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Results for “Puberty, Precocious”

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At least 451 records · Page 25Linked to original sources
PubMed1988

Do some patients with fragile X syndrome have precocious puberty?

We report on an 8 1/2-year-old white girl with fra (X) syndrome; she had mental deficiency, hyperactivity, speech disturbances, slightly prominent ears, mild joint laxity and 20% fra (X) expression. Additional findings include idiopathic precocious puberty and a right ovarian cyst. Ovarian cysts have been reported previously in heterozygous females, but to our knowledge idiopathic precocious puberty is a new finding in this syndrome. Whether precocious puberty is a coincidental finding in this patient or a previously unreported manifestation of the fra (X) syndrome is not clear.

Female↗
PubMed1995

Precocious puberty and decreased melatonin secretion due to a hypothalamic hamartoma.

Hypothalamic hamartomata are benign malformations of the brain consisting of heterotopic nervous tissue, and are often associated with precocious puberty and gelastic seizures in early childhood. We report for the first time the melatonin plasma values of a girl with central precocious puberty and gelastic seizures due to a hypothalamic hamartoma. The melatonin plasma levels were low for the chronological age but appropriate for the pubertal status, making a causal relationship between lowered melatonin plasma levels and precocious puberty possible.

Female↗
PubMed2025

Polycystic ovary syndrome and idiopathic central precocious puberty: two sides of the same coin?

PURPOSE: Several studies have reported an association between central precocious puberty (CPP) and a higher prevalence of polycystic ovary syndrome (PCOS), raising the hypothesis that CPP may act as an early-life indicator of increased PCOS risk. This review investigates the shared genetic, epigenetic, and environmental factors potentially underlying CPP and PCOS, with the aim of clarifying their connection and supporting advances in early detection and management. METHODS: A comprehensive literature review was conducted using the PubMed/MEDLINE database, prioritizing research from the past two decades, supplemented by key studies from earlier years. This research included studies on genetic and epigenetic factors, endocrine-disrupting chemicals (EDCs), and metabolic influences related to CPP and PCOS. Both original research and review articles were selected, focusing on the identification of pathophysiological mechanisms and risk factors linking these disorders. RESULTS: Genome-wide association studies (GWAS) have linked genetic variants in the kisspeptin and neurokinin B signaling pathways to increased gonadotropin-releasing hormone (GnRH) secretion, triggering early puberty. Moreover, increased GnRH pulsatility contributes to elevated luteinizing hormone (LH) levels, altered LH/follicle-stimulating hormone (FSH) ratios, and ovarian hyperandrogenism—key pathophysiological features of PCOS. Additionally, epigenetic modifications, particularly changes in DNA methylation at CpG sites, have been observed in both CPP and PCOS. A hyperandrogenic intrauterine environment and inadequate fetal growth contribute to prenatal epigenetic alterations, while postnatal factors such as obesity, insulin resistance, and exposure to EDCs further influence epigenetic modifications. Although insulin resistance and hyperandrogenism are central features linking CPP to PCOS, the precise mechanisms underlying these associations remain complex and not yet fully elucidated. CONCLUSIONS: Identifying shared genetic and environmental factors influencing early puberty onset and PCOS highlights the importance of close clinical monitoring in early life, though preventive interventions remain unproven. Further research is needed to clarify these mechanisms, which will support the development of more precise prevention and treatment strategies in clinical practice.

Humans↗
PubMed1984

Precocious puberty: a follow up study.

Follow up of women previously seen between 1951 and 1971 with precocious puberty showed that most had normal menstrual cycles and that fertility was generally normal in those with 'constitutional' precocious puberty. Three patients, however, with the McCune-Albright syndrome had not yet proved to be fertile.

Adolescent↗
PubMed1989

Treatment of precocious puberty using an intranasal luteinizing hormone-releasing hormone analogue: Buserelin.

