PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Puberty, Precocious”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMed1996

[Precocious puberty].

Explore the source record for details and available documents.

Antineoplastic Agents, Hormonal↗
PubMed2001

Adrenocorticotropin-dependent precocious puberty of testicular origin in a boy with X-linked adrenal hypoplasia congenita due to a novel mutation in the DAX1 gene.

Primary adrenal insufficiency is a rare condition in pediatric age, and its association with precocious sexual development is very uncommon. We report a 2-yr-old Brazilian boy with DAX1 gene mutation whose first clinical manifestation was isosexual gonadotropin-independent precocious puberty. He presented with pubic hair, enlarged penis and testes, and advanced bone age. T levels were elevated, whereas basal and GnRH-stimulated LH levels were compatible with a prepubertal pattern. Chronic GnRH agonist therapy did not reduce T levels, supporting the diagnosis of gonadotropin-independent precocious puberty. Testotoxicosis was ruled out after normal sequencing of exon 11 of the LH receptor gene. At age 3 yr he developed clinical and hormonal features of severe primary adrenal insufficiency. The entire coding region of the DAX1 gene was analyzed through direct sequencing. A nucleotide G insertion between nucleotides 430 and 431 in exon 1, resulting in a novel frameshift mutation and a premature stop codon at position 71 of DAX-1, was identified. Surprisingly, steroid replacement therapy induced a clear decrease in testicular size and T levels to the prepubertal range. These findings suggest that chronic excessive ACTH levels resulting from adrenal insufficiency may stimulate Leydig cells and lead to gonadotropin-independent precocious puberty in some boys with DAX1 gene mutations.

Adrenal Gland Diseases↗
PubMedDate not supplied

Central precocious puberty in a girl with triple X syndrome and neonatal diabetes mellitus associated with paternal isodisomy of chromosome 6.

We describe a girl with triple X syndrome and paternal isodisomy of chromosome 6 (UPD6), who developed neonatal diabetes mellitus (NDM) and precocious puberty. At birth she presented growth retardation and congenital anomalies (ventricular septal defect, macroglossia, umbilical hernia). Diabetes mellitus (DM) was diagnosed at 31 days of life and treated with insulin for 13 months. DM recurred at 4 years of age and since that time it required insulin, in spite of preserved beta-cell function. Tall stature was present from early childhood. At 7 years of age the girl presented central precocious puberty, height velocity further increased, but her near-final height was normal. This patient is unique in that precocious puberty has never been described in triple X females. Moreover it is a further example of paternal UPD6 causing NDM with a predisposition to type 2 DM in later life.

DNA↗
PubMedDate not supplied

Precocious puberty in a patient with indicanuria.

A 7-5/12 year-old girl, who was followed-up after diagnosis of indicanuria, presented with symptoms of bilateral breast enlargement. Her breast development was at Tanner stage II. No pubic or axillary hair was observed. Pelvic ultrasonography revealed multiple follicles on both ovaries. Basic endocrinological evaluation and cranial magnetic resonance imaging (MRI) were normal. The diagnosis of precocious puberty was established with respect to the pubertal response to GnRH stimulation test. Although precocious puberty has been reported associated with some metabolic diseases, this is the first description in a patient with indicanuria. The question of whether precocious puberty in our patient with indicanuria is a coincidence or whether it is related to metabolic changes activating the hypothalamo-pituitary-gonadal axis remains open.

Amino Acid Metabolism, Inborn Errors↗
PubMed1999

Combined use of growth hormone and gonadotropin-releasing hormone analogues in precocious puberty: theoretic and practical considerations.

The rationale underlying the use of gonadotropin-releasing hormone analogues (GnRHa) to treat patients with central precocious puberty is reviewed. GnRHa are now considered the treatment of choice for patients with central precocious puberty, but the adult heights that these patients attain often fall short of what would be expected according to their genetic potential. This has led to investigations of whether adding growth hormone to GnRHa therapy can improve adult height. The results of recent combination trials are presented and analyzed.

