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PubMed1980

Involvement of a cholinergic mechanism in the mediation of hippocampal influences on female sexual maturation and somatic development.

Female Wistar rats were bilaterally lesioned in the anterior part of the ventral hippocampus (VHPC) at 21, 26 or 32 days of age. Irrespective of the age at lesioning a significant delay of vaginal opening and of the first ovulation was recorded. This delay of the onset of puberty was consistently associated with a retardation of the body weight increase. Both the puberty-delaying and growth-retarding effects of VHPC lesions produced on day 21 could be prevented by daily s.c. injections of 50 micrograms/100 g b.w. pyridostigmine from day 21 till vaginal opening, but not by the administration of 2 mg/100 g/day pargyline. The findings suggest a cholinergic mediation of stimulatory effects exerted by the hippocampus on sexual maturation and somatic development.

Animals↗
PubMed2006

[Sexual development of children and teenagers in the families deported from Abkhazia (dynamic observation)].

The aim of the study was the evaluation of physical and pubertal development of children from the families deported from Abkhazia who were exposed to significant psycho-somatic stress and prolonged socio-economical infringement. Dynamic observation started in 1998. Children, 9-15 years of age, have been studied. 200 children have been selected by the individualised methods (115 were girls and 85 were boys). In parallel children of appropriate age and gender groups from the local families have been studied. The investigations were conducted according to the generally accepted schemes and tables suggested by Tenner (17), for girls and by V.M. Vedenski (8) for boys, respectively. The analysis of obtained results showed that the total percent of delayed puberty in studying group was 21.4% versus 30.0% in the groups of 1998. Consequently, index of delay in control group was equal to 3.9% (2005) and 5.0% (1998). The group, exceeding the norms of puberty (accelerates) was 4.8% versus 11.2% in control group in comparison with the data of 1998--5.4% versus 15.0%, respectively. It should be concluded that due to the obtained results, comparing with the analogic groups of 1998, the number of delayed puberty has been reduced by approximately 9.0%. The number of cases exceeding the norms of puberty has been decreased slightly.

Adolescent↗
PubMed1985

Estrogens before birth and development of sex-related reproductive traits in the female guinea pig.

Influences of estrogens on the differentiation of psychosexual traits in the female guinea pig were studied. Pregnant animals were injected intramuscularly with either 1, 2, or 3.3 micrograms estradiol benzoate (EB) or with 1 or 3 micrograms diethylstilbestrol dipropionate (DESDP). Injections were started on the 29th day of pregnancy, given daily for 6 days, and continued every other day until parturition. Female offspring were evaluated for onset of puberty, ovarian function, and lordosis and mounting behavior in adulthood. Prenatal treatment with 3 micrograms DESDP caused delayed puberty, impaired ovarian function, reduced responsiveness of lordosis to EB and P in adulthood (defeminization), augmented mounting in the absence of hormones (masculinization), and reduced responsiveness of mounting to exogenous EB and P in adulthood (defeminization). Prenatal treatment with 1 microgram DESDP produced similar but less pronounced effects. Prenatal treatment with 3.3 micrograms EB also caused a delay in puberty. However, responsiveness of lordosis to EB and P in adulthood was enhanced by treatment with either 1 or 3.3 micrograms EB prenatally. Further, neither mounting in the absence of hormones nor mounting in response to EB and P in adulthood were affected in any measurable way by any prenatal treatment with EB. These results show that estrogens can have masculinizing and defeminizing effects on sexually dimorphic reproductive traits in guinea pigs. The failure of EB to duplicate or parallel the effects of DESDP is not completely understood at this time, but it may indicate that less of the active substance reaches the target tissues following maternal and placental metabolism of EB than of DESDP.

Animals↗
PubMed2000

Delayed growth and puberty in patients with Gaucher disease type 1: natural history and effect of splenectomy and/or enzyme replacement therapy.