Fourteen patients with precocious puberty were treated for 1-3 years with 900-1800 micrograms/day of intranasal (i.n.) Buserelin. The peak luteinizing hormone and follicle-stimulating hormone responses to intravenous luteinizing hormone-releasing hormone were reduced significantly 4 weeks after starting treatment and remained suppressed while the patients were on treatment. Two patients were withdrawn because of drug non-compliance. Three patients showed regression of pubertal changes, four patients showed no progression and five patients showed progression of breast size or pubic hair staging after 1.5-2 years of treatment. Treatment was changed to the subcutaneous route in two patients because of hormonal escape and accelerated skeletal maturation. The mean growth velocity decreased from 10.78 cm/year (s.e.m. = 0.64) to 7.06 cm/year (s.e.m. = 0.85) after 1 year of treatment (P less than 0.005). After an increase in dosage (from 900 micrograms/day to 1800 micrograms/day) in most patients, further significant falls in growth velocity to 5.29 cm/year (s.e.m. = 0.45), 4.63 cm/year (s.e.m. = 0.8) and 5.06 cm/year (s.e.m. = 0.5) were observed at 18, 24 and 30 months, respectively, compared with the pretreatment value (P less than 0.001). With treatment, the increased rate of skeletal maturation normalized. In 10 patients who had completed 2 years of treatment, the height standard deviation score for bone age improved from a pretreatment value of -2.42 +/- 0.42 to -1.6 +/- 0.42 after 2 years of treatment (P less than 0.01), indicating an improvement in height prognosis. It is concluded that i.n. Buserelin at a dose of 1800 micrograms/day is effective in the treatment of most but not all patients with precocious puberty.

Administration, Intranasal↗
PubMed1988

Intranasal LH-RH analogue treatment of precocious puberty.

The agonistic analogues of luteinizing hormone releasing hormone were used in the treatment of precocious puberty (pp) in children. 12 children with pp were treated for 6 months with an intranasal LH-RH analogue (C6-C3-C2-naphtyl/D-alanine)-LHRH. The majority of the children had central precocious puberty. Only one child had peripheral pp. Laboratory assessment of estradiol, testosterone, LH and FSH levels revealed that 1,000 micrograms/day of this analogue diminished the hormone levels only in the group of children with central and combined pp. Bone age, pelvic ultrasound examination, sexual development and growth rate were determined pre-, during and after the treatment. The growth velocity decreased and gonadal and sexual characteristic ceased advancing after the LH-RH therapy. Biochemical and hematological studies performed in our children did not show any significant changes during the treatment periods. No adverse effects were noted from the intranasal therapy. We conclude, that intranasal therapy is safe, convenient and effective in pp, but not of peripheral origin.

Administration, Intranasal↗
PubMed1999

A novel luteinizing hormone receptor mutation in a patient with familial male-limited precocious puberty: effect of the size of a critical amino acid on receptor activity.

Familial male-limited precocious puberty (FMPP) is a form of luteinizing hormone-releasing hormone (LHRH)-independent isosexual precocious puberty caused by gain-of-function mutations of the luteinizing hormone/chorionic gonadotropin receptor (hLHR). The most common mutation is 1733 A>G, which causes substitution of Asp-578 by Gly. In this study, a male infant presented at the age of 20 months with accelerated sexual development was analyzed for the presence of activating mutations of the hLHR. Analysis of exon 11 of the hLHR gene by genomic polymerase chain reaction (PCR), asymmetric PCR, and dideoxy sequencing identified a single base substitution, 1734 T>A, which led to the replacement of Asp-578 by Glu. The same mutation was found in the mother. Expression of the mutated hLHR in HEK 293 cells demonstrated elevated basal levels of intracellular cAMP in the transfected cells confirming the constitutive activating nature of the mutated hLHR. A possible genotype-phenotype relationship of the hLHR mutations was examined by a comparison of the in vitro activities of the hLHRs carrying the Asp578Gly, Asp578Tyr, Asp578Trp, and Asp578Glu mutations in HEK 293 cells. A positive correlation between the size of the substituting amino acid and the basal level of intracellular cAMP of cells expressing the mutated receptor was demonstrated.

