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Results for “Central precocious puberty”

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13 recordsLinked to original sources

PubMed1978

Hypothalamo-pituitary-gonadal function in male central precocious puberty.

Eleven boys aged 1-10 years with central precocious puberty were studied. According to the pubertal development six were classified as P2, one as P3 and four as P5. In all cases plasma testosterone levels were definitely elevated (1.7-5.8 ng/ml) when compared with pre-pubertal controls. Peak values after HCG (3 X 1500 units) in four of the boys were in the high adult range. The binding capacity of serum testosterone oestradiol binding globuline (TeBG) ranged between 0.5 and 7.30 microgram/dl. Basal plasma levels of LH and FSH were respectively 2.06 +/- 0.64 and 1.2 +/- 0.25 miu/ml, and peak levels after LHRH (0.1 mg/m2) 13.9 +/- 3.7 and 2.6 +/- 0.43 miu/ml respectively. The data demonstrated a significant increase of plasma testosterone and post LHRH LH peak levels in boys with central precocious puberty when compared with pre-pubertal controls. The patients at stage P2 exhibited high levels of plasma testosterone contrasting with the degree of pubertal maturation, high values of TeBG and low response to LHRH which were in the pre-pubertal range. These findings suggest that the testicular sensitivity to LH increases early in boys with central precocious puberty, while the testosterone responsiveness, both at peripheral and hypothalamic levels, is delayed.

Child↗

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↗

PubMed2026

Biallelic EZH1 Nonsense Novel Variant in Two Siblings with Neurodevelopmental Disorder and Central Precocious Puberty: A Case Report from a Consanguineous Saudi Family.

Neurodevelopmental disorders (NDDs) are a group of conditions that impair the development and function of the central nervous system. Recently, variants in the EZH1 gene have been associated with neurodevelopmental disorders. Here, using whole-exome sequencing coupled with confirmatory Sanger sequencing, we identified a homozygous nonsense variant in EZH1 in two affected siblings. Both parents were heterozygous carriers of the variant. The variant is predicted to result in a 44-amino acid C-terminal truncation within the catalytic SET domain, leading to loss of protein function. RT-qPCR analysis revealed significantly reduced EZH1 mRNA expression in patient-derived peripheral blood cells. The index patient (female) also exhibited elevated gamma-glutamyl transferase (GGT) levels and hypoalbuminemia, whereas the affected male presented with central precocious puberty. This study further expands the clinical, genetic, and molecular spectrum of EZH1-associated neurodevelopmental disorders by demonstrating that reduced EZH1 expression is consistent with a loss-of-function disease mechanism.

Child↗

PubMed1976

The neuro-radiological examination of endocrine disorders of central origin in the child (precocious puberty, hypopituitarism).

The neuro-radiological findings in 38 cases of precocious puberty of central origin and 9 cases of hypopituitarism (craniopharyngiomas excepted), are reported. The radiological examination consisted of plain films of the skull and pneumo-encephalography. In the 9 cases with hypopituitarism radiological examination was normal in 4 and localised but quite diverse anomalies were discovered in 5. Out of 38 patients presenting with isosexual precocious puberty, 29 were female and 9 male. Out of the 29 girls, neuro-radiological examination was normal in 20 and showed a hypothalamic anomaly in 9. Out of the 9 boys, 8 had a hypothalamic anomaly, and only one examination was normal. In precocious puberty we found 1 ectopic pinealoma and 2 gliomas of the chiasma. In these three cases the clinical context and radiological examination made the diagnosis obvious. Masses were discovered in 7 (3 spongioblastomas and 4 heterotopias). In 2 cases (spongioblastomas) neurological symptoms were present and made an operation mandatory. In 5 cases (1 spongioblastoma, 4 heterotopias) precocious puberty was an isolated finding. It was not possible to make, on a clinical or radiological bases, a distinction between spongioblastoma and heterotopia. As time has passed the role of surgery has changed. Formerly, surgery aimed at excision of the lesion, but with advances in medical treatment surgical intervention is now directed towards biopsy and the histological study of lesions which may be treated by radiotherapy.

Adolescent↗

PubMed1978

Asymmetric ovarian enlargement in idiopathic precocious puberty.

A patient with precocious puberty is presented in whom the pneumogynogram showed only one enlarged ovary. Because tumor could not be excluded, the patient had exploratory operation six weeks later. Both ovaries and the uterus were enlarged, compatible with the central stimulation seen in idiopathic precocious puberty. Care should be used in interpreting pneumogynograms as evidence of possible ovarian tumor in young girls with precocious puberty who have only modest unilateral ovarian enlargement.

Child↗

PubMed1979

Fibrous dysplasia and precocious puberty (McCune-Albright syndrome).

A patient with fibrous dysplasia and precocious puberty, with pneumogynographic demonstration of an enlarged uterus and ovaries at age 16 months has been followed up to age 14 years. The pneumogynographic findings and the chemistries implicate central nervous system stimulation as the cause of the precocious puberty.

Air↗

PubMed1975

Giant axonal neuropathy. A clinical entity affecting the central as well as the peripheral nervous system.

An 8-year-old girl had progressive muscle weakness and a unique posture of the lower limbs, areflexia, distal sensory impairment, and remarkably kinky hair. Histologic examination of the sural nerve showed giant axons filled with neurofilamentous masses. The clinical and histologic findings resembled those of recent cases reported as "giant axonal neuropathy." Our patient's precocious puberty, Babinski's sign, and electroencephalographic abnormalities suggested central nervous system involvement. Two cases previously reported and the present one appear to represent a new clinical entity that affects the central and the peripheral nervous system.

