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PubMed1972

Plasma and urinary luteinizing hormone levels in the diagnosis of endocrine disease.

The diagnostic value of measurements of plasma and urinary luteinizing hormone (LH) has been studied in 209 patients with endocrine disease. In 44 patients puberty was either delayed or had failed to occur. In those with chromosomal abnormalities the LH levels were often within the normal range, whereas those with a pituitary cause usually had low levels. In boys with delayed puberty plasma LH levels rose before physical changes occurred and had prognostic value. In patients with later gonadal failure, men with impotence or infertility, and women with secondary amenorrhoea LH assays proved of little value, although in one case a premature menopause was suspected and six patients with anorexia nervosa had low LH levels.Sixty patients with disorders of the hypothalamicpituitary area were studied. Levels of LH were measured and considered in relation to the other anterior pituitary hormones. Impairment of LH secretion was one of the first effects on hormone production of disease affecting this area, and this was, of course, most readily detected in postmenopausal women.The normal ranges of both plasma and urine LH are wide and there seems to be considerable day-to-day variation, especially of urinary output. Several samples should, therefore, be measured if therapeutic decisions are involved.

Adolescent↗
PubMed1989

Endogenous opioid regulation of pulsatile luteinizing hormone secretion during sexual maturation in the female sheep.

The developing female sheep, which attains puberty after 25 weeks of age, was used as an experimental model to investigate the role of endogenous opioid peptides in the control of pulsatile LH secretion during sexual maturation. Treatment of ovary-intact prepubertal sheep at 12 weeks of age with the opiate antagonist naloxone resulted in a dose-dependent increase in LH secretion. Subsequent studies used ovariectomized (OVX) lambs implanted with capsules containing 17 beta-estradiol to provide a constant, ovarian steroid feedback signal throughout development. Naloxone treatment (hourly iv injections of 1 mg/kg BW for 4 h) produced an increase in the frequency of episodic LH secretion at all prepubertal ages, when lambs were highly sensitive to the estradiol negative feedback. However, increases in LH pulse frequency were also induced by naloxone treatment at a postpubertal age in estradiol-treated OVX sheep, indicating that opioid inhibition is still present at a time when sensitivity to the feedback effects of ovarian steroids is markedly reduced and endogenous LH secretion is increased. These observations in ovary-intact and estradiol-treated OVX lambs suggest that opioid mechanisms inhibit pulsatile tonic LH secretion during both the prepubertal and postpubertal periods. Endogenous opioid inhibition of LH secretion is not dependent on the presence of ovarian steroids, as evidenced by the response to naloxone 3 weeks after removal of an estradiol implant from OVX lambs, when LH pulse frequency was already high. Naloxone treatment increased LH pulse frequency further, at both a prepubertal age (18 weeks) and a postpubertal age (38 weeks). Naloxone also increased LH pulse frequency in OVX lambs in which LH secretion was inhibited chronically by progesterone rather than by estradiol. The response to naloxone was similar in postpubertal P-treated OVX lambs and age-matched prepubertal P-treated OVX controls in which puberty had been delayed by means of an inhibitory seasonal photoperiod. In addition, after removal of steroid implants to allow LH secretion to increase, the degree of inhibition of LH secretion by the opiate agonist morphine was similar between age-matched postpubertal sheep and those with photoperiodically delayed puberty. We conclude that endogenous opioid mechanisms are an important inhibitory mechanism controlling pulsatile LH secretion in the developing sheep. However, changes in opioid inhibition are unlikely to underlie the decrease in sensitivity to steroid negative feedback and increase in pulsatile LH secretion that occur at puberty.

Animals↗
PubMed1991

[The responsibility of medicine in adolescence].

Adolescence is a not very well defined time period between childhood and the adult age. The self esteem of an adolescent is neither that one of a child nor that one of an adult. If somatic, psychologic or psychosomatic complications or problems occur within this period, most of the adolescents disagree to be treated by a pediatrician, but they also disagree to be treated by "doctors for the elderly". Most of the complications or problems are specific for that age period; they are not well known to all medical doctors. Because of these reasons, specialists in adolescent medicine are mandatory for proper treatment. The most important problems or complications are dealing with puberty (early or delayed puberty, acne), growth, sexuality and sexual behavior, contraception, chronic disease and drugs.

Adolescent↗
PubMed1981

Failure to demonstrate a significant influence of ovarian maturity on the onset of puberty in female rats.