Body Height↗
PubMed1987

The effect of cyproterone acetate on the growth of children with central precocious puberty.

We have examined the growth and skeletal maturation of 19 children (6 male, 13 female) with central precocious puberty. The aetiology in nine patients (5 male, 4 female) was secondary to a hypothalamic hamartoma. Six children (2 male, 4 female) received no treatment whereas 13 children (4 male, 9 female) were treated with cyproterone acetate in a mean dose of 68 mg/m2 per day (range, 34-260) for a mean duration of 4.5 years (range, 0.8-7.9). There was no significant difference between height SDS for bone age at the beginning and end of observation in either treated or untreated groups. No significant relationship between the mean dose of cyproterone acetate used and change in height SDS for bone age could be determined. We conclude that cyproterone acetate has no beneficial effect on the growth prognosis of children with central precocious puberty.

Body Height↗
PubMed1984

Treatment of precocious puberty with LHRH analogue in combination with cyproterone acetate-further experience.

Six girls and one boy with precocious puberty were treated with a superactive LHRH analogue (D-TRP6-LHRH) for periods ranging from 1 year to 2 years and 3 months. In the first phase of the treatment it was administered in combination with cyproterone acetate (CyA) to counteract an early stimulatory effect until inhibition of gonadotrophin secretion was achieved. The gonadotrophin-dependent signs i.e. gonadarche, showed sustained arrest and even regression. Gonadal sex steroids decreased but the adrenal androgens were unaffected. In four patients who showed progression of the angrogen-dependent signs (adrenarche), despite suppression of gonadotrophins, increasing the dosage of the LHRH analogue was ineffective and combined therapy with CyA was reinstituted in three of them because of accelerated growth and bone maturation. It is concluded that at present the treatment of choice for precocious puberty is the daily administration of a superactive LHRH analogue such as D-TRP6-LHRH, together with CyA in the initial stage, and at a later state if adrenarche progresses too rapidly.

Androgens↗
PubMed1984

Idiopathic precocious puberty in the chimpanzee: a case report.

A female chimpanzee developed premature sex skin swelling, breast budding, advanced bone age, and moderate estrogen effect of the vaginal cytology. Extensive radiographic and hormonal studies excluded all the known causes of precocious puberty and pseudopuberty, yielding a diagnosis of idiopathic true precocious puberty. To our knowledge this is the first observation of idiopathic true precocious puberty in a chimpanzee.

Animals↗
PubMed1993

Histrelin. A review of its pharmacological properties and therapeutic role in central precocious puberty.

Histrelin is a synthetic gonadotrophin-releasing hormone (GnRH) agonist which, when administered over a prolonged period, suppresses the release of gonadotrophins from the anterior pituitary. Data from clinical trials undertaken in small numbers of patients with idiopathic central precocious puberty have demonstrated that histrelin 8 to 10 micrograms/kg/day administered subcutaneously desensitises the anterior pituitary to gonadotrophin secretion within 3 months, ablating the pubertal gonadotrophin response to GnRH stimulation and reducing circulating gonadal sex steroid levels. When histrelin is administered to treat central precocious puberty, the rate of secondary sexual maturation is slowed and in some cases there is a reversal of maturation which occurs before initiation of treatment. Of equal importance, histrelin therapy appears to have decelerating effects on skeletal maturation, allowing more statural growth; an increase in final adult height is predicted from available data, but will need to be confirmed in long term follow-up studies currently being undertaken. The most common adverse event reported during histrelin therapy was a skin reaction at the site of subcutaneous injection. Few patients have discontinued therapy because of any adverse event. Although experience with histrelin is limited, the absence of effective clinically available alternatives and the demonstrated efficacy of histrelin justifies its place as a first-line therapy for patients with central precocious puberty.

Amino Acid Sequence↗