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At least 19 recordsLinked to original sources
PubMed1978

The effect of LH-RH infusion on serum LH, FSH and testosterone in boys with advanced puberty, delayed puberty and hypogonadotrophic hypogonadism.

LH-RH injection and infusion studies were performed in advanced puberty, delayed puberty and hypogonadotrophic hypogonadism. No differential diagnosis could be made between delayed puberty and hypogonadotrophic hypogonadism using LH-RH injection. In the LH-RH infusion studies evidence was obtained that stimulation of the pituitary during 4 h results in continuously rising LH levels in advanced puberty and in delayed puberty while in hypogonadotrophic hypogonadism the secretory capacity of the pituitary is gradually exhausted. This phenomenon can be used in the differential diagnosis between delayed puberty and hypogonadotrophic hypogonadism. Though the FSH data point in the same direction they are not useful in this connection as the overlap between the different categories was considerable.

Adolescent↗
PubMedDate not supplied

[Delayed puberty].

Delayed puberty can be defined as the absence of any signs of puberty in subjects that have attained an age at the upper limit (+2DS) for the onset of puberty, that means 13 years in girls and 14 years in boys. The causes of delayed puberty can be classified into three groups, functional temporary impairment in gonadotropin and sex steroid secretion (most frequently constitutional delay of puberty), hypothalamo-pituitary failure with deficiency in gonadotropin secretion, primary gonadal failure with increased gonadotropin levels. The Authors discuss about etiology, diagnostic testing and therapeutic approach in these conditions. The majority of children with delayed puberty are males that have only a constitutional delay of growth and puberty. It is difficult, in teenage years, to distinguish this common and benign condition from true gonadotropin deficiency, in spite of the variety of endocrine tests developed for this purpose. Individuals with constitutional delayed puberty with a bone age greater than 11.5 years, show after triptorelin stimulation an increase in LH capable of distinguishing them from patients with gonadotropin deficiency. In our opinion this could be an important screening test to exclude gonadotropin deficiency in boys with delayed puberty.

Adolescent↗
PubMed1995

Investigation of delayed puberty.

Delayed puberty is defined arbitrarily on the basis of statistical consideration, when no signs of puberty have occurred at 2.0 SD (13.4 years in girls and 13.8 in boys) above the mean chronological age for the onset of puberty. The vast majority of these patients have no endocrine abnormality and their pubertal development and growth spurt are simply consequences of primary delay (constitutional delay of growth and puberty (CDGP)) or secondary delay due to a chronic disease of childhood, such as asthma. However, a small proportion may have pathological causes of delayed puberty which must be careful identified as specific management may be required. Associated with delayed puberty, the growth spurt is always delayed which is why the condition is described as delayed growth and puberty. Short stature and lack of sexual development may lead to emotional and social difficulties and in some patients their consequences can persist when 'normal' height and full sexual maturation are attained. Recent data also suggest that a delay in the 'tempo' of pubertal maturation may interfere with the normal bone accretion occurring during puberty, later causing osteoporosis. Such findings suggest that a new approach in delayed puberty may be necessary not only for psychological reasons but also for optimizing bone mass accretion.

Adolescent↗
PubMedDate not supplied

Delayed puberty.

Delayed puberty is a frequently encountered problem causing much anxiety to patient and parents alike. Proper understanding of the normal pubertal events and its variation sets off the background to understand disorders leading to delayed puberty. An orderly clinical approach combined with continued observation helps to arrive at a final diagnosis in most of the patients. The treatment modalities available, even if not curative, can achieve the goals of management set off at the end of evaluation of the patient.

Adolescent↗
PubMed1981

Delayed puberty.

Delayed puberty is the cause of much distress to adolescents and with modern techniques it is possible to arrive at a therapy-orientated diagnosis in the majority of instances. A relatively wide choice of therapeutic interventions is now available and may be employed, even in endocrinologically normal patients, if the situation warrants. In such patients, ther duration of therapy is very short. In patients with pathological causes of delayed puberty, the aim must be to reproduce the normal pubertal changes over the normal span of time and large doses of sex steroids should not be used early in the induction of puberty.

Adolescent↗
PubMed1982

[Investigation of delayed puberty].