Ovaries of 23- and 35-day-old rats were transplanted under the kidney capsules of 31- and 23-day-old females, respectively. The recipient rats were ovariectomized on the fourth day after transplantation, and the onset of puberty was recorded. Neither the age and body weight at vaginal opening and first ovulation nor the length of the first ovarian cycle differed significantly between the experimental rats and sham-transplanted or untreated controls. Estimation of the serum FSH an LH concentrations before and after ovariectomy provided no evidence that different gonadotropic responses had masked puberty-delaying or puberty-advancing effects of the implanted immature and prepuberal ovaries, respectively. The results suggest that the developmental stage of the ovaries is not a decisive factor in the control of the onset of female puberty.

Animals↗
PubMed1996

Ovarian expression of insulin-like growth factor-I (IGF-I), IGF binding proteins, and growth hormone (GH) receptor in heifers actively immunized against GH-releasing factors.

Active immunization against GRF at 6 months of age delays puberty in beef heifers. The objectives of the present study were to determine whether active immunization against GRF at an earlier age would affect normal onset of puberty and follicular growth and to determine whether these changes were related to alterations in ovarian insulin-like growth factor I (IGF-I) or IGF binding protein (IG-FBP) messenger RNA (mRNA) levels. Heifers were immunized against human serum albumin (HSAi; n = 15) or against GRF conjugated to HSA (GRFi; n = 18) at 3 months of age. A third group of heifers was not immunized (CON; n = 16). Immunization against GRF delayed puberty beyond 13 months of age in 75% of treated heifers. Unilateral ovariectomy at 191 days of age revealed that the delay in puberty was associated with a reduction in the number of large ( > or = 7 mm in diameter) follicles. Large follicles were present in only 22% of GRFi heifers compared to 77% of HSAi heifers. The number of small ( < or = 3 mm in diameter) and medium (4 to 6 mm in diameter) follicles was not affected by GRFi. The percentage of 1- to 3-mm follicles that were atretic was not different between HSAi (65%) and GRFi (62%) heifers. Unilateral ovariectomy had no effect on age at puberty. Immunization against GRF decreased (P < 0.01) concentrations of IGF-I in serum (23 +/- 2 ng/ml) compared to HSAi heifers (109 +/- 11 ng/ml). IGF-I levels in follicular fluid (FFL) of medium and small follicles were also decreased by GRFi from 82 +/- 3 ng/ml in HSAi heifers to 48 +/- 6 ng/ml (P < 0.01). Levels of IGFBP-3 (determined by ligand blot analysis) in serum and FFL of small follicles were decreased by GRFi (P < 0.01). In contrast, IGFBP-2 serum levels were increased from 422 +/- 32 ng/ml in HSAi heifers to 657 +/- 6 ng/ml in GRFi heifers (P < 0.05). Likewise, IGFBP-2 levels in FFL from small and medium follicles were increased from 785 +/- 44 ng/ml to 926 +/- 44 ng/ml (P < 0.05). Ligand blot analysis indicated that IGFBP levels were lower in FFL from large vs. small follicles. The band intensities of IGFBP-4 and -5 were drastically reduced ( > 80%) while the decreases in IGFBP-2 and -3 were less marked ( < 50%). The decreased levels of IGFBP-5 in FFL from large follicles was not associated with an increase in proteolytic fragments detectable by immunoblot analysis. While mRNA transcripts for IGF-I, GH receptor, and IGFBP-2, -3, -4, and -5 were readily detectable in ovarian tissue, GRFi had no effect on ovarian levels of mRNA for each of these proteins. This suggests that the decrease in follicular development associated with GRFi may be related to changes in circulating IGF-I and/or IGFBPs.

Animals↗
PubMed1980

Twenty-four hour profiles of serum prolactin during male puberty with and without gynaecomastia.

Twenty-four hour profiles of circulating prolactin have been documented in eight boys with simple delayed puberty, eleven with gynaecomastia, three of whom were retested following its spontaneous resolution, and two normal adult men. Mean 24 h prolactin levels in four boys with delayed puberty and ten with gynaecomastia exceeded the mean levels for the two adult men. A sleep-associated rise in prolactin levels occurred at all stages of puberty irrespective of the presence or absence of gynaecomastia, and in some subjects peaks also occurred during the daytime. Boys with gynaecomastia had higher 24 h means levels of prolactin (P less than 0.05), higher daytime levels (P less than 0.05) and higher sleep-associated levels (P less than 0.05) than did control subjects. These were not related to the degree or duration of the gynaecomastia, but 24 h mean levels of prolactin and oestradiol were positively correlated. In one subject who had had transient galactorrhoea, high levels of circulating prolactin, oestrone and oestradiol fell following spontaneous resolution of the gynaecomastia. We believe that oestrogen: androgen imbalance during the daytime is the major cause of pubertal gynaecomastia, with hyperprolacinaemia (which may cause galactorrhoea) sometimes occurring as a response to relative hyperoestrogenaemia.