BACKGROUND: Growth retardation in childhood was only recently recognized as a prominent feature of Gaucher disease type 1, but there are few data on both the pubertal development and the final outcome of growth and sexual maturation. OBJECTIVE: To investigate the natural pattern of growth and puberty in patients with Gaucher disease type 1 and the effect of splenectomy and enzyme replacement therapy. METHODS: We retrospectively analyzed growth and puberty in 57 patients with Gaucher disease type 1; 52 were followed since childhood and/or prepuberty and 42 have reached sexual maturity and final height. In the analysis we considered severity of disease, time of splenectomy, and start of enzyme replacement therapy. RESULTS: Deceleration of growth at age 3-5 years was observed in 30 of 57 patients followed since early childhood while untreated: height-SDS decreased from -0.34 +/- 0.42 at age 0-3 years to -1.93 +/- 0.95 (P < 0.01) at age 7-10 years and was more pronounced with severe disease. A high prevalence (59.6%) of delayed puberty, which was more frequent with severe disease, was observed in 47 patients followed before and throughout puberty. No primary endocrine pathology was found. All patients, untreated as well as treated, with growth and pubertal delay had a spontaneous catch-up, achieved full sexual maturation, and most (83.3%) reached a final height within the range of parental height-standard deviation score. Splenectomy (partial and/or total) performed in 20 patients while still growing had a beneficial effect on growth, which was temporary in some and did not affect puberty. ERT improved growth in 11 patients who started therapy before puberty, as evidenced by a progressive increase in the height-SDS, and seemed to normalize the onset of puberty. CONCLUSIONS: Growth retardation in childhood and delay of puberty are characteristic of Gaucher disease type 1 and are more frequent with severe disease. There is a spontaneous catch-up later in life and most patients reach a final height within their genetic growth potential. Enzyme replacement therapy apparently normalizes growth and possibly also the onset of puberty.

Adolescent↗
PubMed1986

Peripheral anosmia affects puberty-influencing chemosignals in mice: donors and recipients.

A series of five experiments tested the effects of peripheral anosmia on both donors and recipients of urinary chemosignals that accelerate and delay puberty in female mice. Control tests determined that the manipulations, in and of themselves, did not bring about any changes in release or reception of the chemosignals. Rendering mice peripherally anosmic using a solution of zinc sulfate did result in effects on both donors and recipients. For donors, release of the substances in male urine, urine from females in estrus, or urine from pregnant or lactating females, all of which accelerate female puberty, were not influenced by peripheral anosmia. Peripheral anosmia did, however, bring about the cessation of release of the substance in the urine of grouped adult females that delays sexual maturation in conspecific females. Peripherally anosmic young female recipients of the chemosignals were accelerated in their sexual development when the treatment applied involved urine from pregnant or lactating females. However, the acceleratory effects normally produced by male urine or urine from females in estrus did not occur in peripherally anosmic young females. The substance in the urine of grouped adult females did not produce delays in puberty when the recipient females were rendered peripherally anosmic prior to urine treatment.

Animals↗
PubMed1999

Pubertal growth as a determinant of adult height in boys with constitutional delay of growth and puberty.

In boys with constitutional delay of growth and puberty, adult height may be inconsistent with parental (target) height. We aimed at studying which period of growth was important to account for adult height being above or below target height. In this retrospective study, adult height measured after 20 years in 39 patients was compared with target height and height data obtained at about 6 and 12 years of age and at diagnosis of delayed puberty (mean 14.6 years). Twenty-eight patients were untreated while 11 received testosterone enanthate (50 or 100 mg/month for 6 months). The growth data from both groups were pooled since they were not different. On average, the adult height standard deviation score (-0. 6 +/- 0.8, mean +/- SD) was similar to target height (-0.5 +/- 0.6). There were, however, marked individual differences since adult height varied between 1.7 SD (11 cm) below target height and 1.4 SD (9.5 cm) above target height. Multiple regression analysis showed that the most significant determinant of the difference between adult height and target height was height catch up during puberty (p < 0.002). We conclude that the magnitude of height catch up during puberty is a significant determinant of adult height in boys with constitutional delay of growth and puberty. Thus, optimizing pubertal growth may be a relevant therapeutic aim for adult height in boys with short stature and delayed puberty. Copyrightz1999S. KargerAG,Basel

Adolescent↗
PubMed1994

The effect of changing gonadotropin-releasing hormone pulse frequency on puberty.

