Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Puberty, Delayed”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1981

Hypernatraemia, diabetes mellitus, hyperprolactinaemia, retarded growth and delayed puberty in a 14 year old girl. Effect of bromocriptine treatment.

Investigations in a 14 year old girl with arrested growth for 2 years, delayed pubertal development, hypernatraemia without thirst, diabetes mellitus and hyperlipaemia are reported. The hypernatraemia was accompanied by a low vasopressin concentration with an abnormal response to thirst, high plasma renin but normal plasma aldosterone concentrations. Treatment with vasopressin and increased fluid intake decreased serum sodium levels. Serum gonadotrophins were low; GH response during an insulin tolerance test was subnormal and basal serum Prl concentration was elevated. Bone age, thyroid function and adrenal function were normal. After initiation of bromocriptine treatment her growth accelerated and regular menstruations commenced. The serum gonadotrophin levels increased and showed pulsatile release. A hypothalamic disorder is suggested, but no cerebral lesion could be demonstrated.

Adolescent↗
PubMed1990

[Gonadotropic function of the hypophysis in girls with delayed puberty].

Radioimmune assay of serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in 216 girls aged 13-18 years with pubertal delay (PD) unrelated to gonadal dysgenesis have shown that LH and FSH levels were normal in 48.1%; one or both gonadotropins were decreased in 17.1%, only LH level was increased in 13.9% and only FSH level in 12.6%. Hypergonadotropinemia was seen in 8.3% of the patients. Bioassay of total gonadotropin excretion was performed in 117 patients. Comparison of the radioimmune and biological assays suggested misproduction of the biologically active gonadotropins in a proportion of girls with PD. Hypoestrogenism in normogonadotropic PD appears to be related to regional blood and lymph flow disturbance.

Adolescent↗
PubMed1993

Androgen-stimulated pubertal growth: the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty.

The purpose of this study was to investigate the roles of androgenic and estrogenic mechanisms in the stimulation of structural growth and plasma GH in male puberty. To resolve these two possible mechanisms, we compared the effect of two androgens in the treatment of constitutional delay in growth and adolescence: an aromatizable androgen, testosterone (T), and a nonaromatizable androgen, dihydrotestosterone (DHT). Nine adolescent males, Tanner stage 1 or 2, were studied before and during treatment with T enanthate (group A) or DHT heptanoate (group B). After 2.5 months of treatment, the height velocity (HV) was 12.6 +/- 2.8 cm/yr (n = 3) in group A and 8.9 +/- 1.7 cm/yr (n = 6) in group B, both within the range of peak HV for pubertal males. In group A, the integrated concentration of GH (ICGH) increased from 3.12 +/- 0.90 to 13.67 +/- 6.0 micrograms/L (P < 0.05), and plasma insulin-like growth factor-I (IGFI) increased from 126.7 +/- 2.5 to 350.3 +/- 20.3 micrograms/L (P < 0.01); plasma T increased from 0.8 +/- 0.5 to 33.8 +/- 11.0 nmol/L (P < 0.001), and the LH response to LHRH decreased from 27.6 +/- 10.7 to 5.9 +/- 2.5 IU/L (P = NS). In group B, ICGH decreased from 4.32 +/- 0.61 to 2.39 +/- 0.42 (P < 0.025), and IGF-I decreased from 218.3 +/- 39.2 to 184.0 +/- 15.8 (P = NS). Plasma T increased from 2.0 +/- 0.5 to 2.7 +/- 0.8 (P = NS), and the LH response to LHRH decreased from 45.7 +/- 14.5 to 10.7 +/- 5.8 (P < 0.05). To further evaluate the mechanism of the effect of DHT on plasma GH, seven male subjects with adolescent gynecomastia were treated with DHT heptanoate, and their responses were studied at 1 week and 3.5 months. ICGH decreased in conjunction with a decrease in the integrated T concentration (r = -0.77; P < 0.001) and to a slight degree with decreasing plasma estradiol (r = -0.39; P < 0.2). Plasma IGF-I did not show a significant change in the subjects with gynecomastia. Thus, the increase in GH at puberty in males appears to be due to an estrogen-dependent mechanism. The suppressive effect of DHT on GH secretion may be due to either suppression of estradiol production or a direct effect. Acceleration of HV into the peak pubertal range by DHT without an increase in plasma GH suggests that an increase in GH is not necessary for the pubertal growth spurt.