Adolescent↗
PubMed2000

Pheromones cause disease: the exocrinology of anorexia nervosa.

The aetiology of anorexia nervosa is exocrinological. This notion is supported by physical evidence in animal models with directly comparable symptomatology. Anorexia nervosa (AN) syndrome would be a puberty delay caused by reception and autoreception of conspecific pheromone emissions: a pheromone-induced puberty delay (PIPD). As such, it would be amenable to medical treatment drawing from forty years of research in animals. This hypothesis is testable. For instance, since food ad libitum is a prerequisite for PIPD, occasional supervised fasting in healthy peripuberal subjects should prevent AN. Besides, tolerating an untestable thought disease (1,2) with symptoms of a curable well-understood animal condition would be anti-scientific and perpetuates medical disaster. Even their endocrinologies are identical. Pheromone feedback tunes animal appetites and immunity to available resources and prospects. In addition to timing puberty, pheromones regulate fertility. Pheromones will probably be implicated in the aetiology of the psychiatric and autoimmune diseases. This is the second in a series of twelve papers to explore this contention systematically.

Animals↗
PubMed1997

[Constitutional delay of growth and puberty in male].

Constitutional delay of growth and puberty (CDGP), featuring short stature, delayed puberty and delayed bone age, is the most common condition in pediatric endocrine clinic and becomes an important differential diagnosis in boys with short stature. The conventional management is to assure eventual development of puberty and normal final stature. Treatment with androgens to induce secondary sex characteristics is given only when the boy is under psychosocial stress. Recent reports revealed poor final height outcomes. The results of growth hormone treatment in idiopathic short stature, including CDGP, has not been successful. New findings showed that adults with a history of delay puberty had significant osteopenia and may have a risk of fracture, and that suppression of spinal growth was closely related to pubertal delay, leading to short stature. These two facts suggest the necessity of induction of puberty in normal timing.

Adolescent↗
PubMed1983

Cognitive and neuropsychological test performance of persons with abnormalities of adolescent development: a test of Waber's hypothesis.

20 children with idiopathic precocious puberty, 27 adolescents with clinically delayed puberty, and an equivalent number of controls matched for age, sex, and IQ were given a battery of tests. These included measures of verbal and spatial abilities and a task assessing hemispheric lateralization using a dichotic listening procedure. Comparisons with matched controls revealed poorer verbal and spatial abilities for precocious males and poorer verbal, but better spatial, abilities for precocious females. Delayed developing males demonstrated superior verbal skills compared with controls, whereas delayed developing females did more poorly than controls in both verbal and spatial areas. On the dichotic task, the only group differing from controls was the delayed developing males, who demonstrated stronger lateral asymmetries. It was suggested that the present findings, which are not consistent with those of former investigations, may reflect methodological differences between studies and the disruptive influence of atypical pubertal onset on normal patterns of sex difference in cognitive functioning.

Adolescent↗
PubMed1983

Delay of puberty onset in males due to suppression of growth hormone.

Infection with Spirometra mansonoides at 22 days of age was associated with delayed sexual maturation in the male rat. Balanopreputial separation occurred at 46.7 +/- 0.8 days in controls and at 50.6 +/- 0.9 days in worm-treated rats (p less than 0.02). This was accompanied by a delay in the normal prepubertal testicular and seminal vesicle weight increases. LH remained normal but serum FSH was depressed as early as 25 days of age. The castration response in worm-treated rats was comparable to that of controls, when the FSH levels were normalized as percentages of resting level. The LH response to castration was diminished. The acute FSH and LH response to GnRH was normal and pituitary stores of gonadotrophin, as estimated by radioimmunoassayable concentrations of FSH and LH, were normal. It can be concluded that puberty onset in males is not linked to body weight gain pe se, and that the absence of endogenous GH secretion affects both sexual maturation and gonadotrophin secretion in the prepubertal period.

Animals↗
PubMed1997

Disorders of puberty: inactivating and activating molecular mutations.