We have examined the effect of using different pulse frequencies of exogenous GnRH to induce puberty and the time relationship among LH, FSH, sex steroids, and GH in these individuals. Five girls and three boys with delayed puberty received exogenous GnRH at either 3-h frequency (slow) or every 45 min (fast). Treatment was initially given overnight and increased to 24 h when breast stage 3 in girls or testicular volume of 10 mL in boys was attained. Twenty-four-hour gonadotropin profiles were performed after 5 days, 1 month, 3 months, 6 months, and 1 yr of treatment. Temporal relationships among LH, FSH, and estradiol; LH and testosterone; GH and estradiol; and GH and testosterone were examined by cross-correlation. There was no difference in the rate of pubertal progress between the groups. Mean serum gonadotropin and sex steroid levels did not differ. LH was correlated with estradiol for both groups at 240 min (slow group, r = 0.54; fast group, r = 0.50). Estradiol correlated with LH at 300 min in the slow group (r = -0.41) and 200 min in the fast group (r = -0.37). FSH correlated with estradiol at 140 min in the slow group (r = 0.62) and 160 min in the fast group (r = 0.50). A rise in estradiol occurred 140-160 min after a rise in FSH and 240 min after a rise in LH. A rise in estradiol was followed 200-300 min later by a fall in LH. LH was correlated with testosterone at 60 min in the slow group (r = 0.73) and at 40 min in the fast group (r = 0.55). Testosterone correlated with LH at 420 min in the slow (r = -0.67) and 460 min in the fast group (r = -0.40). A rise in LH was followed 40-60 min later by a rise in testosterone. A rise in testosterone was followed by fall in LH 420-460 min later. GH correlated with estradiol at 320 min in the slow group (r = 0.37) and 380 min in the fast group (r = 0.38). A rise in GH was followed, after 320-380 min, by a rise in estradiol. There was a correlation between GH and testosterone in the slow group after 280 min (r = 0.44). A rise in GH was followed by a rise in testosterone after 280 min. The pituitary-gonadal axis is sufficiently robust to allow puberty to progress with different fixed pulse frequencies. There is a temporal relationship among LH, FSH, and estradiol secretion and between LH and testosterone secretion. We have demonstrated the feedback effect of sex steroids at the level of the pituitary and the time course of the effect of GH on gonadal function.

Adolescent↗
PubMed1995

Oxandrolone therapy in constitutionally delayed growth and puberty. Bio-Technology General Corporation Cooperative Study Group.

BACKGROUND: Male adolescents with constitutional delay of growth and puberty may have significant psychosocial difficulties related to their sexual immaturity and short stature. The purpose of this study was to test the hypothesis that 1 year of oxandrolone therapy would increase growth velocity and thereby improve psychosocial functioning in boys with constitutional delay of growth and pubertal development. METHODS: Forty boys (ages 11 to 14.7 years) with delayed pubertal development and short stature were recruited from the pediatric endocrine clinics of 14 medical centers. The boys were randomized using a block design stratified for age to receive either oxandrolone (0.1 mg/kg daily for 1 year) or an identical-appearing placebo tablet, using a double-masked design. RESULTS: Growth velocity in the oxandrolone-treated boys was significantly greater than in the control boys (9.5 vs 6.8 cm/y). Likewise, the mean height SD score increased 0.41 in the oxandrolone group, whereas it decreased 0.03 in the control group. Those in the oxandrolone group gained 2.4 kg more than those in the placebo group. Mean predicted adult heights did not change in either group. The mean rates of pubertal progression were equivalent in both groups. Self-image (Piers-Harris Self Concept Scale) and social competence (Child Behavior Profile) were normal at baseline in both groups and did not change significantly over the course of the study in either group. No complications of oxandrolone therapy were identified. CONCLUSIONS: This randomized, placebo-controlled trial demonstrates that low-dose oxandrolone can increase both height and weight velocity in boys with delayed puberty safely. Under the conditions of this study, however, the increased growth velocity in the oxandrolone-treated boys was not associated with a greater improvement in psychosocial status compared with the control boys.

