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PubMed1996

[The function of the hypothalamo-hypophyseal-gonadal system in patients with Friedreich's ataxia].

Both the decrease of reproductive adaptation and effect of reproductive compensation were revealed in 19 cases of Friedreich's ataxia (FA). Retardation of sexual development was observed, the degree of which correlated with the age of disease manifestation. By means of radioimmunoassay basal and stimulated secretion of hypophysial and peripheral sex hormones were examined in 6 males and 9 females (17-30-years). The gonadal hypofunction was observed as the consequence of hypothalamo-hypophysial insufficiency. The decrease of follicle stimulating hormone and prolactin levels was found. The conclusion was made that pathological process in FA involves hypothalamus that causes in turn insufficiency of norepinephrine and epinephrine hypothalamic neurotransmission.

Adolescent↗
PubMed1997

Inhaled corticosteroids: clinical relevance of safety measures.

There seem to be individual, end organ, and tissue variations in responsiveness to glucocorticoids. In some children, 400-800 micrograms/day of inhaled steroid reduces cortisol excretion and short-term growth of the lower leg. These effects only become clinically relevant if the capacity of the adrenal gland to respond to stress is impaired or there is an adverse effect on bone metabolism and height velocity. Low morning plasma cortisol or reduced the cortisol excretion suggests the possibility of adrenal suppression. A stimulation test using adrenocorticotrophic hormone 500 ng is safer and more discriminating than using adrenocorticotrophic hormone 250 micrograms. For research purposes, measurement of urine cortisol metabolites over 24 hours closely approximates adrenal corticosteroid production. The dynamics of bone turnover of children are different to those of adults. Biochemical and physical studies of bone metabolism of children are hampered by a lack of age- and sex-specific normal values. Osteocalcin is probably the marker of choice for bone formation and pyridinium crosslinks for bone resorption. Bone density data in asthmatic children are limited, but so far reassuring. Knemometry is a sensitive technique for comparing the systemic absorption of different inhaled steroids, but does not relate to long-term growth. Growth velocity in asthmatic children is influenced by seasonal variation, delay in puberty, disease severity, and the use of oral steroids. These variables must be taken into account when assessing the effects of inhaled steroids. Height measurements made over a period of less than 1 year are liable to error and misinterpretation. There is no evidence that inhaled steroids, when appropriately prescribed in standard doses, have an adverse effect on long-term growth. However, children taking above-standard doses of inhaled steroids need their growth monitored using stadiometric measurements every 3-4 months by trained personnel using regularly calibrated equipment.

Adolescent↗
PubMed1996

The role of luteinizing hormone-beta gene polymorphism in the onset and progression of puberty in healthy boys.

An immunologically anomalous LH with two point mutations in its beta-subunit gene (Trp8Arg and Ile15Thr) has recently been described. This polymorphism is common in Finland; 28% of the population are homo- or heterozygous for the variant allele. To assess the effect of the LH variant on LH action, we correlated its presence in a group of 49 healthy boys with the onset and progression of puberty. This group was followed-up longitudinally from a mean age of 11.7 +/- 0.1 yr for 3 yr at 3-month intervals. In addition, we studied the prevalence of the variant LH in boys with constitutional pubertal delay (testicular volume < or = 4 mL after 13.5 yr of age). The LH beta gene status of each subject in this study was judged from a single venous blood sample using two immunofluorometric LH assays with different combinations of monoclonal antibodies: one detecting both the variant and wild-type LH, and the other detecting only wild-type hormone. Of the boys with pubertal onset at a normal age, 36 (74%) were homozygous for the wild-type LH beta allele, 12 (24%) were heterozygous, and 1 (2%) was homozygous for the variant LH beta allele. Clear differences in pubertal parameters were found between the boys with normal and mutated (homo- or heterozygous) LH genotypes. During the follow-up, the boys with the mutated genotype had smaller testicular volumes (P < 0.03), were shorter (P < 0.02), had slower growth rates (P < 0.04), and had lower serum insulin-like growth factor I-binding protein-3 levels (P < 0.03) than the boys with the normal LH genotype. In the boys with delayed onset of puberty, the frequency of the variant LH beta allele did not differ from that in the reference population, indicating that the variant LH is not associated with conditions due to disturbed control of the reactivation of GnRH secretion. We conclude that during the progression of puberty, the variant LH may be less active in stimulating testicular growth than wild-type LH. Thus, the gene may affect tempo, contributing to the wide normal variation in pubertal progression in healthy boys. Our results also suggest that the variant LH not only affects the course of puberty, but is already involved in the regulation of the GH-insulin-like growth factor I axis during childhood.

