Early Pubertal Girls Research Articles

Growth hormone response to growth hormone releasing hormone 1-40 in Turner's syndrome.

The response of growth hormone (GH) to acute administration of GH-releasing hormone 1-40 (GHRH) was evaluated in 12 patients with Turner's syndrome and in 12 prepubertal or early pubertal girls. In 7 of 12 patients GHRH induced a definite increase (greater than 10 ng/ml) of plasma GH levels. In 5 patients there was a poor GH rise after GHRH administration (less than 10 ng/ml). Overall, the mean GH response of patients was significantly lower than that of normal girls. Five out of 7 patients with a 45 X,O karyotype had a reduced GH rise after GHRH, while all patients with non X,O karyotype (mosaicism and/or 46 X,iX) had a normal GH response to GHRH. Although the cause of short stature in patients with Turner's syndrome is most likely multifactorial, a reduced pituitary GH reserve, as documented by the reduced GH response to GHRH in some of our patients, may contribute to the growth impairment in this disorder.

Prolonged pulsatile administration of luteinizing hormone-releasing hormone in prepubertal children: diagnostic and physiologic aspects.

In order to test gonadotropic function 30 prepubertal and 2 early pubertal girls and boys were treated with LH-releasing hormone (LRH) in a pulsatile fashion for 7 days. LRH was administered iv either in a dose of 10 micrograms every 90 min or in a dose of 20 micrograms/1.73 m2 every 96 min. On days 1 and 7, just before as well as at the end of LRH treatment, a LRH test (100 micrograms/m2 iv) was performed. In 27 patients a LRH test was repeated 4 (day 11) or 7 days (day 14) after LRH withdrawal as well. Plasma LH, FSH, and estradiol or testosterone levels were estimated during the LRH tests on days 1, 7, and 11/14. The patients were divided into 4 groups: group 1 consisted of 2 girls and 1 boy with gonadal failure, group 2 of 1 girl and 2 boys with intact pituitary and gonadal function, group 3 of 11 girls and 13 boys with various central endocrine disorders, and group 4 of 1 girl and 1 boy with pubertal arrest of unknown origin. In group 1 LRH treatment elicited an increase of both gonadotropins into the castrate range, whereas gonadal steroids did not increase. In group 2 baseline LH as well as the response to LRH increased on day 7. In the boys FSH changed similarly. In the girl baseline FSH increased, but the high FSH response of day 1 decreased. Estradiol and testosterone levels were elevated on day 7. These changes during LRH treatment are similar to those during normal pubertal development. When the LRH test was repeated on day 11/14 basal levels had returned into the prepubertal range and a high response of LH especially was found in all 3 subjects. Patients of group 3 were separated into two subgroups: group 3a, those with, and group 3b, those without an increase of gonadal steroids on day 7 of LRH treatment. Since an increment must be the result of increased gonadotropin stimulation, this probably indicates intact gonadotropic function. Group 3a had a pattern of gonadotropin secretion similar to group 2. In group 3b basal and peak LH levels were lower on day 7 compared to group 3a, whereas FSH levels did not differ. Four or 7 days after LRH discontinuation (day 11/14) basal gonadotropin levels were in the original low range. In the LRH test mean LH peak level of group 3a was 43.7 U/liter, of group 3b 13.1 U/liter (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Lipid profiles in young, female gymnasts

Abstract The relationship between the plasma lipid profile and gymnastic training was evaluated in prepubertal and early pubertal girls. The plasma lipids and lipoproteins were measured in 24 elite gymnasts (age ± s.e.: 12.2 ± 0.3 years), 42 recreational gymnasts (aged 12.0 ± 0.2 years) and 16 control girls (aged 12.0 ± 0.3 years). The girls were matched for sexual maturation (breast development stages 1–3) and for chronological age. The lipid profile of the elite gymnasts was similar to that of the control girls. In the recreational group the level of HDL‐C, the HDL‐C to total plasma cholesterol (TC) and HDL‐C to LDL‐C ratios were higher in comparison with the controls and the talented group (P <0.05). Moreover, this group had the lowest level of LDL‐C in comparison with the other two groups. The results suggest that in children, as in adults, regular physical activity is associated with a lipid profile which is favourable in reducing risks to the cardiovascular system. This benefit was not evident in th...

