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Results for “Puberty, Precocious”

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PubMed2006

Induction of precocious puberty in heifers I: enhanced secretion of luteinizing hormone.

In beef heifers weaned between 3 and 4 mo of age and fed a high-concentrate diet, approximately 50% reach puberty before 300 d of age (precocious puberty). The objectives of this experiment were 1) to determine whether precocious puberty could be induced experimentally by weaning heifers early and feeding a high-concentrate diet, and 2) to determine the dynamics of secretion of LH associated with precocious puberty. Crossbred Angus and Simmental heifer calves were weaned at 73 +/- 3 d of age and 115 +/- 3 kg of BW and fed a high-concentrate (60% corn; HI, n = 9) or control diet (30% corn; CONT, n = 9). Heifers were fed individually, and target BW gains were 1.50 and 0.75 kg/d for the HI and CONT treatments, respectively. Heifers were weighed every 2 wk. Blood samples were collected weekly and assayed for progesterone concentration to determine age at puberty. Serial blood samples were collected at 20-min intervals for 24 h at mean ages of 102, 130, 158, 172, 190, 203, 217, 231, and 259 d and assayed for LH concentration to evaluate the dynamics of secretion of LH. Heifers fed the HI diet exhibited greater BW gain (P < 0.01) than CONT heifers (1.27 +/- 0.05 vs. 0.85 +/- 0.05 kg/d, respectively). As a result, BW in the HI treatment was greater (P < 0.01) than in the CONT treatment by 188 d of age and remained different through the end of the experiment. Precocious puberty occurred in 8 of 9 heifers fed the HI diet and 0 of 9 heifers fed the CONT diet. Age at puberty was reduced in the HI (P < 0.01) compared with the CONT heifers (262 +/- 10 vs. 368 +/- 10 d of age, respectively). Body weight at puberty was also reduced in the HI (P < 0.05) compared with the CONT treatment (327 +/- 17 vs. 403 +/- 23 kg, respectively). Heifers attaining puberty during the experiment continued with subsequent luteal phases as evidenced by cyclic patterns of progesterone concentrations. Frequency of pulses of LH (pulses/24 h) increased with age (P < 0.01) for both treatments. Heifers in the HI treatment exhibited a greater number of pulses of LH (P < 0.01) than those in the CONT treatment by 190 d of age and in all subsequent collection periods (treatment x age, P < 0.05). Mean LH concentrations also increased with age (P < 0.01) for both treatments but did not differ between treatments. In conclusion, precocious puberty induced by early weaning and feeding of a high-concentrate diet is preceded by increasing frequency of pulses of LH.

Aging↗

PubMed1976

A female case of the HCG-producing ectopic pinealoma associated with precocious puberty.

A female case of precocious puberty associated with HCG-producing ectopic pinealoma was reported. The patient, a 5-year-old girl, was referred to the hospital because of headache and choked discs. Physical examination revealed normal physical growth with breast enlargement. Endocrinological study revealed a high plasma HCG concentration of 1192 ng/ml with a normal FSH level. None of HCG, LH and FSH did respond to the LH-RH test. A partial resection of the tumor and an external X-ray irradiation relieved the symptoms and breast enlargement subsided with a remarkable decrease in the plasma HCG level. Histological examination revealed two-cell-pattern pinealoma and electron microscopic findings showed abundant secretory granules in the dark cells. HCG content in the tumor was as high was 400 ng/mg of acetone dried tumor tissue, but no FSH was detectable. Hitherto, all of the reported cases of precocious puberty associated with pineal tumors have been exclusively boys. A normal level of plasma FSH concentration with a somewhat elevated prolactin level might be a contributory factor for the development of precocial sexual development in the present case.

Child, Preschool↗

PubMed1991

[Undulating course of precocious puberty].

The normal course of precocious puberty is progredient resulting eventually in full sexual maturation. In few cases a transient form of the disease has been recorded, characterized by a temporary appearance of signs of sexual maturation. We report on a female patient with an undulating course of the disorder: after precocious initiation of puberty, a temporary interruption and subsequent resumption of sexual maturation occurred. Presently, the patient is successfully treated with an LHRH-analogon. Within the framework of this case problems in diagnosis and treatment of precocious puberty are being discussed.

Age Determination by Skeleton↗

PubMed2006

Hypomelanosis of Ito associated with precocious puberty.

