypothalamic hamartoma. Eleven of 32 children (34%) who underwent measurement of the mean nighttime spontaneous GH level had levels below the normal range for prepubertal children (less than 1.2 microgram/L). Despite the high incidence of subnormal GH levels, there appeared to be no relationship between the GH levels of these children and their growth characteristics. The height, growth velocity, bone maturation rate, predicted height, and insulin-like growth factor-I levels were not different between the children with low GH levels and the children with normal GH levels. Conversely, the GH levels were not different between the children with subnormal growth rates and the children with normal growth rates. Thus, variation in the growth rates of these LHRHa-treated children with central precocious puberty could not be explained by variation in the stimulated or spontaneous secretion of GH. In attempting to understand the high incidence of low GH levels in children with precocious puberty, we examined the relationship between GH level and body mass index (BMI). Both the stimulated (r = -0.33; P less than 0.002) and the spontaneous (r = -0.61; P less than 0.0002) GH levels were inversely related to BMI. Moreover, the children with precocious puberty as a group had significantly elevated BMI [1.2 +/- 0.1 (+/- SE) SD units] compared to normal children of the same age (P less than 0.0001). Thus, increased body mass may explain the high incidence of subnormal GH levels in these patients, and normative GH levels adjusted for body mass are needed before it can be concluded that the apparently subnormal GH levels in LHRHa-treated children with precocious puberty are in fact low.

Adolescent↗

PubMed1985

Testolactone treatment of precocious puberty in McCune-Albright syndrome.

Current medical and surgical therapies of precocious puberty in McCune-Albright syndrome are often unsatisfactory. We used an aromatase inhibitor, testolactone, to treat precocious puberty in a girl with McCune-Albright syndrome. This child was unresponsive to 28 weeks of treatment with the long-acting agonist of LRH, D-trp6-pro9-NEt-LRH. During testolactone therapy, menses ceased, bone age advancement and height velocity diminished, and plasma oestradiol levels were suppressed. Serum gonadotrophin levels remained in the prepubertal range. Testolactone may be an effective therapy of precocious puberty in girls with McCune-Albright syndrome.

Androstenedione↗

PubMed1992

The natural history of autonomous gonadal function, adrenarche, and central puberty in gonadotropin-independent precocious puberty.

Gonadotropin-independent precocity (GIP) is a syndrome marked by precocious pubertal development in the absence of pubertal levels of gonadotropins. To investigate the discrete patterns of central nervous system, gonadal, adrenal, and skeletal maturation in this syndrome, we conducted longitudinal studies spanning up to 10 yr in two such affected individuals. A cross-sectional analysis of adrenal androgen secretion was performed in nine additional patients to assess further the time course of adrenarche in GIP. Serial evaluations revealed progression of secondary sexual characteristics, statural growth, and skeletal maturation, all consistent with ongoing exposure to pubertal gonadal steroid levels. On the other hand, adrenarche (n = 11) and spontaneous and GnRH-stimulated gonadotropin secretion (n = 2) progressed in chronological age-appropriate manners despite long term pubertal levels of gonadal sex steroid secretion. After the development of central puberty, as documented by the appearance of pulsatile gonadotropin secretion, we sought to determine whether the potential for gonadal autonomy persisted. Despite complete pituitary desensitization induced by administration of a GnRH agonist, both patients studied demonstrated an ongoing capacity to secrete pubertal levels of gonadal steroids. Our study suggests that the timing of adrenarche and central puberty in these subjects with GIP was apparently unaltered by prolonged exposure to gonadal steroids. Subsequent to the development of central puberty, pulsatile gonadotropin secretion may override and, thus, mask the underlying defect(s) in adolescents and adults with histories of GIP.

Adrenal Glands↗

PubMed1992

Hypothalamic hamartoma and precocious puberty: report of a case.

Hypothalamic hamartoma is reported to be associated with precocious puberty. Here, the authors present a seven-year-old girl whose onset of puberty occurred at the age of two. Under the impression of idiopathic precocious puberty, cyproterone acetate was initially tried. Since the effect of her medication was not satisfactory, it was discontinued at the age of five years and 11 months. However, rapid advance of bone age and vaginal spotting recurred after the withdrawal of treatment. She was re-evaluated at the age of six, and a magnetic resonance image (MRI) study of the head revealed a hypothalamic hamartoma. At that time, a long-acting analog of luteinizing hormone-releasing hormone (LHRHa), leuprolide acetate, was prescribed. Her secondary sex characteristics regressed and her hypothalamic-pituitary-gonad axis was suppressed after treatment. The clinical presentation, mechanism and treatment of precocious puberty caused by hypothalamic hamartomas are fully discussed in this report.

Child↗

PubMed1985

Spontaneous gonadotrophin pulsatility and ovarian morphology in girls with central precocious puberty treated with cyproterone acetate.

We have studied four girls with central precocious puberty treated with cyproterone acetate for a mean of 3.6 years (range 1.5-6.3 years). Pelvic ultrasound assessment demonstrated suppression of the ovarian morphology of central precocious puberty despite the presence of spontaneous pulsatile gonadotrophin secretion at night. We suggest that the previously reported effects on gonadotrophin secretion induced by cyproterone acetate therapy, administered in recommended doses, are minor and that the predominant effect of cyproterone acetate in the treatment of girls with central precocious puberty is direct inhibition of ovarian steroidogenesis.

Child↗

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↗

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↗

PubMed1994

Laboratory monitoring of children with precocious puberty.

It is necessary not only to perform laboratory tests for the correct diagnosis of children with precocious puberty, but also to monitor laboratory tests to ensure adequacy of therapy. Careful laboratory testing is a requisite in the differentiation of central from peripheral precocious puberty. It is also required to determine whether the patient who presents with early physical changes of pubertal development with peripheral precocious puberty has evidence of pubertal hormonal secretion. The most useful single test is gonadotropin-releasing hormone (gonadorelin) stimulation of luteinizing hormone release. The same stimulation test is also indicated to verify the adequacy of suppression of gonadotropin secretion among patients with central precocious puberty who are being treated with gonadotropin-releasing hormone analogue. It is necessary to know which gonadotropin assay is being used and the range of normal levels to correctly interpret the tests.

Child↗

PubMed1990

[Diagnostic differentiation between precocious puberty and premature thelarche using ultrasonography and the stimulated LH/FSH quotient].

True precocious puberty represents a serious developmental disorder necessitating immediate therapeutic measures, whereas premature thelarche is a harmless variation from the norm. For the differential diagnosis the ultrasonographic evaluation of the internal genitalia is of value. Girls with precocious puberty reveal a statistically significantly greater uterus length and volume as well as ovarian size. The stimulated LH/FSH quotient allows verification of the diagnosis. This value is found always to be greater than 1 in precocious puberty and always less than 1 in premature thelarche.

Adolescent↗