Recent developments have increased our understanding of the molecular mechanisms that are responsible for several disorders of puberty. Specific gene mutations have been identified in three syndromes, one that is associated with delayed puberty (Kallmann syndrome) and two that are associated with precocious puberty (McCune-Albright syndrome and familial male precocious puberty). Mutations in the KAL gene have been shown to be responsible for cases of X-linked Kallmann syndrome. This gene encodes a protein that is believed to be involved in neural target recognition and protease inhibition. In McCune-Albright syndrome, heterozygous, postzygotic somatic mutations of the alpha-subunit of the stimulatory guanine nucleotide binding protein Gs have been shown to stimulate constitutive G protein activation and long-term cyclic adenosine monophosphate production. Similarly, familial male precocious puberty has been linked to gain-in-function mutations that result in increased levels of cyclic adenosine monophosphate; however, these mutations are found in the luteinizing hormone receptor gene itself. The clinical manifestations and the recent molecular advances in each of these three syndromes are explored.

Cyclic AMP↗
PubMed1992

[Disorders of puberty and gonadal disorders in the child].

Normal puberty has a characteristic harmony or consonance between the individual modalities of sexual maturation. Thus, the objective description and detailed knowledge of physical pubertal development is the basis of the clinical analysis of pubertal disorders. An aim of the review is to provide details of the visible changes the clinician must note in order to document the normal progression of puberty. Disorders of puberty can be classified by the timing of onset of sexual characteristics into either precocious or delayed puberty. A more useful concept, however, than the abnormalities of timing of puberty is whether the pubertal development is true (consonant) or if there is a pseudo-puberty (absence of consonance). This is of greater significance in relation to the pathophysiology and, therefore, the investigations and therapies which will be required. The use of either well known or new agents that may be used for treatment of pubertal disorders are presented.

Adolescent↗
PubMed1998

Growth and management of short stature in thalassaemia major.

UNLABELLED: With modern treatment and longer survival of patients with homozygous beta-thalassaemia endocrine dysfunction assumes greater importance. Short stature, delayed puberty and hypogonadism are major problems in both adolescent and adult patients. Growth failure has been attributed to GH deficiency (hypothalamic or pituitary), hypothyroidism, delayed sexual maturation, hypogonadism, diabetes mellitus, zinc deficit, low Hb levels, bone disorders and desferrioxamine toxicity. The present report concentrates on the incidence of short stature among children aged 7-8 years (n = 50) and young adults aged 20-29 years (n = 93) with blood transfusion dependent homozygous beta-thalassaemia appropriately treated who have entered and completed puberty spontaneously (n = 45) or with treatment (n = 48) and have attained final height. It also concentrates on the role of GH in the growth retardation of 65 blood transfusion dependent thalassaemia major patients, their GH response to provocative stimulation, the effect of rhGH therapy on growth and final height in 13 patients who had GH deficiency and the effect of long acting androgens on growth and final height of 11 short boys with thalassaemia major, delayed puberty and normal GH secretion. CONCLUSION: 8% of young boys with thalassaemia major aged 7-8 years have short stature. 12% of the older boys and 15% of the older girls without endocrinopathies had height < 3rd percentile. This incidence was 29% when endocrinopathies were present. GH deficiency is rare among short blood transfusion dependent thalassaemia major patients (20%) and seems to play a limited role in the etiology of growth retardation. One year treatment with rhGH improved growth rate and predicted height without causing serious metabolic problems. Long term administration of rhGH is also safe and promising. Patients with thalassaemia major can achieve acceptable final heights but below their target heights with rhGH therapy. Low dose long acting sex steroid treatment in boys with delayed puberty, delayed bone age and without GH deficiency for a year or more is safe and can produce similar results to those obtained with rhGH therapy.

Adolescent↗
PubMedDate not supplied

[Physiology of pubertal maturation].

Most important features of puberty are described. The puberty is the age of development of sexual characters. In females it appears between 10 and 15 years +/- 1 year whereas in males signs of puberty are visible between 11 and 15 years. In our country menarche appears at the mean age of 12 years and 2 months +/- 1 year and 2 months. Precocious puberty in females is that which appears before 8 years and 6 months and in males before 10 years. Delayed puberty is that which appears in females after 15 years and in males after 16. Nowadays is possible to keep off puberty when it is too soon by means of an analogous of LH-RH and as the result the subject reaches a better statural growth. The puberty should not be confused with the adolescence which is characterized by psycho-social maturity.

Adolescent↗
PubMed1984

Urinary chemosignals from mice (Mus musculus): acceleration and delay of puberty in related and unrelated young females.

