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We studied 49 boys and girls with delayed physical sexual maturation during treatment with sex steroids. We found significant agreements, but also some disagreements between physicians' and subjects' Tanner sexual maturity ratings. We found neither effects of treatment with sex steroids nor gender differences, comparing ratings between physicians and patients.
Two hundred fourteen crossbred gilts, born in January through March and June through July of two different years, were raised in total confinement until 100 to 120 days of age and then moved to an outside dirt lot (non-confined) or to a single pen in a confinement, finishing building (confined). Beginning at 150 days of age, estrus was checked daily with a boar to determine percentage of gilts that attained puberty and age at first estrus, and weekly blood samples were collected and analyzed for progesterone by radioimmunoassay to determine age at first ovulation. In the Jan.-Mar. born gilts, 75.4% of the non-confined gilts and 37.4% of the confined gilts attained puberty by 270 days of age (P<.001). Although differences were not significant in the gilts born in June-July, more non-confined gilts (62.6%) than confined gilts (50.9%) attained puberty. Of the 121 gilts that ovulated, only 1 non-confined and 3 confined gilts did not exhibit estrus. Average age at first estrus or at first ovulation were similar for confined and non-confined gilts. Adrenal gland weights at 250 to 270 days of age were similar also for confined and non-confined gilts. Based on the results of this study, we conclude that total confinement housing can reduce, by as much as 50%, the proportion of gilts that attain puberty by 8 to 9 months of age and that time of year may influence the extent of delayed puberty.
There is evidence that the capacity to synthesize gonadotropins is less in teenage boys with gonadotropin deficiency (GD) than in those with constitutional delay of puberty (DP). We hypothesized that this might predispose the latter group to have a greater pituitary-testicular response to the potent long-acting GnRH agonist nafarelin. We evaluated GD patients 14.3-24.0 yr of age (n = 8) and prepubertal DP boys 14.8-17.6 yr of age (n = 3). In most subjects the response to nafarelin was compared to that of frequent nocturnal blood sampling for LH and testosterone levels. All subjects received a single dose of nafarelin (1.0 micrograms/kg, sc), and blood was then sampled at 0.5- to 4.0-h intervals for 24 h. Patients with GD could not be distinguished from those with DP by pubertal staging criteria or by baseline values of LH, FSH, or testosterone. Patients with GD exhibited no rise in plasma LH levels during sleep, in contrast to those with DP. All GD patients had LH and FSH responses distinctly less than those of the DP group between 3-24 h postnafarelin. The peak incremental responses of GD and DP to nafarelin were, respectively: LH, 5.5 +/- 2 3 (+/- SEM and 77.2 +/- 8.6 IU/L (P less than 0.02); FSH, 2.7 +/- 1.2 and 9.4 +/- 0.8 IU/L (P less than 0.005). Testosterone peak responses were lower as well (0.26 +/- 0.2 vs 1.6 +/- 0.5 nmol/L, P = 0.05). This pilot study suggests that the response to a single test dose of nafarelin distinguishes GD from DP in the teenage years as well as does measurement of nocturnal LH levels. The testosterone response to the GnRH agonist adds a new dimension to GnRH testing. Nafarelin also allows assessment of the bioactivity of endogenous gonadotropin, is a more potent stimulus of pituitary-testicular function than endogenous GnRH secretion, and is more cost-effective than nocturnal sampling.
This study was conducted to determine whether the seasonal delay in puberty in autumn is driven by individual differences in night-time melatonin secretion in domestic gilts at the attainment of puberty. A group of spring-born gilts (n = 30) were expected to reach puberty in autumn by the age of 7 months. Eighteen of these gilts were selected in pairs on the basis of matched days of birth. By the expected time, half of the animals showed oestrous symptoms (group CYCLING, n = 9) with the rest remaining silent (group SILENT, n = 9). Afterwards, all gilts were fitted with indwelling jugular catheters for frequent blood sampling. Blood samples were collected from all animals three times during the day followed by three times in the night at 2-h intervals for 48 h. The samples were analysed by a commercial radioimmunoassay (RIA). The results show a consistent 25-fold rise (on average) in night-time melatonin concentration in every animal sampled with group averages ranging from 0.28 +/- 0.04 to 0.37 +/- 0.06 pg/ml at day and from 10.20 +/- 2.16 to 10.67 +/- 0.05 pg/ml at night. Night-time group mean values between CYCLING and SILENT gilts did not differ significantly (10.26 +/- 0.67 and 10.38 +/- 0.94 for the CYCLING; 10.67 +/- 0.05 and 10.20 +/- 2.16 for the SILENT). When 10 pg/ml was used as a threshold value, six individuals did not reach it during the night (low responders). Two of these gilts were CYCLING and four were SILENT. In conclusion, the results presented imply no involvement of the level of night-time melatonin concentration in the seasonal delay of puberty in gilts.