Adolescent↗
PubMed1991

Role of pulsatile luteinizing hormone releasing-hormone therapy in males with idiopathic hypogonadotropic hypogonadism and delayed puberty.

The aim of our work was to review the literature to evaluate the importance of pulsatile LHRH administration therapy in males with idiopathic hypogonadotropic hypogonadism (IHH) and delayed pubertal development. Among the various routes of administration (iv, sc, nasal) we believe that sc administration is better in IHH males whereby a long-term therapy is needed. With regard to the differential diagnosis of pubertal delay, the diagnostic use of LHRH administration for a short-period is still being debated. Biochemical controls show that response to therapy is quick in all of the subjects treated. 30-50% of IHH subjects can obtain adequate sperm production. The appearance of antibodies to LHRH is a rare phenomenon. We can conclude that pulsatile sc therapy is more physiological and better tolerated for a longer time.

Adolescent↗
PubMed2000

Short stature and delayed puberty in gymnasts: influence of selection bias on leg length and the duration of training on trunk length.

BACKGROUND: Delays in bone age, the onset of puberty, and skeletal growth in gymnasts could be, in part, the reason for an interest in gymnastics, rather than being the result of vigorous exercise. We hypothesized that short stature and delayed bone age are present at the start of gymnastics, and training delays growth, producing short stature, even after retirement. METHODS: Sitting height and leg length were measured in 83 active female gymnasts, 42 retired gymnasts, and 154 healthy control subjects. Results were expressed as age-specific SD scores (mean +/- SEM). RESULTS: In the cross-sectional data, active gymnasts had delayed bone age (1.3 +/- 0.1 years), reduced height -1.32 +/- 0.08 SD, sitting height -1.24 +/- 0.09 SD, and leg length, -1.25 +/- 0.08 SD (all P <.001). However, in those training for less than 2 years, the deficit was confined to leg length (-0.8 +/- 0.2 SD). During 2 years of follow-up of 21 gymnasts, only the deficit in sitting height worsened (by 0.4 +/- 0.1 SD). In 13 gymnasts followed up in the immediate 12 months after retirement, sitting height accelerated, resulting in a lessening of the deficit in sitting height by 0.46 +/- 0.14 SD (P <.01). Adult gymnasts who had been retired for 8 years had no deficit in sitting height, leg length, or menstrual dysfunction. CONCLUSIONS: Short stature in active gymnasts is partly due to selection of individuals with reduced leg length. Reduced sitting height is likely to be acquired but is reversible with cessation of gymnastics. A history of gymnastic training does not appear to result in reduced stature or menstrual dysfunction in adulthood.

Adolescent↗
PubMed2004

Increase of serum leptin after short-term pulsatile GnRH administration in children with delayed puberty.

OBJECTIVE: Leptin is known to play an important role in pubertal development in humans, probably acting as one permissive factor for the onset of puberty. Leptin serum concentrations change during pubertal development and an initial increase before the onset of puberty has been reported. The underlying mechanism for this increase in leptin levels is unknown. We hypothesized that the pulsatile release of GnRH stimulates leptin metabolism. In this study, the effect of short-term pulsatile GnRH administration on leptin levels in children with delayed onset of puberty was investigated. METHODS: Nineteen children (15 males and four females, mean age 15.5 years, range 13.1-20.5 years), who underwent evaluation for delayed sexual maturation, were included in the study. Sixteen subjects received 36 h of pulsatile intravenous GnRH, using an infusion pump that released 5 microg GnRH every 90 min. Serum concentrations of LH, FSH, testosterone, estradiol and leptin were analysed before and up to 36 h after GnRH administration. Eight patients received a single dose GnRH-agonist stimulation test (buserelin acetate test, 10 microg/kg body weight) with a 24-h follow-up (five patients underwent both tests). RESULTS: Mean (+/-s.e.m.) serum leptin increased significantly (P<0.01) after 36 h of pulsatile GnRH administration (7.26+/-1.35 vs 9.75+/-1.76 ng/ml). In contrast, no increase in leptin concentrations was observed after administration of a single dose of buserelin. CONCLUSIONS: These findings suggested that the increase in serum leptin at the onset of puberty is triggered by the pulsatile release of GnRH.

Adolescent↗
PubMed1985

GnRH and HCG tests are both necessary in differential diagnosis of male delayed puberty.