A series of five experiments was carried out to determine the possible differential effects that urinary chemosignals from genetically related and unrelated donors have on puberty onset in female mice. The first four experiments, with a laboratory mouse strain, demonstrated no differential acceleration or delay of sexual maturation, with respect to a close genetic relation between donors and recipients, due to the chemosignals from estrous, diestrous, pregnant, or lactating females or grouped females. In the last experiment, wild stock Mus were used; all of the results were comparable to those found in laboratory stocks. There were no instances of differential acceleration or delay based on close genetic relatedness of donors and recipients. The results conform with a general hypothesis that the urinary chemosignals in mice communicate information about the adequacy of reproductive conditions to conspecifics.

Animals↗
PubMed1992

End-stage renal disease and primary hypogonadism associated with a 46,XX karyotype.

OBJECTIVE: To determine the cause of absent sexual development in a 17-year-old girl with end-stage renal disease. DESIGN: Case study. PARTICIPANT: Seventeen-year-old girl with end-stage renal failure. INTERVENTIONS: None. MEASUREMENTS/MAIN RESULTS: The patient had phenotypically normal external female genitalia, müllerian duct hypoplasia, and no ovaries. Her serum gonadotropin levels were in the castrate range at baseline and after gonadotropin-releasing hormone stimulation. Her karyotype, in lymphocytes and cultured fibroblasts, was 46,XX. Analysis of genomic DNA, following polymerase chain reaction-amplication with oligonucleotide primers corresponding to the Y-encoded zinc finger protein ZFY and the testis-determining SRY gene, showed Y chromosome material in a male control but none in the patient. CONCLUSIONS: The results suggest a diagnosis of Frasier syndrome, a disorder characterized by true gonadal dysgenesis and end-stage renal disease occurring in normal phenotypic girls. Although previously reported only in individuals with a 46,XX karyotype, our studies indicate that Frasier syndrome may also occur in 46,XX girls. Delayed puberty is not uncommon in renal failure. This case illustrates the importance of measuring gonadotropin levels in teenage girls with delayed puberty and renal failure, particularly if the origin of the renal disease is obscure.

Adolescent↗
PubMed2004

Phenotypic analysis and growth response to different growth hormone treatment schedules in two siblings with an inactivating mutation in the growth hormone-releasing hormone receptor gene.

Mutations in the GHRH receptor (GHRHR) gene (GHRHR) are emerging as a common cause of familial isolated growth hormone deficiency (IGHD) type IB. The use of gonadotropin-releasing hormone (GnRH) analogues has been advocated as a tool to delay puberty in patients with isolated GH deficiency (IGHD), allowing longer time for the beneficial effect of exogenous human GH (hGH) treatment on growth. We describe two male siblings with IGHD due to a homozygous missense GHRHR mutation who, because they were started on hGH therapy at different ages, presented with different height SDS at the onset of puberty and therefore had different predicted target heights. The shorter brother was treated with GnRH analogue plus hGH for 3 years, whereas the other brother received only hGH. Despite different predicted heights at the onset of puberty, they attained similar final heights. We conclude that in patients with IGHD, GnRH analogue treatment should be considered to delay puberty and obtain a maximal growth response if hGH treatment is started in late childhood and the predicted height at puberty onset is below the genetic target.

Adolescent↗
PubMed1992

Pre- and postweaning excretion of puberty-influencing chemosignals in house mice.

Pre- and postweaning excretion of urinary chemosignals that influence puberty in female house mice were tested. The dependent variable used to assess the effectiveness of urine samples collected from donor mice was the age of first vaginal estrus in young female mice. Preweaning excretion of the puberty-delaying chemosignal by females was affected by litter sex composition; this effect interacted with the age of the young donor females. In litters of all females, the substance occurred from about the age of 9 days and in litters with 6 females and 2 males the delay substance was released from about the age of 17 days. Grouping dams during gestation but not prior to conception resulted in excretion of the puberty-delaying substance in the female progeny from the age of 17 days or possibly earlier. Young male mice do not excrete the puberty-accelerating chemosignal prior to the age of puberty. However, giving young males injections of testosterone resulted in an earlier first excretion of the acceleratory signal, suggesting that the machinery for chemosignal production is operative prior to the time of sexual maturity. Caging young males with an adult female prior to puberty resulted in earlier excretion of the puberty-accelerating substance, while caging young males with adult males retarded excretion of the substance. The findings are discussed in terms of early hormone effects on behavior and with regard to consequences for the chemosignal systems in house mice.

Animals↗