Plasma levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), dehydroepiandrosterone (DHA), dehydroepiandrosterone-sulphate (DHA-S), 17-hydroxyprogesterone (17P), androstenedione (A), testosterone (T), dihydrotestosterone (DHT) and estradiol (E2) were measured in basal conditions in eleven young women from 16 to 25 years of age characterized by delayed puberty. The gonadotropin response to LHRH (50 microgram iv) was also tested in these cases. The results, as far as gonadotropins and E2 are concerned, indicate that delayed pubertyin girls is a heterogeneous disorder: an impairment in the negative feedback between E2 and FSH coexists with a reduced ovarian response to endogenous gonadotropins. All cases showed evidence of a more or less pronounced delayed adrenarche, which was demonstrated by the markedly reduced levels of DHA-S and DHA (with the exception of this latter steroid in two cases with idiopathic hirsutism). Furthermore, the very low plasma progesterone (P) levels in all cases suggest the existence of impaired delta 5 - delta 4 isomerase activity in the adrenal cells. Despite the low levels of A and T, DHT is within the upper limits of the normal range in all cases.
Hyperprolactinaemic hypogonadism in adults is a well defined disease with clinical symptoms like ovarian hypofunction or amenorrhea and galactorrhea in females and loss of sexual activity in males. In pediatrics this special form of hypogonadism is almost unknown. Typical manifestation is delay in puberty or pubertal arrest. We describe a 20 year old man with signs of delay of puberty. Endocrinological work-up revealed a decreased pulse frequency of luteinizing hormone resulting in pathologically low testosterone concentrations. The final cause of hypothalamic hypogonadism was a prolactin producing pituitary microadenoma. During long-term treatment with a dopaminergic drug the elevated prolactin levels decreased to the normal range and testicular function normalized as shown by growth of the testes and increasing testosterone levels.
The effect of pregnant mare serum gonadotropin (PMSG) or estradiol cyclopentylpropionate (EC) on the induction of estrus, duration of estrus, and serum progesterone concentration after estrus was evaluated in 8 gilts with delayed puberty. Four gilts were given 500 IU of PMSG IM and 4 were given 2 mg of EC, IM. The inactive status of the ovaries at the time of treatment was verified by serum progesterone values of less than 0.5 ng/ml in serial samples collected before treatment. The 4 EC-treated gilts came into estrus at a mean of 3.5 days after treatment, but 1 of the gilts did not form corpora lutea. Three PMSG-treated gilts came into estrus at a mean of 4.0 days after treatment. The remaining PMSG-treated gilt remained anestrus and did not form corpora lutea. The mean duration of estrus in EC-treated gilts was 5.25 days compared with 2.0 days for PMSG-treated gilts (P less than 0.05). Serum progesterone concentrations were higher in PMSG-treated gilts than in EC-treated gilts at 8, 11, and 17 days after treatment (P less than 0.05).
Using a sensitive measuring device, 3-day hCG administration (Pregnyl; 1500 IU daily) was shown to temporarily increase ulnar growth velocity from prepubertal (0.40 +/- 0.35 mm/3 weeks to pubertal values (1.1 +/- 0.64 mm/3 weeks) in 10 boys with delayed puberty. This growth-promoting effect of diagnostic hCG administration, which was demonstrable for 3--9 weeks, was associated with an overt rise in plasma testosterone from 129 +/- 126 to 818 +/- 419 ng/100 ml and an approximate doubling of the serum alkaline phosphatase activities from 193 +/- 46 to 376 +/- 115 U/liter, suggesting an initiated growth spurt.