Adolescent↗
PubMed2006

Reproductive toxicity of trenbolone acetate in embryonically exposed Japanese quail.

This study was conducted to assess the effects of a one time embryonic exposure to trenbolone acetate on reproductive development and function in Japanese quail (Coturnix japonica). Embryos were exposed to either 0.05, 0.5, 5, or 50microg trenbolone or a sesame oil vehicle control at embryonic day 4. Onset of puberty, gonadal histopathology, sperm motility, cloacal gland size, and male copulatory behavior were assessed in adults. Trenbolone delayed onset of puberty in males, inhibited cloacal gland development, and reduced male reproductive behaviors. Industry laboratories have shown trenbolone acetate to be non-teratogenic in mammalian studies. Our study, however, shows that this one time in ovo exposure delayed onset of puberty in and suppressed adult copulatory behavior in quail males. These results suggest that this one time embryonic exposure to trenbolone may have disrupted development of either the central nervous system or the hypothalamic-pituitary-gonadal axis. This is the first study to demonstrate a demasculinizing effect on copulatory behavior in Japanese quail from embryonic exposure to a non-aromatizable androgenic chemical. More studies are needed to determine the mechanisms behind the observed effects.

Animals↗
PubMed1982

Plasma albumin, parasitic infection and pubertal development in Egyptian boys.

Pubertal stage was assessed in 453 Egyptian boys aged from nine to 17 years. Weights and albumin concentrations were measured and parasites identified from stool samples. The mean age to reach each stage of puberty was significantly delayed in the presence of low albumin levels and parasites. The magnitude of the delay was greater for genital stage 2 than for later stages. Weight was also lower in children with reduced albumin concentration or parasites. Among children of the same age, weight and albumin were positively correlated (P less than 0.001), suggesting that albumin status is involved in the timing of puberty.

Adolescent↗
PubMed1999

Deficits in female reproductive function in GH-R-KO mice; role of IGF-I.

Mice homozygous for targeted disruption of the GH receptor/GH binding protein gene (GH-R-KO mice; -/-) exhibit reduced plasma IGF-I levels, elevated plasma GH levels, and dwarf phenotype. Although most GH-R-KO mice are fertile, age at first conception is greatly delayed in -/- x -/- matings. Here we report that the age of vaginal opening is significantly delayed in GH-R-KO vs. normal mice, but it can be advanced by treatment with recombinant human (rh)IGF-I. In pregnant GH-R-KO females, fetal size is reduced and pregnancy is prolonged while placental weight is, unexpectedly, increased. Alterations in fetal and placental weight are related to maternal rather than fetal genotype. Moreover, litter size and body weight of newborn pups are significantly reduced in GH-R-KO vs. normal females. Reduction in litter size reflects both dam and sire effects. We conclude that GH resistance and consequent reduction in peripheral IGF-I levels is associated with delay of female puberty, alterations in fetal and placental growth, delay of parturition, and reduced litter size.

Animals↗
PubMed1993

Anti-müllerian hormone and testosterone serum levels are inversely during normal and precocious pubertal development.