The discriminative power of the gonadotropin releasing hormone test and the human chorionic gonadotropin (HCG) test in the diagnosis of gonadotropin deficiency was studied in 73 boys referred because of delayed pubertal development or suspicion of gonadotropin deficiency. Hypogonadotropic hypogonadism was confirmed by clinical follow-up in 21 of the boys and excluded in the others because of normal pubertal development. Those latter boys served as a reference group. The post-HCG serum testosterone level was subnormal in hypogonadotropic hypogonadism on 12 of 19 occasions (in the reference group on two of 46 occasions) and the post-gonadotropin releasing hormone serum luteinizing hormone level was subnormal on fourteen of 22 occasions (zero of 65). Four of the seven boys with hypogonadotropic hypogonadism who had normal post-HCG testosterone levels had subnormal peak luteinizing hormone levels. Of the remaining three boys, two had low basal testosterone levels. Combining the two tests therefore improved the diagnostic accuracy.

Adolescent↗
PubMed1991

Therapeutic indications for delayed puberty and hypogonadism in adolescent boys.

Testosterone and synthetic androgens have formerly been used indiscriminately, but are now applied more selectively. They are the only treatment of primary hypogonadism, but are also useful in gonadotropin deficiency and constitutional delay. 17-Alkylated androgens are no longer used. Oral testosterone undecanoate is not suitable for adolescents because of unreliable absorption. The prototype disorder where replacement is necessary is congenital anorchia. As a physiological replacement, an initial dose of 35 mg/m2 per month for 6 months, followed by 70 mg/m2 for 1 year, and 150 mg/m2 thereafter, is recommended. No general rules can be given for other types of primary hypogonadism. In testicular atrophy after cryptorchidism, defects of testosterone biosynthesis, galactosemia or other causes, it is advisable to carry out periodic testosterone determinations and to wait until the levels drop below normal. Progress has been made in the treatment of gonadotropin deficiency, and pulsatile gonadotropin-releasing hormone (GnRH) has been shown to be effective in the hypothalamic type. Nevertheless, androgens still have a temporary place in this condition. In constitutional delay of growth and adolescence, treatment is not necessary somatically, but there are often psychosocial reasons. Gonadotropins, GnRH or growth hormone (GH)-releasing hormone have been used. Also treatment with human GH is successful in accelerating height velocity. The most simple and economic treatment is still testosterone in a physiological dose for 3-6 months. Oxandrolone or other synthetic androgens have no advantages.

Adolescent↗
PubMed1993

[Hypogonadism and delayed puberty. Indications for androgen treatment in adolescents].

Testosterone and synthetic androgens were once used somewhat uncritically; on account of the undesired side effects that are now known to occur, however, they should be employed very selectively, in particular in the young patient. Although the main indication is primary hypogonadism, they are also employed in the treatment of gonadotropin deficiency and constitutionally delayed growth and development. While, for the treatment of congenital anorchism a therapeutic scheme could be developed which closely approximated the physiological conditions, no generally applicable treatment schemes could be established for other forms of primary hypogonadism. In the case of constitutional retardation of growth and development, treatment is not indicated, for somatic reasons, although severe psychosomatic disturbances may make treatment necessary in many cases.

Adolescent↗
PubMed1976

Mean 24-hour growth hormone and testosterone concentrations in relation to pubertal growth spurt in boys with normal or delayed puberty.

The mean growth hormone concentration during 24-hour period in 7 boys of short familial stature and a growth rate of 3.2-5.4 cm/year was between 1.0 and 4.6 ng/ml serum. In 7 boys with pubertal growth spurt and familial tallness (growth rate 7.2-11.0 cm/year) it varied from 0.97 to 4.4 ng/ml and in 6 boys with constitutional delay of puberty (a growth rate of 4.2-5.2 cm/year prior to puberty) from 1.3 to 4.3 ng/ml. No correlation was found between the 24-hour mean growth hormone concentration and the mean 24-hour testosterone concentration in serum or the growth rate, but a correlation was found between testosterone and the growth rate. It is concluded that the growth spurt in puberty is not due to a change in growth hormone concentration but rather to the increase of androgen production in puberty.

Adolescent↗
PubMed1990

Delayed puberty in girls having biliary atresia.