BACKGROUND: Female genital mutilation (FGM) is commonly practiced mainly in a belt reaching from East to West Africa north of the equator. The practice is known across socio-economic classes and among different ethnic, religious, and cultural groups. Few studies have been appropriately designed to measure the health effects of FGM. However, the outcome of FGM on intersex individuals has never been discussed before. CASE PRESENTATION: The patient first presented as a female with delayed puberty. Hormonal analysis revealed a normal serum prolactin level of 215 Micro/L, a low FSH of 0.5 Micro/L, and a low LH of 1.1 Micro/L. Type IV FGM (Pharaonic circumcision) had been performed during childhood. Chromosomal analysis showed a 46, XY karyotype and ultrasonography verified a soft tissue structure in the position of the prostate. CONCLUSION: FGM pose a threat to the diagnosis and management of children with abnormal genital development in the Sudan and similar societies.
We have reviewed the growth of 98 boys and 34 girls with constitutional delay of growth and puberty followed until final height. At presentation chronological age was 14.1 (1.3) years (SD) in the boys and 13.0 (1.3) years in the girls. At presentation all patients were either prepubertal or in early pubertal maturation (4 ml testicular volume in the boys and breast stage II in the girls). Twenty-nine boys (30%) and 2 girls (6%) were treated with either sex or anabolic steroids. Mean height SDS in the boys at presentation was -2.7 (0.7) which rose to -1.9 (0.9) at final height attainment. This was significantly lower than the predicted final height SDS of -1.4 (0.8) and mid-parental height SDS of -0.5 (0.7). Similar results were obtained for the girls with a height SDS at presentation of -3.2 (0.8) which increased to -2.3 (0.7) at final height which was significantly lower than predicted final height SDS of -1.7 (0.6) and mid-parental height SDS of -0.8 (0.8). Both sexes had a relatively short sitting height at presentation; sitting height SDS -3.4 (1.0) and subischial leg length SDS -2.2 (1.0) in the boys and sitting height SDS -3.6 (1.1) and subischial leg length SDS -2.5 (0.7) in the girls. The relative disproportion between the segments had no significant change at final height. We are unable to explain the failure to achieve final height potential and the relatively disproportionate stature. Our data suggest that the late timing of the onset of puberty may be deleterious to spinal growth and consequently final height.(ABSTRACT TRUNCATED AT 250 WORDS)
Thirty-three crossbred gilts that were raised in total confinement were randomly allotted to two adjacent pens in a finishing unit at 144.7 +/- .5 days of age and 58.0 +/- 1.7 kg body weight. At approximately 253 days of age, 16 gilts were group fed a daily dose of 20 mg of Regu-mate per gilt for 18 days and 17 control gilts were group fed the same diet without Regu-mate for 18 days. Ovarian morphology was examined on 11 or 12 days after the last feeding of Regu-mate. Based on estrous behavior and ovarian morphology only one Regu-mate gilt displayed an estrus but did not ovulate and only three of the control gilts displayed estrus and ovulated at least once before the start of treatment. Three of the 16 Regu-mate gilts displayed estrus and ovulated 7.3 +/- .3 days after the last feeding and within the same time period the 3 control gilts, which previously displayed estrus, continued to have estrous cycles. One additional control gilt displayed estrus and ovulated 5 days after the last feeding of the control diet. Therefore, the proportion of gilts that displayed estrus and ovulated by the end of the experimental period were similar for the treated (25.0%) and control (23.5%) groups. Based on these results we conclude that treatment of gilts in a state of confinement-induced delayed puberty with 20 mg Regu-mate daily for 18 days failed to result in a synchronized onset of puberty in a significant proportion of gilts.
Studies relating to the psychosocial aspects of short stature and pubertal delay are reviewed. Although IQ scores show a statistical correlation with stature, significant intellectual, psychological, or academic deficits have not been consistently demonstrated for short children. However, hypopituitary growth failure is associated with poor social adjustment as an adult despite growth hormone therapy. The reasons for this remain unclear. Constitutional pubertal delay in boys can lead to social and academic problems. Treatment with a short course of testosterone can be beneficial in selected cases. Psychosocial considerations should play a major role in the treatment of short stature and pubertal delay.