Anti-Müllerian hormone (AMH), also called Müllerian inhibiting substance or factor, is produced by Sertoli cells from fetal life until puberty. In the present study, AMH, testosterone (T), LH, and FSH were measured by immunochemical methods in the serum of 50 boys with normal or delayed pubertal development, 4 patients with suspected androgen insensitivity, and 11 patients with either central (CPP) or gonadotropin-independent (GIPP) precocious puberty to investigate the hormonal regulatory mechanisms of AMH secretion at puberty. An inverse relationship between AMH and T levels was demonstrated. In boys with normal or delayed puberty with T concentrations below 6.7 nmol/L, AMH values were elevated (mean +/- SEM, 22.4 +/- 3.1 micrograms/L) and widely dispersed. In subjects with T levels over 6.7 nmol/L, AMH levels were uniformly low (3.4 +/- 0.5 micrograms/L), except in patients with suspected androgen insensitivity. No significant relationship was found between AMH and gonadotropin levels. Similar results were obtained in patients with either CPP or GIPP. Longitudinal studies were performed on four boys with CPP and two with GIPP before and after treatment. At the time of diagnosis, the T concentration was high, and AMH levels were usually low in CPP and GIPP patients alike. When appropriate treatment was initiated, the T concentration was normalized within 2-4 weeks, but restoration of prepubertal AMH levels required several months. Mature Sertoli cells were observed in testicular biopsies performed in three patients with untreated GIPP. Our results suggest that gonadotropins are not directly implicated in repression of AMH synthesis at puberty, but, rather, that the decrease in AMH production is the consequence of an androgen-mediated, long term, reversible chain of events leading to morphological and functional maturation of the Sertoli cells. Thus, the fall in serum AMH levels appears to be an excellent marker of Sertoli cell pubertal development.

Adolescent↗
PubMed1993

Disorders of puberty in boys.

Puberty is the last phase of the complex process of sexual maturation, a process by which an individual acquires reproductive competency. This article reviews the physiologic and physical changes of normal puberty and the causes of either delayed or precocious sexual development of boys.

Adolescent↗
PubMedDate not supplied

Gonadotropin secretion in infantile rats exposed to ethanol in utero.

Previous studies have shown that fetal alcohol exposure (FAE) alters reproductive function in both male and female rats. In females, FAE delays the onset of puberty, reduces a preovulatory-like LH surge, and results in an early onset of acyclicity. In males exposed to ethanol in utero, the perinatal surge of testosterone is reduced. During the infantile period of the female rat, there is a dramatic increase in plasma follicle-stimulating hormone (FSH), which is thought to play a role in initiating ovarian activity and perhaps the onset of puberty. In this study, we determined the effects of FAE on the patterns of gonadotropin secretion during the infantile period [postnatal days (PND) 8-21] in both male and female rats. Timed pregnant dams were fed a liquid diet containing 35% ethanol-derived calories during the final week of gestation. Control dams were fed either an isocaloric diet with sucrose substituted for ethanol (pair fed, PF) or laboratory chow (chow fed, CF). Male and female pups were sacrificed on PND 8, 10, 12, 15, 18, and 21, and trunk blood was collected. In males, LH levels decreased to a nadir on PND 18, and this decrease was blunted by FAE (p < 0.05). In contrast, FSH secretion was not altered by FAE. In females, plasma FSH levels were greater than males, and increased to peak on PND 12. This FSH peak was significantly delayed in FAE females (p < 0.02). There was no age-related change in LH levels in FAE females, and LH levels were not altered by FAE. The delayed peak of FSH secretion by FAE correlates with the delay in puberty previously seen in females. To investigate this further, we examined the possibility that the delay in the peak of serum FSH in FAE females is due to a reduced number of FSH-producing gonadotrophs. FSH-containing gonadotrophs were identified by immunocytochemistry. Cell counts of FSH-immunoreactive cells in pituitaries from PND 8, 15, and 21 control-fed and FAE female rats showed developmental increases in the number of FSH gonadotrophs per unit area (p < 0.001), but no treatment differences were observed. Overall, these data show that fetal alcohol exposure can alter gonadotropin secretion in infantile life in male and female rats. Importantly, the delay in FSH secretion in females may ultimately play a role in the delay in puberty observed in the FAE female rat.