Delayed puberty is defined as the total or almost total absence of development of sex characteristics at an age exceeding the mean by two standard deviations: approximately 15 years in boys and 13 years in girls. A double sense has been given to this term, which is usually applied to permanent hypogonadism as well as to normal but delayed maturation. In practice, certain signs can assist formulation of a prognosis, and if necessary the type of therapy required. Data on which can be based the diagnosis, surveillance, and medical conduct in sexually immature adolescents are discussed. Their interpretation is simple when elevated gonadotrophins levels indicate a primary gonadal lesion, or when the delayed puberty results from a general disease disturbing body maturation. In other cases, interpretation of data is often very difficult and is sometimes a very slow process. Because of these difficulties, the diagnosis between simple delay and gonadotrophic insufficiency is discussed in this report on the basis of a retrospective study conducted for a long enough period to have arrived at a definite conclusion.

Adolescent↗
PubMed1980

Puberty delay by a urinary cue from female house mice in feral populations.

Urine produced by wild female house mice, living in high- and low-density populations and confined to areas within a highway cloverleaf, was tested for its ability to delay puberty in juvenile female mice. Only urine collected from females in the dense population at its maximum density delayed puberty in test females. Urine collected when the population was less dense, or from a population that remained sparse, failed to delay puberty. These results suggest that a urinary factor present at high densities may delay puberty and thus help to slow further population growth.

Animals↗
PubMed1985

Effect of density, duration of grouping and age of urine stimulus on the puberty delay pheromone in female mice.

The ability of urine from female mice to delay puberty in test females was directly related to the density and duration of grouping of females. When females were removed from group housing their urine lost its ability to delay puberty within 10 days. No interactive effects were observed between duration and density of grouping on the onset of pheromone release after grouping or on the persistence of pheromone release after re-isolation. Urine from grouped females lost its ability to delay puberty in test females after 7 days of exposure to air.

Animals↗
PubMed1998

Delayed puberty in obese boys: comparison with constitutional delayed puberty and response to testosterone therapy.

OBJECTIVE: To evaluate the results of a brief course of testosterone therapy in boys with delayed puberty and to compare the responses seen in boys with constitutional delayed puberty (CDP), boys with obesity, and boys with possible gonadotropin deficiency. DESIGN AND SETTING: A retrospective chart review was done for 36 boys aged 14 years or older, seen between 1983 and 1996 because of delayed puberty, who were given 4 monthly injections of testosterone, 100 mg/mo, and had adequate follow-up. RESULTS: There were 23 boys whose findings before and after treatment were consistent with a diagnosis of CDP. Testosterone treatment increased the growth rate from 4.3 cm/y to 11.2 cm/y (P <.00001), and mean testis length increased 0.6 to 0.8 cm in all (from a mean of 2.9 to 3.6 cm, P <.00001) in the 4 months after testosterone treatment. Serum testosterone 4 months after therapy was higher than that before therapy (P =.00003). Of 5 boys with growth hormone deficiency but unknown gonadotropin status, 2 had lack of progression after testosterone therapy and were believed to have permanent gonadotropin deficiency. Seven of the 36 boys were obese (body mass index, >25), and 6 had a response to testosterone similar to boys with CDP with clear pubertal progression. One obese boy and one nonobese boy were diagnosed as having isolated gonadotropin deficiency. CONCLUSIONS: Monitoring the growth and genital responses to a 4-month course of testosterone injections helps to differentiate CDP from gonadotropin deficiency in boys with delayed puberty. Obese boys constitute a distinct category of boys with pubertal delay in terms of their growth, but their response to testosterone is similar to that observed in boys with classic CDP.

Adolescent↗
PubMed1986

Pulsatile gonadotropin-releasing hormone treatment in idiopathic delayed puberty.