The fetal environment is now recognized as a key determinant of the adult phenotype, being linked to development of diseases, including hypertension, as well as the timing of puberty. Such links may be related, in part, to the level of fetal exposure to maternal glucocorticoids in utero, which is normally regulated by placental expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD). The present study examined whether manipulation of fetal glucocorticoid exposure, either directly or indirectly via 11beta-HSD inhibition, influences the subsequent timing of puberty. Administration of dexamethasone acetate at low (LDEX, 0.25 microg/ml drinking water) or high doses (HDEX, 1 microg/ml) or carbenoxolone (CBX, 2 x 10 mg/day, sc; an inhibitor of 11beta-HSD) to pregnant rats from day 13 to term (day 23) reduced offspring birthweight (LDEX: 9%; HDEX: 27%; CBX: 8%) and resulted in a subsequent delay in the onset of puberty in females (control: 41.4 +/- 0.5; LDEX: 44.8 +/- 0.7; HDEX: 48.5 +/- 0.4; CBX: 43.6 +/- 0.5 days). Importantly, the effects of CBX were not observed in the absence of maternal adrenals, indicating that they were mediated by increased fetal exposure to endogenous maternal glucocorticoids. In contrast, maternal treatment with metyrapone (MET; an inhibitor of glucocorticoid synthesis; 500 microg/ml drinking water from day 13) increased birthweight by 5% and advanced puberty onset in male offspring (control: 48.8 +/- 1.0; MET: 45.7 +/- 0.8 days). Changes in the timing of puberty onset were not attributable to changes in either bodyweight at puberty or peripubertal plasma leptin concentrations. Peripubertal plasma LH was also unaffected in animals with delayed puberty but was elevated in male offspring of MET-treated mothers. Collectively, these results demonstrate that fetal glucocorticoid exposure is an important determinant of the timing of puberty onset in postnatal life, and that this effect is operable within the normal physiological range of glucocorticoid concentrations.
Two adolescent boys with 45,X/46,XY (XO/XY mosaicism), presented in adolescence with pubertal delay and short stature. Both patients had a history of hypospadias repair, but otherwise normal male genitalia. Scrotal testes were present bilaterally, and no Müllerian structures were identified by pelvic ultrasound. The XO/XY mosaicism suggests that this chromosomal abnormality might be more common in phenotypic males than previously recognized. Because of the increased incidence of testicular neoplasia in patients with XO/XY mosaicism, it is important to document this chromosomal abnormality. We recommend cytogenetic analyses for boys with pubertal delay and hypospadias. If XO/XY mosaicism is documented, the patient must be closely followed for possible development of testicular failure and/or gonadoblastoma.
Sleep-related gonadotropin rhythms are specific for puberty. Sleep-dependent increases of prolactin, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were studied in 6 boys and 1 girl with constitutional delay of growth and puberty. The purpose of this study was to determine whether gonadotropin rhythms occur in the same hormonal sequence in children with constitutional delay of puberty as in normal children. At the onset of puberty a sleep-related FSH increase was detectable, followed by LH-rhythms 1 to 2 years later. The findings of a sleep-dependent FSH increase excludes a hypogonadotropic hypogonadism and triggers the development of secondary sex characteristics.
BACKGROUND AND OBJECTIVE: Tests for growth hormone (GH) deficiency are not always helpful in the differential diagnosis of physiological delay of growth and puberty and GH deficiency. PATIENTS AND METHODS: To enhance diagnostic specificity, we used a single dose testosterone priming before repeating the arginine stimulation test in 26 boys with short stature and only early signs of puberty who failed to show an adequate response of serum GH in the first test. RESULTS: 77% (20/26 patients) increased their serum GH peak to more than 10 ng/ml, whereas six patients were still below this concentration. CONCLUSION: We propose that testosterone priming is a useful tool to distinguish between physiological delay of growth and puberty and GH deficiency and should be included in the diagnostic procedure.
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Eleven boys, mean age 15.3 years (range 13.2-17.5), with pubertal delay in association with steroid therapy for steroid-sensitive nephrotic syndrome and following renal transplantation were treated with oxandrolone 2.5 mg daily for a mean of 0.50 years (range 0.34-0.61). Mean growth velocity increased from 3.9 cm/year (range 1.1-6.3) to 6.1 cm/year (range 2.0-14.4) and was maintained at 6.1 cm/year (range 0.4-10.2) (P less than 0.05). However, there was no significant difference in growth between the treated boys and age- and puberty-matched controls. Elevation of blood cyclosporin A and creatinine levels occurred in the transplant patients. Oxandrolone may initiate a pubertal growth spurt in patients taking steroid therapy for renal disease, but should be used with extreme caution because of potential side-effects.