Adolescent↗
PubMed2002

Adrenocorticotrope deficiency with clinical evidence for late onset in combined pituitary hormone deficiency caused by a homozygous 301-302delAG mutation of the PROP1 gene.

Combined pituitary hormone deficiency (CPHD) can be caused by mutation of the pituitary transcription factors POU1F1 or PROP1. More recently mutations in the HESX1, the LHX3 and LHX4 transcription factor genes have also been described as a cause in patients with CPHD. In most patients the disorder is characterized by an impaired production of GH, TSH, PRL and gonadotropins. In some cases of CPHD adrenocorticotropin deficiency is also present. We report the progressive CPHD and its molecular etiology in a woman with CPHD presenting with first symptoms of ACTH/cortisol deficiency at the age of 48 years. The 49 year old patient's initial symptoms were growth retardation at the age of 2 years and symptoms of hypothyroidism at the age of 5 years. The patient never entered puberty spontaneously. No familial history of delayed puberty, growth retardation or other symptoms of CPHD were present. At the age of 48 years the patient presented with the first symptoms of hypocortisolism such as recurring hypoglycaemias and hyponatriaemia with coma. Cortisol, ACTH, TSH, fT3, fT4 and GH as well as LH, FSH and PRL were measured in basal conditions. GH, cortisol and ACTH were also measured in response to an Insulin Tolerance Test. Molecular analysis was performed by PCR amplification and sequencing of exon 1-3 of the PROP1 gene. The patient had insufficiencies of TSH, LH, FSH and GH. PRL was normal. Serum cortisol was low and basal ACTH was normal. However, there were no responses of cortisol, ACTH and GH to hypoglycaemia. Magnetic resonance imaging showed a hypoplastic anterior pituitary lobe. Direct sequencing revealed a homozygous 2 base-pair deletion 301-302delAG in exon 2 of the PROP1 gene. This case suggests that in patients with CPHD ACTH producing cells may be involved at a rather late age.

Adrenocorticotropic Hormone↗
PubMed1999

Combined use of growth hormone and gonadotropin-releasing hormone analogues: the national cooperative growth study experience.

Gonadotropin-releasing hormone ana-logues (GnRHa) are used to treat central precocious puberty. They also are used to delay puberty in short children with a prognosis for impaired adult height. In both cases, growth hormone (GH) treatment is sometimes added. To determine how North American pediatric endocrinologists are using the combination of GH and GnRHa, we searched the National Cooperative Growth Study (NCGS) database and identified 509 patients who were treated with both. Among them were 139 patients with a diagnosis of precocious puberty. Most of these (82%) also had GH deficiency (GHD). Of the 370 patients who did not have precocious puberty, 71% had GHD. There were 200 patients with precocious puberty who were treated with GH but not with GnRHa. The children who were given GH alone (77% of whom had GHD) were much younger than the children who were given both GH and GnRHa (5.7 +/- 2.9 years for those who were not treated with GnRHa vs 9.1 +/- 2.7 years for those who were). Data on both predicted adult height before GH treatment and near- adult height were available for 141 of the patients who were given both GH and GnRHa. There was a statistically significant increase in near-adult height over pre-GH predicted adult height in girls with precocious puberty (5.4 +/- 4.3 cm) and without precocious puberty (3.0 +/- 6.1 cm). There was no statistically significant gain in height for boys who did not have precocious puberty (1.3 +/- 6.8 cm). There were too few boys with precocious puberty (n = 7) to enable meaningful conclusions. In a multiple regression analysis of data on girls who did not have precocious puberty, duration of GH treatment was the most important variable predictive of height gain.gonadotropin-releasing hormone, growth hormone, precocious puberty, idiopathic growth hormone deficiency, organic growth deficiency, idiopathic short stature.

Body Height↗
PubMed2006

Worster-Drought syndrome (congenital bilateral perisylvian syndrome) with posterior pituitary ectopia, pituitary hypoplasia, empty sella and panhypopituitarism: a patient report.