Hypomelanosis of Ito has been associated with precocious puberty in two cases. This study reports a third case involving a female with hypomelanosis of Ito including severe mental retardation and seizure disorder with autonomic symptoms (gastroesophageal reflux and asthma). At age 5 she developed vaginal discharge, thelarche, and adrenarche. Soon after, she died of pneumonia stemming from her neurologic deficits. A postmortem examination revealed normal gonads and endocrine organs. The breasts and vulva were prematurely developed. Central nervous system findings included megalencephaly, neuronal eosinophilic inclusions, leptomeningeal neuroglial heterotopias, and cortical dysplasia. Both previously reported cases of hypomelanosis of Ito associated with precocious puberty had abnormal gonads and responded to cyproterone acetate therapy, indicating a peripheral mechanism of precocious puberty (gonadotrophin-independent). The current case, which was autopsied, lacks significant gonadal pathology, and has extensive neurologic involvement that suggests that a central mechanism of precocious puberty (gonadotrophin-dependent) can also be associated with hypomelanosis of Ito.

Brain↗

PubMed1987

Precocious puberty after traumatic brain injury.

After traumatic brain injuries in 33 prepubertal children, precocious puberty was observed in seven. Precocious puberty developed significantly more frequently in girls than in boys (54.5 versus 4.5%, P less than 0.01). Six children with precocious puberty were in coma for greater than or equal to 2 weeks. Follow-up computed tomography revealed cerebral atrophy or focal encephalomalacia in all children with and 69% of children without precocious puberty. There were no striking differences in incidence of motor or cognitive deficits or posttraumatic epilepsy in children with and without precocious puberty. In four of five children, basal sex steroid levels were elevated, and the response to luteinizing hormone releasing hormone stimulation revealed a pubertal pattern after the appearance of secondary sex characteristics.

Brain Injuries↗

PubMed1986

The NIH experience with precocious puberty: diagnostic subgroups and response to short-term luteinizing hormone releasing hormone analogue therapy.

Between 1979 and 1983, 129 children (95 girls) with precocious puberty were referred to the National Institutes of Health and received treatment for at least 6 months with the long-acting LHRH analogue D-Trp6-Pro9-NEt-LHRH. The majority (107 of 129) of the children had central precocious puberty mediated by activation of the hypothalamic-pituitary-gonadal axis in association with hypothalamic hamartomas (24 of 107) or other central nervous system lesions (21 of 107), or idiopathic precocious puberty (62 of 107). Hypothalamic hamartomas or other central nervous system lesions were a frequent cause of central precocious puberty in girls (27 of 87), but idiopathic precocious puberty was still the most frequent diagnosis (63%). Idiopathic precocious puberty was uncommon in boys (6%). The patients with peripheral precocious puberty included six girls with McCune-Albright syndrome and six boys with familial male precocious puberty. These children had peripheral sex steroid secretion in the absence of hypothalamic-pituitary-gonadal axis maturation. The children with combined peripheral and central precocious puberty included nine children with congenital adrenal hyperplasia and one girl with a virilizing adrenal tumor. In the patients with central precocious puberty or combined peripheral and central precocious puberty, LHRHa therapy caused suppression of gonadotropin and sex steroid levels (P less than 0.001), stabilization or regression of secondary sexual characteristics, and decreases in growth rate and in the rate of bone age maturation (P less than 0.005). Patients with peripheral precocious puberty, however, had no significant change in gonadotropin or sex steroid levels, growth rate, or the rate of bone age maturation, and no improvement in secondary sexual characteristics. Thus, LHRHa is an effective treatment of central precocious puberty and combined peripheral and central precocious puberty, but is ineffective in the therapy of peripheral precocious puberty.

Adrenal Hyperplasia, Congenital↗

PubMed1998

Exaggerated 17-hydroxyprogesterone response to short-term adrenal stimulation and evidence for CYP21B gene point mutations in true precocious puberty.

OBJECTIVE: Following the observation of two patients affected by true precocious puberty who went on to develop polycystic ovary syndrome (PCOS) and who were found to be heterozygotes (carriers) for 21-hydroxylase deficiency (21-OHD), we decided to evaluate the frequency of heterozygosity for adrenal 21-OHD in patients with true precocious puberty. STUDY DESIGN: We investigated 32 girls affected by true precocious puberty, by the single-dose ACTH stimulation test, HLA typing and the molecular analysis of the CYP21B gene encoding for the 21-OH enzyme, in order to detect gene deletions or point mutations. Twenty-eight cases were on LHRH analogue treatment and the remaining four, untreated owing to parental refusal, were investigated 0.5-1.5 years after spontaneous menarche. RESULTS: After ACTH testing, 13 out of the 32 (41%) cases displayed higher 17-hydroxyprogesterone (17-OHP) levels than normal but less than those found in patients affected by nonclassical adrenal hyperplasia (CAH); these levels were similar to those observed in obligate heterozygotes for CAH due to 21-hydroxylase deficiency (21-OHD). HLA typing showed a significantly increased frequency of the HLA alleles A28 and B14 which are peculiar to the HLA haplotypes of nonclassical CAH due to 21-OHD. Molecular analysis of the CYP21B gene showed that in four out of the 10 tested patients with an exaggerated 17-OHP response there were heterozygous point mutations of the CYP21B gene. In contrast, no CYP21B gene abnormalities were detected in the eight tested patients with normal 17-OHP. No differences were found between carriers and non-carriers of the 21-OHD with regard to age at onset of precocious puberty, clinical features, bone age acceleration and gonadal suppression induced by LH-RH analogue treatment. Two out of the four untreated patients who were investigated after menarche were found to be carriers of the 21-OHD; these girls showed signs of androgen excess, irregular menses and polycystic ovaries. CONCLUSIONS: A high frequency of heterozygosity for adrenal steroid 21-OHD was found in our patients with true precocious puberty. This adrenal defect does not seem to influence the pattern of central precocious puberty, but these patients require long-term follow-up as they might go on to develop polycystic ovary syndrome (PCOS). Whether or not heterozygosity of the 21-OHD may be related to the premature activation of the hypothalamo-pituitary-gonodal axis remains to be defined.