Biliary atresia patients have several problems even after undergoing successful Kasai operation. Fourteen female patients have been followed for over 12 years after successful Kasai original portoenterostomy procedures. The oldest patient is 21 years of age. All patients are jaundice-free, but 10 patients have a history of esophageal varices and/or hypersplenism. Five patients complain of menstrual disorders. The average age of menarche was delayed 1 year, 9 months, compared with Japanese controls. Two cases of 11 (18.2%) presented primary amenorrhea after 14 years, 6 months, which is mean + 2SD of Japanese controls. Four cases of 11 (36.4%) showed secondary amenorrhea. Unestablished menstrual cycles after 2 years of menarche were observed in two patients of nine (22.2%). Four cases had regular menstruation. Five patients showed delay in the development of pubic hair and breasts. Six patients showed atypical body height velocity pattern that showed no peaking, and one patient showed no growth spurt. All the patients with amenorrhea had portal hypertension. In hormonal evaluation, the patients with menstruation showed normal or slightly good reaction of luteinizing hormone and follicle stimulating hormone in the luteinizing hormone-releasing hormone test, having normal to high estradiol levels. The patients with menstrual abnormality showed overreaction of LH, having normal estradiol levels.

Adolescent↗
PubMed1980

Delayed puberty in males with chronic renal failure.

The effects of chronic renal failure on the pituitary-testicular axis of 31 males, aged 11.7 to 20.0 yr (mean, 16.0 yr) were studied. Nine patients not on hemodialysis (group I) had serum creatinines between 2.5 and 8.0 mg/dl, 10 patients were on hemodialysis (group II) and 12 patients had received a renal transplant (group III). The Tanner stage of pubertal development was delayed relative to chronologic age. Testosterone (T), delta 4-androstenedione (delta 4), and urinary 17-keto steroids were normal when related to pubertal stage in groups I and II; and dehydroepiandrosterone (DHEA) and DHEA sulfate (DS) were in the low normal range. In group III, adrenal androgens (delta 4, DHEA, DS) were decreased as a consequence of prednisone therapy whereas T was normal. Luteinizing hormone levels were normal in all. Follicle-stimulating hormone levels were normal in all. Follicle-stimulating hormone (FSH) was significantly increased in groups I and II. In group III, FSH was normal in 6 of 9 patients with serum creatinine concentrations < 2 mg/dl. FSH levels were uniformly elevated in Tanner I-V patients with creatinines > 2 mg/dl. The data shows that FSH is elevated in patients with chronic renal failure even in prepuberty and early adolescence. This may reflect damage to germinal epithelium prior to the advent of spermatogenesis, whereas Leydig cell function appears to remain intact.

Adolescent↗
PubMed1991

Testosterone esters advance skeletal maturation more than growth in short boys with chronic renal failure and delayed puberty.

Four young males with chronic renal failure and absent or stagnant puberty were treated with testosterone esters. Endocrine evaluation before therapy showed low plasma follicle stimulating hormone (FSH) levels and relatively high luteinizing hormone (LH). Following therapy skeletal maturation accelerated more than growth velocity, resulting in a lower predicted adult height. In three patients osteoporosis increased or rickets developed. Testosterone therapy was effective in developing sex characteristics, but endogenous pubertal development was not stimulated. Growth velocity was increased, but the effect on growth was more than outweighed by bone age acceleration.

Adult↗
PubMed2005

Isolated 17,20-lyase (desmolase) deficiency in a 46,XX female presenting with delayed puberty.

OBJECTIVE: To investigate the cause of hypergonadotropic hypogonadism. DESIGN: Case report and literature review. SETTING: University Departments of Pediatric Endocrinology and Obstetrics and Gynecology. PATIENT(S): A 13.5-year-old girl with absent puberty and growth retardation. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Detailed biochemical, radiological, and molecular analysis, including pelvic ultrasound, basal steroid hormone analysis in serum and aspirated follicle fluid, serum steroid measurement after ACTH (Synachten) and human chorionic gonadotropin (hCG) stimulation, and molecular analysis of CYP17. RESULT(S): This girl with hypergonadotropic hypogonadism (LH 65 U/L, FSH 50 U/L) had a 46,XX karyotype, small uterus and enlarged cystic ovaries, and markedly delayed bone age (9 years). Basal (serum, follicular) and stimulated (serum) steroid hormone levels were consistent with isolated 17,20-lyase deficiency whereas relatively normal P and 17-hydroxyprogesterone concentrations were detected together with very low androstenedione, T, and E(2) levels. CONCLUSION(S): Isolated 17,20-lyase deficiency should be considered in the differential diagnosis of hypergonadotropic hypogonadism in 46,XX females, and follicular fluid steroid analysis is a useful adjuvant test. Failure to detect mutations in CYP17 raises the possibility of a novel association of these phenotypes.