Axons↗

PubMed1977

[Central nervous manifestations of neurofibromatosis in children (author's transl)].

Serious central nervous manifestation of neurofibromatosis have been reported in 11 children aged 1,5-12 years. According to the present literature we conclude: 1. Central nervous lesions of neurofibromatosis are common even in childhood. 2. About two thirds of these patients suffer from brain tumors. 3. The tumors involve the suprasellar region in many cases. 4. By this localisation endocrine manifestations, especially precocious puberty, are frequent.

Astrocytoma↗

PubMed1976

Studies on the puberty-controlling function of the mediocortical amygdala in the immature female rat.

The puberty-controlling function of the mediocortical amygdala in immature female rats was investigated by lesioning this region at different ages and by studying the effects on the onset of spontaneous and experimentally-induced precocious puberty. At 21 days of age, bilateral lesions in the anterior mediocortical amygdala (AMCA) caused precocious puberty and enhanced the puberty-accelerating effect of bilateral lesions produced simultaneously in the medial preoptic area (MPA). Similar lesions, ineffective on day 26, delayed the onset of puberty when produced on day 32 in otherwise untreated rats. Lesions in the posterior mediocortical amygdala (PMCA) at 26 or 32 days of age postponed puberty in untreated rats and inhibited the advancement of their 1st pubertal ovulation that resulted from damage to the ventromedial-arcuate region (VAH) or daily administration of 0.05 mug estradiol benzoate (EB) per 100 g b.w. The results confirm earlier findings of different gonadotropin-controlling activities of the AMCA and PMCA in immature female rats and suggest maturational changes in the function of both areas. The gonadotropin-inhibiting action exerted by the AMCA at 3 weeks of age is lost when puberty approaches; a gonadotropin-stimulating activity seems to develop in both the AMCA and PMCA.

Age Factors↗

PubMed1977

Hypothalamic hamartoma: a source of luteinizing-hormone-releasing factor in precocious puberty.

The presence of a hypothalamic hamartoma and precocious puberty in a 19-month-old boy provided an opportunity to study their relation. Excised tissue had the ultrastructural characteristics of an independent neuroendocrine unit -- i.e., neurons containing neurosecretory granules and blood vessels with fenestrated endothelium and double basement membranes. Immunofluorescence studies using specific antibody to luteinizing-hormone-releasing factor showed antigenicity to the factor in the hamartoma. The testicular-hypothalamic-pituitary axis was tested. Clomiphene unresponsiveness suggested a lack of maturation of central-nervous-system events characteristic of normal puberty. The negative feedback system between gonad and brain was intact but partially resistant to steroid suppression. These studies suggest that hypothalamic hamartomas may cause precocious puberty by autonomous production and release of luteinizing-hormone-releasing factor into vessels that communicate with the pituitary portal blood system.

Brain Neoplasms↗

PubMed1978

Premature craniosynostosis: A common complication of juvenile thyrotoxicosis.

Cranial vault suture opacification (apparent closure) and bone age were evaluated roentgenographically in ten children with thyrotoxicosis. The bone age was advanced greater than 2 SD in only one. In comparison to 96 control children of similar age, craniosynostosis was present in each of the patients with thyrotoxicosis. Children with advanced bone age, nine due to virilizing adrenal hyperplasia and three with precocious puberty, had normal radiographic patterns of cranial suture closure. Thyrotoxic premature craniosynostosis did not interfere with continued head circumference growth nor did it result in clinical or radiographic evidence of increased intracranial pressure. We conclude that premature craniosynostosis appears to be a common feature of juvenile thyrotoxicosis. Investigation of the possible long-term adverse effects of this entity on central nervous system function is advocated.

Adolescent↗

PubMed1976

Changes in the concentration of LH, FSH and estrogen in the immature female rat during precocious sexual maturation induced by electrochemical stimulation of the brain.

Electrochemical stimulation of the hypothalamus of 23-day-old female rats induced precocious puberty as judged by occurrence of vaginal opening, the degree of uterine hypertrophy, changes in ovarian steroid content and incidence of first ovulation. Three types of responses were observed: (I) pubertal ovulation within 96 h; (II) pubertal ovulation within 120 h, and (III) vaginal opening at 120 h not followed by ovulation. All treated animals showed a sustained increase in the LH/FSH ratio in both pituitary and plasma. Plasma estrogen was also increased 1 h after stimulation. A preovulatory rise in plasma estrogen and gonadotropins was noted in type I and type II animals. These data lend further support to the suggestion that brain stimulation causes a release of gonadotrophins which induced ovarian steroidogenesis leading to an ovulatory gonadotropin surge via a positive feedback effect.

Animals↗

PubMed1978

Sexual precocity in association with septo-optic dysplasia and hypothalamic hypopituitarism.

Sexual precocity in association with abnormalities of the central nervous system is well known, but its occurrence with hypothalamic hypopituitarism is most unusual. We report five females with septo-optic dysplasia, blindness, and multiple pituitary tropic hormone deficiencies: all were growth hormone and adrenocorticotropic hormone deficient; two had diabetes insipidus; one had sexual precocity, and one had early pubertal maturation, whereas three were prepubertal and responded to administration of synthetic gonadotropin-releasing hormone. These children retained ability to secrete gonadotropins despite the presence of anterior hypothalamic disease. Experimental data from primates plus our observations on these patients raise questions about the role of the anterior hypothalamus in gonadotropin secretion in man.

Adolescent↗