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 433 records · Page 24Linked to original sources

PubMed1995

Central precocious puberty following feminizing right ovarian granulosa cell tumor.

A 7-month-old girl presented with ascites and breast enlargement due to right ovarian granulosa cell tumor. After tumor removal, the clinical signs of incomplete precocious puberty regressed. Four years later, the patient reappeared with signs of precocious puberty. Our investigations proved that this was not due to tumor recurrence, but it was a true central precocious puberty. She responded well to therapy with a luteinizing hormone releasing hormone agonist, and 3 years after onset of this therapy, she is growing at a normal prepubertal rate.

Antineoplastic Agents, Hormonal↗

PubMed1999

[Precocious puberty secondary to an intramedullary germinoma].

BACKGROUND: hCG secreting tumors are responsible for 21% of precocious puberties in boys. Usual localizations are hepatic, cerebral, mediastinal and gonadic. CASE REPORT: A 4-year-old boy developed precocious puberty with rapid evolution. Serum beta hCG suggested germinal etiology, but radiological procedures failed to find any usual localization. Further occurrence of pain in the legs led to carry out a lumbar puncture. The high cerebrospinal fluid/blood gradient of beta hCG suggested the presence of an intramedullar tumor. Medullar magnetic resonance imaging found a large tumor facing L1 and L2. CONCLUSION: To our knowledge, this localization is described for only the second time.

Cerebrospinal Fluid↗

PubMed1994

Pediatric Adolescent Gynecologic Imaging: Precocious Puberty and Hormone-producing Neoplasms.

Evaluating children with precocious puberty or a hormone-producing neoplasm can be a challenging and time-consuming clinical task that, if done thoroughly, can prove to be well worth the time and effort. A detailed analysis allows the physician to prescribe the best diagnostic and cost-efficient work-up. Here, the author describes the use of various imaging techniques in precocious puberty and neoplasms.

Journal Article↗

PubMed1983

Precocious puberty in a 3-year-old girl associated with a parasellar ganglionic hamartoma.

Precocious puberty due to disorders of the nervous system is uncommon and may arise from neoplastic lesions situated in the pineal gland, hypothalamus, tuber cinereum, and midbrain. Most of these neoplasms maintain connections with or are attached to the central nervous system. Rarely, however, tumors lying free within the meninges may be associated with precocious puberty. A patient with this rare form of precocity who was found to have a parasellar ganglionic hamartoma is described in this report. Her post-operative course was marked by a reversal in her sexual precocity and a subsequent arrest in her accelerated growth rate.

Body Height↗

PubMed1995

A super long-acting LH-RH analogue induces regression of hypothalamic hamartoma associated with precocious puberty.

We treated a 1-year-old female with a hypothalamic hamartoma and precocious puberty with leuprolide acetate depot, a super long-acting hormone-releasing hormone analogue (Tap-144-SR; [D-Leu6-[des-Gly10-NH2] LH-RH ethylamide acetate). The infant's major symptoms were genital bleeding and gynaecomastia. The LH-RH analogue (30 micrograms/kg) was injected subcutaneously once every 4 weeks. Clinical and laboratory manifestations of precocious puberty showed marked improvement. A follow-up after 16 months of treatment, the size of the tumour decreased significantly and remained unchanged for 2 years of further follow-up. To the best of our knowledge, this is the first hypothalamic hamartoma case in whom a decrease of tumour size under treatment with LH-RH analogue has been documented. But, because diagnosis of hamartoma is only based on neuroradiological and not on histological examinations, the possibility of a gangliocytoma cannot be excluded with certainty.

Delayed-Action Preparations↗

PubMed1993

Long-term testolactone therapy for precocious puberty in girls with the McCune-Albright syndrome.