Animals↗
PubMed2006

Bone age and onset of puberty in normal boys.

Many conditions that delay skeletal maturation also delay the onset of puberty, whereas conditions that accelerate skeletal maturation often hasten the onset puberty, raising the possibility that skeletal maturation influences pubertal onset. To determine whether this concordance is also present in normal children, we analyzed data from 30 normal boys participating in a longitudinal study. Height, weight, and serum testosterone concentrations were assessed every 6 months and bone age (Fels method) every year. Pubertal onset was defined by serum testosterone > or =30 ng/dL. The variability in bone age at onset of puberty was not less than the variability in chronological age. In addition, there was no significant correlation between skeletal advancement and pubertal advancement (r=0.01, P=0.9). Similarly, there was not a significant correlation between pubertal advancement and height age advancement, weight age advancement, or BMI age advancement. Our findings do not support the hypothesis that skeletal maturation directly influences the age of pubertal onset in normal boys.

Adolescent↗
PubMed2002

Factors affecting onset of puberty.

In humans, foetal and early postnatal growth failure may have persistent consequences for growth and pubertal development in later life. During this period, the developing organs are still plastic to change their function, which may have long-lasting effects. At the time of onset of puberty, acute factors may also interfere with pubertal development. Malnutrition, as seen in anorexic patients, and chronic diseases with malabsorption or diseases with systemic effects result in a delayed onset of puberty. We have observed an earlier onset of puberty in girls with low birth weight; menarcheal age also tended to be earlier. In boys, a low birth weight tended to be associated with a later development. Two rat models with growth failure based on perinatal malnutrition have been examined, one with intrauterine growth retardation (IUGR) by ligation of the uterine arteries and one with postnatal food restriction (FR) by increasing the litter size postnatally. In both models, the rats had a persistent postnatal growth failure. The onset of puberty in female rats, defined by vaginal opening, was delayed only in the IUGR group. Despite a significantly lower weight, there was no difference in the timing of puberty onset in the FR group. In IUGR rats, the ovaries had fewer follicles, while FR rats had a normal number of follicles but an abnormal maturation pattern. In male rats, both models showed a delayed onset of puberty, defined by the balano-preputial separation, as well as impaired testicular function, shown by decreased testosterone levels. These data indicate that early malnutrition during a critical developmental time window may have long-lasting effects on pubertal development, including gonadal maturation in both humans and rats.

Adolescent↗
PubMed1984

Effects of confinement on attainment of puberty in gilts.

The present work is a review of experiments realized in order to determine the effects of confinement conditions on attainment of puberty in gilts. Few authors have compared age at first estrus or first ovulation of gilts bred in total confinement, in open front buildings and in outdoor dirt lots. Results are not always significant but lead to conclude to a detrimental effect of confinement on attainment of puberty (5 to 17 day delay). Interactions with other factors such as genotype, season of birth, age at treatment explain the differences between results. Large variations are also observed in the response of confined gilts housed in different conditions of intensity and duration of light, temperature and social environment. However, high temperature and individual penning induce a delay in age at puberty (4 to 10 days). Although the sexual development is known to depend on hormonal control, studies regarding the influence of environmental conditions on hormonal secretions are recent, rather scarce and incomplete. Significant variations in the pineal gland activity, the plasma levels of prolactin, LH and estrogens have not yet been associated with confinement, intensity and duration of light. A disruption of the corticosteroid rythm has been observed in individual compared to group penned animals. Estrus response to gonadotropin hormones is not modified but ovarian response to estrogen is reduced by confinement. Further experiments taking into account the existence of interactions between genotype, light and temperature conditions, season of birth and social relations are required in order to investigate more precisely the influence of the different types of environment on the hormonal secretions and consequently the sexual development of gilts.

Age Factors↗
PubMedDate not supplied

Longitudinal estimates of puberty timing in Senegalese adolescent girls.