Worster-Drought syndrome (WDS) (congenital bilateral perisylvian syndrome, congenital pseudobulbar paresia) is characterized by neuronal migration defect, pseudobulbar paralysis, epilepsy, neuromotor retardation and perisylvian dysplasia. We report a patient with WDS associated with posterior pituitary ectopia, pituitary hypoplasia, partial empty sella and panhypopituitarism, not previously reported in the literature. The 16.4 year-old female patient had severe growth retardation with height SDS -4.5, delayed puberty, microcephaly, pes equinovarus deformity, developmental delay, speech disorder and epilepsy. Laboratory findings, which revealed abnormal electroencephalography and bilateral perisylvian cortical dysplasia on cranial magnetic resonance imaging (MRI) were consistent with WDS. Endocrinological evaluation revealed secondary hypothyroidism and combined deficiency of adrenocorticotropin, gonadotropin and growth hormone (GH). Sella MRI showed congenital empty sella, anterior pituitary hypoplasia, ectopic neurohypophysis, and stalk agenesis. Appropriate replacement therapy was started. GH treatment resulted in a final height of 150.3 cm, appropriate for her target height. This is the first reported patient with WDS associated with congenital structural hypothalamic-pituitary abnormalities, including empty sella, pituitary hypoplasia, posterior pituitary ectopia, stalk agenesis and panhypopituitarism. GH has been successful in the treatment of her short stature.

Adolescent↗
PubMed1988

Effects of testosterone therapy for pubertal delay.

We reviewed the effects of a brief course of testosterone enanthate (four intramuscular injections of 200 mg at three-week intervals) on pubertal advancement and final adult height in 50 male patients with delayed puberty. Although those treated with testosterone were slightly older than a group of 38 untreated subjects, the two groups had similar baseline mean bone age delays, height z scores, Tanner stages, predicted adult heights, growth rates, and midparental heights. Four months after baseline, the treated group had a significantly greater mean increase in the height z score and sexual maturation index. At 12 months, the mean increase in the sexual maturation index remained greater in the treated group. Among treated and untreated subjects older than 17 years, there was no significant difference in the absolute height z score. Over 95% of treated subjects were satisfied with the effects of therapy.

Adolescent↗
PubMed1988

Hypogonadotrophic variant of Klinefelter's syndrome. A case report.

A 16-year-old boy with 47,XXY chromosomal complement (Klinefelter's syndrome) presented with delayed puberty and apparent gonadotrophin deficiency. Despite an inadequate growth hormone response to insulin-induced hypoglycaemia and to L-dopa administration, his somatic growth was appropriate for his delay in pubertal development, increasing markedly on testosterone treatment. Patients with Klinefelter's syndrome may have abnormalities of neuro-endocrine regulation.

Adolescent↗
PubMed2006

Growth hormone normalizes pubertal onset in children with cystic fibrosis.

UNLABELLED: Children with cystic fibrosis (CF) have a high incidence of delayed puberty and poor growth. We retrospectively reviewed pubertal maturation data from 105 children with CF who had participated in studies on growth hormone (GH). As part of the GH study, participants were randomized into two cohorts, one of which was treated with GH for 1 year, and then followed off GH, and the other group was first followed off GH, and then treated with GH for 1 year. Pubertal staging was obtained throughout these studies and we have retrospectively analyzed the data. RESULTS: In prepubertal females, GH treatment resulted in a normalized onset of breast development as compared to delayed onset in non-treated females. Females treated during puberty had a normal tempo of breast development. In prepubertal males, GH treatment resulted in a normalized onset of testicular volume compared to non-treated males. Testicular size progression was not accelerated in pubertal boys treated with GH. CONCLUSION: GH treatment normalizes pubertal onset in prepubertal children with CF.

Adolescent↗
PubMed1986

[Growth of anorexic adolescents].

Growth and puberty were studied in 19 children with anorexia nervosa (15 girls and 4 boys), the onset being before puberty or in its early stages. Growth retardation reached 2.04 +/- 1.39 SD, with important individual changes and for some patients a prolonged interruption of growth. Seventeen of 19 patients presented delayed puberty, and in some, hypogonadism persisted after recovery from anorexia nervosa. Endocrine investigations concerning the pituitary somatotropic (GH) and gonadotropic (FSH, LH) secretions, as well as gonadal steroids showed highly variable changes from one patient to another and even variations in the same patient from one test to another. However, no correlation could be found between the hormonal abnormalities and the degree or length of undernutrition. Some patients recovered normal endocrine function when they reached an adequate weight, others kept a lasting deficiency. The endocrine impairment in anorexia, well known in adults, is probably more severe in adolescents.