Adolescent↗
PubMed1985

Pinealectomy delays puberty in ewe lambs.

Fifteen pinealectomized and 15 unoperated ewes were exposed to constant light for 3 weeks before and 10 weeks after lambing. Fourteen pinealectomized and 15 unoperated ewes were allowed to lamb outdoors. Five ewe lambs born in constant light to the 2 groups of dams were pinealectomized at 10 weeks of age. Ewes and lambs were then returned to the field. Puberty (determined by weekly progesterone analysis) was significantly delayed (P less than 0.05) in the pinealectomized ewe lambs. Median pubertal age in pineal-intact ewe lambs was 37 weeks compared to 49 weeks in pinealectomized lambs. Constant light during the first 10 weeks of life had no effect upon puberty onset nor did the pineal status of the dam. Control lambs entered seasonal anoestrus at the time pinealectomized ewe lambs were entering puberty. Pinealectomized lambs entered anoestrus at the same time as control lambs were beginning their second breeding season. These results confirm a key role of pineal-mediated hormonal signals in the control of puberty in the sheep.

Anestrus↗
PubMed1977

A possible mechanism of the puberty-delaying effect of hippocampal lesions in female rats.

Untreated female Wister rats and females in which advancement of the onset of puberty was induced by bilateral lesioning of the medial preoptic area or the ventromedial-arcuate region, or by the daily s.c. injection of 0.05 microgram oestradiol benzoate/100 g b.w., were bilaterally lesioned in the anterior part of the ventral hippocampus at 21 days of age. Irrespective of the applied treatment, a significant delay of vaginal opening and of the first puberal ovulation resulted from the hippocampal lesions. This delay of the onset of puberty was consistently associated with a retardation of the body weight increase, so that the stage of body development necessary for the occurrence of spontaneous or precocious puberty was reached at later ages in these rats. The results suggest that a normal function of the hippocampus may be necessary for adequate somatic development during sexual maturation.

Animals↗
PubMed2006

Metformin therapy during puberty delays menarche, prolongs pubertal growth, and augments adult height: a randomized study in low-birth-weight girls with early-normal onset of puberty.

CONTEXT AND OBJECTIVE: Low-birth-weight (LBW) girls who enter puberty earlier (around 8-9 yr) tend to have earlier menarche, earlier growth arrest, and a shorter adult stature. At present, there is no therapy for most of these girls. In LBW girls with early puberty, hyperinsulinemic insulin resistance could underpin their rapid transit through puberty and their loss of adult stature. We explored the effects of insulin sensitization with metformin during puberty. SETTING, DESIGN, AND PATIENTS: In an open-labeled, prospective study, 22 LBW girls (birth weight < -1.5 sd score for gestational age) with early-normal puberty (stage 2 breast development at age 8-9 yr) were randomized to remain untreated (n = 12) or to receive metformin (850 mg/d; n = 10) for 36 months (mean age at start, 9.0 yr). All girls remained untreated between 36 and 42 months. MAIN OUTCOME MEASURES: Pubertal growth, body composition by absorptiometry, uterine-ovarian size by ultrasound, fasting insulin, glucose, lipids, leptin, IGF-I, and IGF-binding protein-1 were assessed. RESULTS: Metformin treatment resulted in a longer duration from stage 2 breast development to menarche (P < 0.01; median difference, +1.0 yr), taller near-adult height (P < 0.01), and leaner body composition (P < 0.001). Metformin was also associated with lower insulin resistance and leptin and IGF-I levels and higher SHBG and IGF-binding protein-1 levels and with a more favorable lipid profile. Bone mineral density and uterine-ovarian growth were unaffected. CONCLUSION: Metformin treatment for 36 months in LBW girls with early-normal puberty normalized their pubertal progression to menarche and increased height gains up to adult stature. These data support the concept that insulin is a major codeterminant of the pubertal tempo and pubertal height gain in girls.

Body Composition↗
PubMed1986

Puberty delay of bank vole females in a high-density population.

The onset of puberty in bank vole females was studied, with uterine weight, ovarian weight, and the number of large ovarian follicles used as indicators of gonadal activity. Maturation of females born at the beginning of the reproductive season was suppressed by the presence of other females. Puberty of animals born at the end of season was primarily influenced by climatic variation.

Animals↗