Idiopathic delayed male puberty is defined as a delay of puberty beyond the age of 16, with prepubertal testosterone levels, normal gonadotropin responses to GnRH (excluding pituitary failure), and normal androgen responses to a single hCG injection (excluding testicular Leydig cell dysfunction), in absence of serious disease. Ten boys with this condition were evaluated as to their spontaneous LH, FSH, and PRL secretory patterns during a 24-h sampling period (20-min intervals). After this all patients were treated with pulsatile infusions of GnRH (25 ng/kg . pulse every 90 min for 10 days. Two groups could be distinguished by means of their pretreatment LH secretory pattern. Five patients had nighttime pulsatile elevation of LH levels, as usually occurs in early puberty. The other five patients did not have such a pattern (prepubertal type). The GnRH treatment resulted in increased LH and testosterone levels in both groups. All patients with pretreatment nighttime pulsatile LH secretion had steady pubertal development during the post-GnRH treatment observation period, whereas the other patients did not. In conclusion, among a number of tests, including chronic pulsatile GnRH treatment for 10 days, only the nocturnal LH secretory pattern differentiated delayed puberty from permanent hypothalamic hypogonadism in boys.

Adolescent↗
PubMed1992

Therapeutic strategies in a male with delayed puberty.

Therapeutical strategies in male with delayed puberty. Delayed puberty (absence of pubertal modifications after 14-15 years of age) due to transitory deficit of LHRH secretion often constitutes a difficult differential diagnostic problem for conditions of permanent LHRH deficit which can be identified only after 18 years of age in the idiopathic hypogonadotropic hypogonadism. After a period of clinical observation short-term therapy with pulsatile LHRH administration may take place. Therapy can be necessary: to document the functional integrity of the pituitary-gonadal axis; to promote pubertal modification such as to improve and physiologically sustain the patient; to tray a neuroendocrine activation of endogenous LHRH-LH secretion. Also delayed puberty linked to uremia seems to respond to short-term pulsatile LHRH administration. Pulsatile LHRH administration is the most physiological therapeutical approach to subject with delayed puberty. It seems to constitute a valid alternative to the therapy with testosterone or gonadotropins.

Adolescent↗
PubMed1997

Delayed puberty in girls with cystic fibrosis despite good clinical status.

BACKGROUND: Previous studies have shown that puberty is delayed among patients with cystic fibrosis (CF). Malnutrition has been considered the main etiologic factor. Today with improved medical therapy and nutritional support, most CF patients obtain an almost normal nutritional status. OBJECTIVES: To investigate whether pubertal development among female CF patients at the Stockholm CF Center was normal and, if not, what other parameters besides nutrition might influence this. METHODS: Seventeen patients were studied retrospectively regarding age at peak height velocity and menarche. Menarcheal age (MA) was compared with normal population data and related to clinical and nutritional status, genotype, oral glucose tolerance test (OGTT), and essential fatty acid levels. RESULTS: The mean age at peak height velocity (12.9 +/- 0.8 years) and at menarche (14.9 +/- 1.4 years) was significantly higher in the CF patients compared with normal controls (11.9 +/- 1.0 years and 13.0 +/- 1.0 years, respectively). No correlation was found between menarchal age and nutritional or clinical parameters. The patients with pathological OGTT without overt diabetes were significantly older at menarche (15.8 +/- 1.7 years) compared with the patients with normal OGTT (14.3 +/- 0.9 years). The patients who were homozygous for the most common mutation, deltaF508, were significantly older at menarche (15.2 +/- 1.9 years) than those who were not (14.7 +/- 0.9 years). CONCLUSIONS: Pubertal delay still existed among the CF patients despite good clinical status. The patients homozygous for deltaF508 and those with pathological OGTT showed the most delayed puberty.

Adolescent↗
PubMed2002

Delayed puberty in chronic illness.

Delayed puberty can be defined as the lack of pubertal development at an age of 2 SD above the mean, which corresponds to an age of approximately 14 years for males and 13 years for females, taking both sex and ethnic origin into consideration. Its incidence associated with chronic illnesses is unknown; however, its clinical importance is relevant due to the larger percentage of patients with chronic disorders surviving until the age of puberty. Virtually every child with any chronic disease could present with delayed puberty (due to recurrent infections, immunodeficiency, gastrointestinal disease, renal disturbances, respiratory illnesses, chronic anaemia, endocrine disease, eating disorders, exercise and a number of miscellaneous abnormalities). Pubertal delay associated with chronic illness is accompanied by a delay in growth and the pubertal growth spurt. The degree to which growth and pubertal development are affected in chronic illness depends upon the type of disease and individual factors, as well as on the age at illness onset, its duration and severity. The earlier its onset and the longer and more severe the illness, the greater the repercussions on growth and pubertal development. The mechanism that trigger the start of physiological puberty remain unknown. Although malnutrition is probably the most important mechanism responsible for delayed puberty, emotional deprivation, toxic substances, stress and the side effects of chronic therapy, among others, have been implicated in the pathophysiology of delayed puberty. Therefore, early diagnosis is essential and appropriate and specific therapy fundamental.