Amino Acid Sequence↗
PubMedDate not supplied

Hypothalamic hamartomas and precocious puberty.

Ten children, five boys and five girls with true precocious puberty at an early age were found to have hypothalamic hamartomas on brain imaging. Very early onset of puberty, varying from a few weeks to three years of age, and rapid progression were characteristic. Accelerated growth velocity and markedly advanced bone age were evident in all. Gonadotropin and gonadal hormone levels were elevated above the prepubertal range. Six children had associated developmental delay or hyperactivity.

Child, Preschool↗
PubMed2006

Sequential comparisons of one-month and three-month depot leuprolide regimens in central precocious puberty.

BACKGROUND: Dosing of monthly depot leuprolide (DL) in central precocious puberty (CPP) varies considerably. U.S. practitioners use 7.5-15 mg, in contrast with the international standard of 3.75 mg. Pubertal suppression using the newer 3-month DL also has been reported from Europe. To date there have been no direct comparisons of these different DL doses. OBJECTIVES: In an open 12-month protocol, we tested the efficacy of three DL doses (7.5 mg- and 3.75 mg-1 month and 11.25 mg-3 month) given sequentially to subjects treated for CPP. Primary outcome measures were stimulated gonadotropin (Gn) levels at 12-wk intervals. The null hypothesis was no difference among doses. METHODS: Both existing and new patients with CPP received our standard therapy (DL 7.5 mg every 4 wk) for a minimum of 24 wk. In subjects with DL-stimulated LH 2 IU/liter or less, the dose was changed to 3.75 mg every 4 wk and evaluated 12 wk later. Subjects who met LH criteria (<4.5 IU/liter) on 3.75 mg then received a single dose of 11.25 mg-3 month and were reevaluated 12 wk later. Serum LH/FSH and sex steroids were obtained 40 min after DL injection. RESULTS: Thirty subjects were enrolled (20 naive; 24 girls, 6 boys), and 21 were evaluated on all three DL doses. DL-stimulated LH levels (mean +/- sd) were 1.30 +/- 0.74, 1.73 +/- 0.99, and 2.13 +/- 1.41 on 7.5 mg, 3.75 mg, and 11.25 mg-3 month, respectively (7.5 vs. 3.75 mg, P = 0.019; 7.5 mg vs. 11.25 mg-3 month, P = 0.004, Wilcoxon ranked sign test). Mean FSH levels were 2.86 +/- 1.91, 3.91 +/- 1.98, and 3.96 +/- 1.34, respectively (7.5 vs. 3.75 mg, P = 0.017; 7.5 mg vs. 11.25 mg-3 month, P = 0.020). No differences were detected in mean sex steroid levels. CONCLUSIONS: Stimulated LH and FSH levels were significantly higher during therapy with both the 3.75 mg and 11.25 mg-3 month depot leuprolide doses, compared with 7.5 mg, contradicting the null hypothesis of no difference. These data suggest that low-dose 1- and 3-month DL preparations are associated with persistently greater gonadal stimulation in most CPP patients, but the LH/FSH results were not corroborated by differences in sex steroid levels. Whether various DL doses lead to long-term therapeutic differences remains to be determined.

Child↗
PubMed2002

CNS germinoma in a boy with simple virilizing 21-hydroxylase deficiency and precocious puberty.

A 6 year-old boy presented with peripheral precocious puberty and was diagnosed as having simple virilizing 21-hydroxylase deficiency based on clinical features and elevated 17-hydroxyprogesterone levels on ACTH stimulation. He was managed with glucocorticoids and mineralocorticoids. Two years later he presented with features of CNS involvement in the form of seizures and raised intracranial pressure with rapid progression of puberty. Contrast enhanced CT scan of brain showed an intraventricular tumor with cerebrospinal fluid cytology suggestive of germinoma. Serum and CSF levels of human chorionic gonadotropin (hCG) and alphafetoprotein (AFP) were elevated, confirming the diagnosis of germinoma.

17-alpha-Hydroxyprogesterone↗