216. Hormonal investigations in “idiopathic” hirsutism

Objective: We hypothesized that there would be evidence of functional ovarian hyperandrogenism in girls with premature pubarche (PP) at diagnosis. Methods: White girls <8 years of age and black girls <6 years with PP (n = 15) were studied. Prepubertal girls (n = 13; 5.3-10.9 years) and early pubertal girls (n = 8) served as control subjects. The biochemical marker for functional ovarian hyperandrogenism was the 17-hydroxyprogesterone (17-OHP), androstenedione (AD), and estradiol (E2) response to subcutaneous leuprolide during adrenal suppression with dexamethasone. This was studied in girls with PP and in control subjects. Results: ACTH stimulated 17-hydroxypregnenolone (17-OH Preg), dehydroepiandrosterone (DHEA), and AD levels, and 17-OH Preg:17-OHP and DHEA:AD ratios were significantly higher in girls with PP than in prepubertal control subjects (n = 18) (P ≤.003). The ovarian response to leuprolide stimulation was comparable in girls with PP and prepubertal control subjects, but the response in prepubertal study subjects was significantly lower than in pubertal control subjects (P =.016 for Δ17-OHP, P =.001 for ΔAD, and P =.026 for ΔE2). Conclusions: Contrary to the hypothesis, PP in girls was not associated with prepubertal evidence of ovarian hyperandrogenism but was associated with functional adrenal hyperandrogenism. (J Pediatr 2002;141:91-8)

Dynamics of basal pituitary gonadotropin secretion and responsiveness to LRH following estradiol benzoate in normal boys.

The influence of a single intramuscular injection of estradiol benzoate (E2B), 2.5-15 micrograms/kg, on the basal estradiol, LH and FSH and their response to LRH stimulation (50 micrograms/m2, i.v.) performed 20 h after E2B injection, was studied in 52 normal boys aged 6-16 9/12 years. The minimal effective dose of E2B was found to be 10 micrograms/kg. This same dose of E2B which increased plasma estradiol level from 15 +/- 8 to 22 +/- 15 pg/ml (mean +/- SD) at 20 h after the intramuscular injection, suppressed basal plasma LH and FSH and their response to LRH in the prepubertal (n = 12), early-pubertal (n = 12) and late-pubertal (n = 8) boys. It is suggested that the maturation of the hypothalamo-pituitary axis in boys during puberty is under the influence of endogenous estradiol.

Dynamics of basal pituitary gonadotropin secretion and responsiveness to LRH following estradiol benzoate in normal girls.

The influence of a single intramuscular injection of estradiol benzoate (E2B), 2.5-15 micrograms/kg, on the basal plasma estradiol, LH and FSH and their response to LRH stimulation (50 micrograms/m2, i.v.) performed 20 h after E2B injection, was studied in 50 normal girls aged 6-17 years. It was found that the minimal dose of E2B which caused a significant change in the basal and/or LRH stimulated LH and FSH levels was 10 micrograms/kg. This dose increased plasma estradiol level by 10-35 pg/ml, i.e. still within the normal range for the appropriate pubertal stage of the subjects. The same dose of E2B significantly suppressed the basal FSH level in most of the prepubertal (n = 8), early-pubertal (n = 9) and late-pubertal (n = 14) girls and the FSH response to LRH in most prepubertal girls. The basal LH was suppressed in most pre- and early-pubertal girls, but increased significantly in 50% of the late-pubertal girls. The LH response to LRH was significantly increased in most of the girls at all pubertal stages. It is suggested that endogenous estradiol is an important mediator in the maturation of the hypothalamo-pituitary axis in girls from mid-puberty onwards, and that the low physiological level of estradiol present in adolescence is sufficient to induce a gradual increase in pituitary sensitivity to LRH and a positive hypothalamo-pituitary feedback.

Maturation of pituitary gonadotropin secreting potentiality in puberty

To investigate the pubertal maturation of gonadotropin (Gn) secretion, early and mid-pubertal girls were received different rates of LH-RH infusion (0.01 and 0.1μg/m2/min for 4h) and a pulse of LH-RH (10μg) at the end of the infusion. Serial blood samples were obtained and serum LH and FSH were measured by RIA. The releasing effect was assessed as the increment of Gn during infusion and the priming effect as that of in response to a pulse. Sexual maturity ratings were recorded according to Tanner (T). I) At the lower infusion rates, there were no elevations of LH in early pubertal girls, whereas in mid-pubertal girls (T3), serum LH levels were markedly increased during infusion. At higher infusion rates, these releasing effects in early pubertal girls were about the same as that on LH. II) In early pubertal girls, the priming effects of LH-RH were minimal at both infusion rates. On the other hand, in mid-pubertal girls, even after much lower rates of infusion (0.001μg/m2/min), the increments of LH by a pulse were significantly greater than that without prior infusion of LH-RH.