Adolescent↗
PubMed1986

Naloxone-induced luteinizing hormone secretion in normal, precocious, and delayed puberty.

The aim of the present study was to evaluate the activity of opiate receptors involved in the control of LH secretion during pubertal development, as determined by the LH response to naloxone. Normal children (n = 28) of both sexes, subdivided according to breast (girls) or testicular (boys) development, and patients with idiopathic precocious puberty (n = 7), delayed puberty (n = 8), or hypergonadotropic hypogonadism (n = 4) were studied. Plasma LH levels were measured after the administration of naloxone (NLX; 0.08 mg/kg BW, iv), GnRH (50 micrograms, iv) or placebo. In healthy subjects, NLX significantly increased plasma LH levels only in girls and boys at the most advanced stage of gonadal maturation. NLX was ineffective in prepubertal and early pubertal children, and it did not significantly alter LH levels in children with delayed puberty or hypogonadism or in most of the children with precocious puberty. GnRH injection consistently increased plasma LH levels in healthy subjects as well as in the children with pubertal disturbances. These results indicate that the LH response to NLX occurs only at the most advanced stages of pubertal maturation when normal or precocious and is absent in early puberty or in children with pubertal disturbances. Furthermore, the results suggest that opioid regulation of LH secretion in humans changes during puberty, reaching an adult-like functional state with maturation of the hypothalamus-pituitary-gonadal axis.

Adolescent↗
PubMed1992

Osteopenia in men with a history of delayed puberty.

BACKGROUND AND METHODS: The effect of delayed puberty on peak bone mineral density in men is unknown. To determine whether such a delay reduces normal peak bone density and leads to osteopenia during adulthood, we measured radial bone mineral density by single-photon absorptiometry and spinal bone mineral density by dual-energy x-ray absorptiometry in 23 men who had a history of constitutionally delayed puberty and 21 men who underwent normal puberty. Their mean ages were 26 and 24 years, respectively. The groups were matched for other factors known to affect bone mass. RESULTS: The mean (+/- SD) radial bone mineral density was significantly lower in the men with a history of delayed puberty than in the normal men (0.73 +/- 0.07 vs. 0.80 +/- 0.05 g per square centimeter; P less than 0.0002). Spinal bone mineral density was also significantly lower in the men with delayed puberty than in the normal men (1.03 +/- 0.10 vs. 1.13 +/- 0.11 g per square centimeter; P less than 0.003). Radial bone density was at least 1 SD below the mean value for the normal men in 15 of the 23 men with a history of delayed puberty, and spinal bone density was similarly decreased in 10 of the 23. CONCLUSIONS: Adult men with a history of constitutionally delayed puberty have decreased radial and spinal bone mineral density. These findings suggest that the timing of puberty is an important determinant of peak bone density in men. Because the peak bone mineral density achieved during young adulthood is a major determinant of bone density in later life, men in whom puberty was delayed may be at increased risk for osteoporotic fractures when they are older.

Absorptiometry, Photon↗
PubMed2003

Delayed puberty associated with inflammatory bowel disease.

Delayed puberty frequently complicates the clinical course of young patients with inflammatory bowel disease, more often in Crohn's disease than ulcerative colitis. Undernutrition has been thought to be the main reason for delayed puberty in these patients. However, puberty may be delayed despite a normal nutritional status. Observations in patients with inflammatory bowel disease and in rats with experimental colitis suggest that inflammatory mediators may have a direct adverse influence, independent of undernutrition, on the onset and progression of puberty. Serum androgens are consistently reported to be reduced in patients with delayed puberty and inflammatory bowel disease. This reduction is not necessarily secondary to a reduction in gonadotrophins as serum concentrations of gonadotrophins have been reported to be normal or even increased in some studies. Management of delayed puberty involves calorie supplements to correct undernutrition and treatment of inflammation. Observations in boys with delayed puberty and controlled studies in experimental models of intestinal inflammation suggest that testosterone therapy can accelerate puberty.

Animals↗