We used the aromatase inhibitor testolactone (40 mg/kg.day) to treat 12 girls with precocious puberty due to the McCune-Albright syndrome for periods of 0.5-5 yr. In the 7 girls who received testolactone for at least 3 yr, the mean +/- SD serum estradiol level was 618 +/- 268 pmol/L at the start of therapy and fell to 156 +/- 84 pmol/L at 1 yr, 116 +/- 48 pmol/L at 2 yr, and 241 +/- 260 pmol/L at 3 yr (P < 0.05 compared to the start of therapy), with recurrent ovarian cysts at 3 yr in 2 patients. These 7 girls averaged 8 menses/yr before therapy. The average frequency of menses decreased to 2 episodes/yr during the first year of treatment, 3/yr during the second year, and 4/yr during the third year. The mean +/- SD testosterone levels were slightly above the normal prepubertal range (0.51 +/- 0.2 nmol/L) before treatment and did not change significantly during treatment. The mean +/- SD androstenedione levels rose from 1.1 +/- 0.6 nmol/L before treatment to 2.1 +/- 0.1 nmol/L at 2 yr and 2.8 +/- 0.1 nmol/L after 3 yr of treatment (P < 0.05 compared to before treatment) and were consistent with normal adrenarche. The mean predicted adult stature was 143.0 +/- 7.8 cm before treatment and 147.3 +/- 11.5 cm at 3 yr (P = NS). In 3 of 12 girls, all with bone age greater than 12 yr, the gonadotropin responses to LHRH indicated early central precocious puberty after 1-4 yr of treatment. The adverse effects of testolactone were transient abdominal pain, headache, and diarrhea in 3 girls and elevated hepatic enzymes in 1 girl who had abnormal liver function before treatment. Six families acknowledged difficulty in adhering to the daily dosing schedule. We conclude that testolactone can be effective in the treatment of LHRH-independent precocious puberty in girls with McCune-Albright syndrome, but that some patients exhibit an escape from the effects of treatment after 1-3 yr.

Age Determination by Skeleton↗

PubMed1984

True precocious puberty complicating congenital adrenal hyperplasia: treatment with a luteinizing hormone-releasing hormone analog.

Congenital adrenal hyperplasia (CAH) is a recognized cause of precocious pseudopuberty. Some children with CAH also develop true precocious puberty with early maturation of the hypothalamic-pituitary-gonadal axis. We have seen four such children (three boys and one girl) who had the diagnosis of CAH made between the ages of 3 and 6 yr. These patients were treated with standard doses of hydrocortisone and fludrocortisone. A diagnosis of true precocious puberty was made because of testicular enlargement in the boys, breast development in the girl, progressive pubic hair development, rapid growth, and rapid bone age maturation. Plasma steroid levels were elevated for age, and gonadotropin levels were within the normal pubertal range, both basally and in response to LHRH stimulation. We treated these children with daily sc injections of a LHRH analog (LHRHa) for 6-18 months in addition to the standard hydrocortisone and fludrocortisone therapy for CAH. LHRHa significantly decreased basal plasma LH and FSH, peak LH and FSH responses to native LHRH, and testosterone levels. Testis size decreased in the males, and breast development regressed in the female. LHRHa therapy led to significant decreases in linear growth rate, ulnar growth rate, and rate of bone age advancement. These results suggest that LHRHa is an effective adjunct to hydrocortisone and fludrocortisone in the treatment of true precocious puberty complicating CAH.

Adrenal Hyperplasia, Congenital↗

PubMed2005

[Treatment of central precocious puberty with Gonadotropin-Releasing Hormone agonist (triptorelin) in girls: breast development, skeletal maturation, height and weight evolution during and after treatment].

Central precocious puberty (CPP) is treated with GnRH analogues to stabilize secondary sexual characteristics and to prevent loss of final height (FH) due to accelerated bone maturation. However, some studies suggest that FH is not always improved and that treatment may induce excessive weight gain. We analysed data from 19 girls treated for CPP with monthly injections of 3.75 mg triptorelin. Pubertal development, bone age, height, weight and body mass index (BMI) were evaluated at start (chronological age: 7.8 +/- 1.8 yrs, mean +/- SD), at the end of treatment (10.6 +/- 1.1 yrs) and at FH (14.9 +/- 2.5 yrs). At start of treatment, breast (B) development was B3 (from 2 to 4), bone age 10.6 +/- 1.7 yrs, height 2.1 +/- 1.1 SDS and BMI 1.3 +/- 0.8 SDS. Treatment stabilized or reduced breast development and decreased bone maturation. Final height was 162.3 +/- 6.6 cm (0.0 +/- 1.1 SDS) and was comparable to predicted adult height at the start of treatment and to corrected mid-parental height. BMI SDS at the start, the end of treatment and at final evaluation were 1.3 +/- 0.8, 1.6 +/- 0.8 and 1.4 +/- 0.9 SDS. In conclusion, in our girls with central precocious puberty, treatment with GnRH agonist stabilized or decreased breast development and stabilized bone maturation, but did not increase neither final height nor weight. Aspects other than height should also be taken into account when considering treatment of children with precocious puberty.

Body Height↗

PubMed1959