Sex-specific sensitivity of the hypothalamic pituitary axis to estradiol benzoate in normal children

The influence of i.m. estradiol benz. (EB)(10-15 mcg/kg) on basal plasma E2, LH and FSH and their response to LRH (50 mcg/m2 i. v.) in normal children was studied. In all pubertal (n=10), early (n=15) and late pubertal (n=6) boys the single EB inj. suppressed basal LH and FSH and their response to LRH. Pre- (n=5) and early pubertal (n=6) girls had suppression of basal LH and FSH but in late puberty (n=14) the basal LH rose from 1.2±0.5 to 3.0±1.6 mIU/ml (p < 0.05) whereas FSH remained suppressed. The mean peak response of LH to LRH following EB (single inj.) was increased in all pubertal stages (to 1.7±0.4, 17.0±14.8 & 27.3±23.6 mIU/ml respectively). FSH response was increased only in early and late puberty (to 13.4±6.0 and 10.5±1.8 mIU/ml respectively). Following 4 daily EB inj. basal plasma LH and FSH levels and their response to LRH in boys (n=22) and girls (n=17) were inconsistently variable in all stages. In conclusion EB modulates the hypothalamic pituitary regulation of gonadotropin secretion, particularly the pituitary response to LRH, which was found to differ at various pubertal stages in normal boys and girls. The sex-specific sensitivity to physiological plasma estrogen levels may be of importance in the maturation of the hypothalamic pituitary axis during puberty.

The effect of chronic childhood malnutrition on growth and gonadotropin excretion during puberty

There is little information available in man regarding gonadal vs. hypothalamic-pituitary contributions to malnutrition-related delayed puberty. To investigate this question, a cross-sectional study was made of 342 rural (R) and 358 urban (U) Kenyan (Bantu) chilren, ages 10-17. Comparative data in early pubertal girls revealed the following mean differences (p<.01) in anthropometry: FSH and LH excretion (mIU/hr) was determined by radioimmunoassay of timed urine specimens. Mean gonadotropin values for individuals in middle and late pubertal stages were similar between the 2 nutritional groups. In early pubertal childhood, however, LH secretion (but not FSH) was lower in malnourished boys (50±7.0 vs. 76±5.5 mIU/hr, p<.05) and girls (55±8.8 vs. 99±12 mIU/hr, p<.01), equivalent to levels in the prepubertal, urban group. On the basis of age urinary gonadotropins were consistently lower in rural children 10-13 yr old. Conclusions: 1) The onset of puberty in man is not determined by size. 2) Gonadotropin relationships to age and pubertal stage in the 2 nutritional categories suggest pituitary rather than gonadal factors mediate the delayed onset of puberty associated with malnutrition.

Hormonal Changes in Girls with Precocious Adrenarche

Serum concentrations of dehydroepiandrosterone, DHA sulfate, estradiol, and prolactin in 20 girls with precocious adrenarche were compared with those of healthy girls of varying age and degrees of breast and sex hair development. Production of adrenal androgens, as reflected by serum DHA and DHA-sulfate concentrations, was significantly increased in PA above that in age-matched control subjects. Surprisingly, in spite of their lack of breast growth, the patients with PA also had serum estradiol levels that were higher than in the prepubertal girls and similar to those found in girls with both breast and pubic hair development. Serum prolactin concentrations in the patients with PA were not increased over those of the age-matched ( 8 years) and early pubertal girls serum prolactin levels were lower. The finding of increased estradiol levels suggests that precocious adrenarche is not a distinct endocrine entity, but merely represents a variant of early adolescence in which estrogen secretion is sufficient to influence adrenal 3β-hydroxysteroid dehydrogenase activity with a resultant rise in DHA production, but not sufficient to produce clinically apparent breast changes. The data do not support a similar role for prolactin.

Hormonal changes in girls with precocious adrenarche: A possible role for estradiol or prolactin

Serum concentrations of dehydroepiandrosterone, DHA sulfate, estradiol, and prolactin in 20 girls with precocious adrenarche were compared with those of healthy girls of varying age and degrees of breast and sex hair development. Production of adrenal androgens, as reflected by serum DHA and DHA-sulfate concentrations, was significantly increased in PA above that in age-matched control subjects. Surprisingly, in spite of their lack of breast growth, the patients with PA also had serum estradiol levels that were higher than in the prepubertal girls and similar to those found in girls with both breast and pubic hair development. Serum prolactin concentrations in the patients with PA were not increased over those of the age-matched (less than 8 years) prepubertal girls. In the older prepubertal ( greater than 8 years) and early pubertal girls serum prolactin levels were lower. The finding of increased estradiol levels suggests that precocious adrenarche is not a distinct endocrine entity, but merely represents a variant of early adolescence in which estrogen secretion is sufficient to influence adrenal 3beta-hydroxysteroid dehydrogenase activity with a resultant rise in DHA production, but not sufficient to produce clinically apparent breast changes. The data do not support a similar role for prolactin.