This study aimed to assess the timing of sexual maturation (breast development and menarche occurrence) among sub-Saharan African adolescent girls from rural areas. In the framework of a longitudinal study of growth at puberty, the stages of pubertal development (Tanner classification) and menarche occurrence were recorded at intervals between 1995 and 2000 in a sample of 406 Senegalese adolescent girls from a rural area. Nutritional status was estimated during infancy, childhood, and adolescence within this sample, and body composition was estimated only during adolescence. At the beginning of the study (1995), the adolescent girls were 11.4 years old (SD = 0.6). At the end of the study, they were 16.5 years old (SD = 0.6). Median and quartile ages at entry into each maturity stage and its confidence limits were estimated by a lognormal parametric survival model. These adolescent girls were shorter and thinner than girls of the same age from developed countries. Median age at the onset of breast development was 12.6 years (95% CI = 12.5-12.8). Median age at the end of sexual maturation and median age at menarche were estimated respectively at 15.8 years (95% CI = 15.7-15.9) and 15.9 years (95% CI = 15.7-15.9). These adolescent girls were less mature than other adolescent girls of the same age from other developing countries. Their puberty was extremely delayed compared to that of adolescent girls of the same age from industrialized countries. Puberty in these Senegalese adolescent girls is delayed by about 3 years. This may be due to malnutrition, significant energy expenditure, and poor diet and living conditions, and possibly to genetic control.

Adolescent↗
PubMed2002

Amplitude of pubertal growth in short stature children with intrauterine growth retardation.

OBJECTIVE: Pubertal growth contributes to 15-18% of adult height. A blunted pubertal peak could contribute to short adult height in short children born with intrauterine growth retardation (IUGR). DESIGN AND METHODS: Pubertal growth, from onset of puberty to final height, was investigated in 75 short IUGR children: 47 were treated with recombinant human growth hormone (GH) (tx) before pubertal onset (mean dose: 0.4 IU/kg/week); 28 were not treated (no-tx). They were compared with 98 normal children. RESULTS: Puberty occurred later in IUGR children than in controls (boys 14.2 +/- 1 years vs. 12.1 +/- 0.8 years; girls 12 +/- 1 years vs. 11.2 +/- 0.8 years; p < 0.0001). In girls, total pubertal growth was similar in all three groups (tx: 19.3 +/- 4.8 cm; no-tx 19.8 +/- 4.9 cm; controls 20.2 +/- 3.9 cm; non-significant). IUGR boys had a reduced pubertal growth (tx: 21.3 +/- 6.2 cm; no-tx: 23.9 +/- 6.1; controls 26.9 +/- 3.9 cm; p < 0.05). The age at puberty onset was the major determinant of pubertal growth amplitude (boys: r = 0.53, p < 0.001; girls: r = 0.45, p < 0.001). IUGR children exhibited little catch-up growth during puberty. CONCLUSIONS: In the present study, we describe a delayed onset of puberty in short children born with IUGR. Moreover, prepubertal GH treatment was associated in boys with a decrease in the amplitude of the pubertal spurt, a finding that should be further evaluated in clinical trials.

Adolescent↗
PubMedDate not supplied

Growth and puberty in thalassemia major.

Growth and sexual development were evaluated in 54 (29 female, 25 male) patients with beta-thalassemia major aged 2.7-21.3 years (mean 10.4 yr). Mean pretransfusion hemoglobin concentration was 7.8 +/- 0.7 mg/dl. All patients except 6 were on desferrioxamine. Age of starting of therapy was 6.8 +/- 3.9 years. Mean SDS values for height, weight and sitting height were significantly lower (p < 0.001) than control cases of similar age. Height deficiency exceeded -2 SD in 18 patients and a delay in bone age (> 2 SD below the mean) was observed in 36 out of 54 patients. Among 11 patients over 14 years, 9 showed delay in onset or progression of puberty and 10 had growth retardation. Height SDS were negatively correlated with chronological age, age of onset of desferrioxamine and present serum ferritin levels (p < 0.001). These findings indicate that abnormal growth and delayed puberty are frequent in transfusion dependent thalassemics. These can be partly overcome by early onset of chelating therapy.