17-alpha-Hydroxyprogesterone↗

PubMed2004

Precocious puberty at an endocrine centre in Jordan.

BACKGROUND: Data from developed countries about precocious puberty are abundant; data from developing countries are limited. Causes are different, and diagnostic and treatment possibilities are very expensive. The present study aimed to display the spectrum of initial presentation and aetiology among children with precocious puberty and to assess any association between th e clinical features and the underlying cause of the condition. PATIENTS AND METHOD: Forty-three girls and seven boys with precocious puberty were diagnosed at the Endocrine Clinic of Jordan University Hospital and at The National Center for Diabetes, Endocrinology and Genetics, Amman, Jordan, between the 1984 and 2003. RESULTS: Mean age for the girls with precocious puberty was 4.1 years +/- 2.5 SD and for the boys was 2.4 years +/- 1.9 SD. Among the girls, 21% presented with breast development only, 9% with pubic hair appearance only and 70% with multiple signs. All the boys presented with pubic hair appearance and enlarged genitalia. Organic causes for precocious puberty were detected in 42% of the girls and in all the boys. Idiopathic precocious puberty was more common among the girls presenting with breast development only (89%) compared with those presenting with multiple presenting signs (50%), and also was more common among girls presenting between 6 and 8 years (82%) than among those presenting < 6 years of age (42%). Congenital adrenal hyperplasia was diagnosed in four boys and four girls, and hypothyroidism in three girls. CONCLUSION: Precocious puberty in the girls was usually of idiopathic origin when it presented with breast development only and at age older than 6 years. Congenital adrenal hyperplasia and hypothyroidism could represent important causes for precocious puberty in our community.

Child, Preschool↗

PubMed1985

Dental development in precocious puberty.

One hundred and one children with precocious puberty were given an oral examination. Dental root development was assessed using panoramic radiographs. All mandibular canines, pre-molars, and molars which could be visualized without apparent distortion were included. The patients were grouped for analysis according to the etiology of their precocity, e.g., McCune-Albright syndrome, familial male, congenital adrenal hyperplasia, central nervous system lesions, and idiopathic precocious puberty. Dental development was significantly retarded relative to their chronological age in patients with idiopathic precocious puberty. However, no significant abnormal dental development was detected in any of the other groups. Individual oral-facial growth and development remain the primary considerations for timing orthodontic treatment.

Age Determination by Skeleton↗

PubMed1977

[Precocious puberty associated with Silver's syndrome].

Precocious puberty has been reported as an important feature of the Silver-Russell syndrome. The present case refers to a boy entered puberty at the chronological age of 11 years and the bone age of 6 years 6/12. Criteria for precocious puberty in this syndrome are discussed by comparison with previously published cases, and it is concluded that abnormalities in clinical pubertal development are quite unusual in this syndrome.

Bone Diseases, Developmental↗

PubMedDate not supplied

The effect of medroxyprogesterone acetate on gonadotropin secretion in girls with precocious puberty.

Plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) as detected by radioimmunoassay have been found to be present in prepubertal children and show a gradual rise until the onset of puberty. Children with idiopathic true precocious puberty have plasma gonadotropin levels which are appropriate for their advanced degree of sexual development. A potent progestational agent, 6-methyl-17-hydroxyprogesterone acetate or medroxyprogesterone has been used in the treatment of precocious puberty and will suppress its physical manifestations. In this study the effect of medroxyprogesterone on gonadotropin levels was investigated in seven girls with true precocious puberty. Plasma LH values were found to be significant lower in patients receiving this agent than in a group of normal prepubertal girls. FSH values did not differ from the control group. One patient was evaluated prior to treatment and showed decreasing levels of LH after therapy was begun. These data suggest that medroxyprogesterone may act on the pituitary-hypothalamic axis to suppress the pubertal levels of LH.

Adult↗

PubMed1950