Adolescent↗
PubMed2005

Reversing sex steroid deficiency and optimizing skeletal development in the adolescent with gonadal failure.

During puberty, the acquisition of skeletal mass and areal bone mineral density (BMD) mainly reflects an increase in bone size (length and perimeters) and not true volumetric BMD. Sexual dimorphism in bone mass and areal BMD is also explained by differences in bone size (longer and wider bones in males) and not by differences in volumetric BMD. Androgens stimulate skeletal growth by activation of the androgen receptor, whereas estrogens (following aromatization of androgens and stimulation of estrogen receptors) have a biphasic effect on skeletal growth during puberty. Recent evidence from clinical cases has shown that many of the growth-promoting effects of the sex steroids are mediated through estrogens rather than androgens. In addition, skeletal maturation and epiphyseal fusion are also estrogen-dependent in both sexes. Nevertheless, independent actions of androgens in these processes also occur. Both sex steroids maintain volumetric BMD during puberty. Androgens interact with the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis neonatally, resulting in a sexual dimorphic GH pattern during puberty, whereas estrogens stimulate GH and hereby IGF-I in both sexes. Hypogonadism in adolescents impairs not only bone size but also maintenance of volumetric BMD, hereby severely reducing peak areal BMD. Delayed puberty in boys and Turner's syndrome in women impair both bone length and size, reducing areal BMD. Whether volumetric BMD is also reduced and whether fracture risk is increased in these conditions remains controversial. Replacing sex steroids according to a biphasic pattern (starting at low doses and ending at high-normal doses) seems the safest approach to reach targeted height and to optimize bone development.

Adolescent↗
PubMed2000

Growth hormone deficiency in one of two siblings with Fanconi's anaemia complementation group FA-D.

Fanconi's anaemia (FA) shows great variability in phenotypic symptoms. We report on two FA siblings of German ancestry with the very rare form of the complementation group FA-D. Both presented with a similar phenotype and mild disease severity but with different growth. In the sister, growth velocity was normal, puberty and menarche occurred spontaneously. Her final height was within her parental target height. The younger brother had a reduced growth velocity, height SDS values below -5.5 SDS, a markedly retarded bone age, and delayed puberty. At the age of 12.9 years, growth hormone deficiency (GHD) was diagnosed and treatment with growth hormone was initiated. Our cases emphasize the heterogeneity of symptoms in FA even in siblings with the same genotype. In FA-children with severe growth retardation, GHD must also be considered.

Abnormalities, Multiple↗
PubMed1992

Daily rhythms of follicle-stimulating hormone in adult anestrous and prepubertal female Turkish hamsters (Mesocricetus brandti).

We tested the hypothesis that daily FSH surges are correlated with the anestrous condition in adult Turkish hamsters. Blood samples were collected from anestrous hamsters on short (12L:12D) and long photoperiods (16L:8D) by cardiac puncture. Both photoperiod-induced anestrous (PIA) and spontaneously anestrous adult Turkish hamsters had a daily rhythm of FSH secretion with maximum hormone concentrations occurring late in the afternoon. We also hypothesized that daily FSH and progesterone surges are correlated with the reproductive response to short photoperiod in prepubertal female Turkish hamsters. Prepubertal hamsters reared on 16L:8D were sampled at 13, 15, 17, 19, and 21 days of age. Only at 19 days was a rhythm of FSH present. Prepubertal female hamsters reared on 12L:12D were sampled at 30, 35, 55, 75, 95, and 115 days of age or until estrous cycles were established. Those hamsters that delayed puberty in response to this short photoperiod had a daily rhythm of FSH and progesterone secretion. Conversely, no daily rhythms were observed in female hamsters that failed to respond to the inhibitory photoperiod with a delay in puberty. These results indicate that the daily rhythm of FSH secretion in the female Turkish hamster is correlated with reproductively inhibited physiological states.

Age Factors↗