Adolescent↗
PubMed1988

Management of idiopathic growth hormone deficient patients during puberty.

Boys with idiopathic GH deficiency, treated with hGH and entering spontaneous puberty, have an onset of puberty and peak height velocity (PHV) at a late chronological age but normal bone age. PHV occurs at G3 with testicular volumes of 6-12 ml. The size of PHV and the height gain after G2 are similar to those of a normal delayed adolescent. In contrast, idiopathic GH deficient girls have an onset of puberty and PHV nearer to a normal chronological age and at an early bone age. PHV occurs at B2 and its size and the height gain after B2 are similar to those of normal girls. The length of time of pubertal growth is shorter in both GH deficient boys and girls. Very late induction of puberty in idiopathic GH deficient boys results in psychosocial damage and in bodily disproportion. It is suggested that induction of puberty be considered no later than 14.5 years in boys and 13.5 years in girls with the use of low-dose sex steroids. The decision to induce puberty should be taken to avoid psychosocial problems and be independent of proof of associated gonadotrophin deficiency. In GH deficient girls with early puberty, therapies to delay puberty may be considered. There are theoretical grounds for increasing the GH dose given during puberty, but present dose-response studies fail to include controls for important biological variables and are so far inconclusive. Cost-effectiveness is an important consideration. Increasing the frequency of injections probably improves the growth effect for a given dose of GH.

Adolescent↗
PubMed1991

Growth hormone response following growth hormone releasing hormone injection in thalassemia major: influence of pubertal development.

Thirty-five patients with thalassemia major, aged 7 to 21 years, were studied to define the relationship between the pubertal development and the growth-hormone (GH) secretion during sleep, after administration of GH-releasing factor (hpGRF 1-44), and betaxolol-glucagon or arginin-insulin. Pubertal development was classified as being appropriate or delayed for chronological age. GH response to pharmacological stimuli and during sleep was not linked to the pubertal development according to the chronological age. The peak of GH secretion after GHRH injection was significantly delayed in thalassemic patients with retarded puberty. The integrated secretion of GH during the 120-min test was slightly but not significantly reduced in these patients. The prepubertal pattern of GHRH response was restored in the patients receiving substitutive therapy by HCG or testosterone. The alteration of GH response to GHRH in thalassemic patients is likely to be only due to delayed puberty and decreased endogeneous GHRH secretion since it is corrected by androgen or gonadotropin replacement.

Adolescent↗
PubMed1993

Effect of deslorelin-induced pubertal delay on the growth of adolescents with short stature and normally timed puberty: preliminary results.

LH-releasing hormone agonist (LHRHa) treatment slows bone maturation and improves adult height in children with LHRH-dependent precocious puberty. To determine whether pubertal delay induced by LHRHa can enhance final height in patients with short stature and a normally timed puberty, we enrolled 43 short children (28 girls and 15 boys) in a double blind, placebo-controlled trial. Patients were assigned randomly to receive either placebo or LHRHa (deslorelin), administered sc at a dose of 4 micrograms/kg.day for a period of 4 yr. This report describes the preliminary results in 16 children who have completed 4 yr of treatment (9 patients in the deslorelin group and 7 patients in the placebo group). Predicted adult height increased significantly in the deslorelin-treated patients, by 7.6 cm compared to the pretreatment baseline and by 10.3 cm compared to that in the placebo-treated patients (P < 0.005). Four of the 16 patients received concurrent GH treatment (3 among the deslorelin-treated patients and 1 among the placebo-treated patients). Omitting these patients from the analysis did not materially affect the results: predicted adult height in the deslorelin-treated patients increased by 7.2 cm compared to the pretreatment baseline and by 10.9 cm compared to that in the placebo-treated patients (P < 0.005). We conclude that pubertal delay induced by deslorelin significantly increases predicted adult height in adolescents with short stature and a normally timed puberty. Whether deslorelin treatment will increase the final height of these patients cannot be determined until they have stopped growing.

Adolescent↗