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 1,189 records · Page 66Linked to original sources
PubMed2005

Pubertal development and its influences on bone mineral density in Australian children and adolescents with cystic fibrosis.

BACKGROUND: Pubertal delay is thought to contribute to suboptimal peak bone mass acquisition in young people with cystic fibrosis (CF), leading to an increased fracture incidence. This study aims to compare pubertal development in young people with CF with that of a local healthy population and assess the influence it has on areal bone mineral density (aBMD). METHODS: Tanner stage, age of menarche, bone age (BA), sex hormone levels and aBMD were examined in 85 individuals with CF (aged 5.3-18.1 years, 39 females) and 100 local controls (5.6-17.9 years, 54 females). RESULTS: Tanner stage and age of menarche were not significantly different between controls and CF. Tanner stage-adjusted mean values for follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T) were lower in males with CF (FSH: P = 0.004, LH: P = 0.01 and T: P = 0.002). Bone age was delayed in adolescents with CF compared to controls (chronological age-BA: controls = 0.13 years (SE = 0.16), CF = 0.95 years (SE = 0.22), P = 0.003). Areal bone mineral density (adjusted for age, sex, height and lean tissue mass) was not significantly different between CF and controls. Moderate negative correlations were found between delayed BA and weight (r = -0.41, P < 0.001) and height (r = -0.41, P < 0.001). CONCLUSIONS: There was no evidence of clinical pubertal delay or low aBMD (adjusted for short stature and lean tissue mass) in young people with CF when compared with a local population, despite lower nutritional markers, height and weight and delayed skeletal maturation.

Adolescent↗
PubMed2003

Effects of perinatal maternal food restriction on pituitary-gonadal axis and plasma leptin level in rat pup at birth and weaning and on timing of puberty.

The effects of maternal 50% food restriction (FR) during the last week of gestation and/or lactation on pituitary-gonadal axis (at birth and weaning), on circulating levels of leptin (at weaning), and on the onset of puberty have been determined in rats at birth and at weaning. Maternal FR during pregnancy has no effect at term on the litter size, on the basal level of testosterone in male pups, and on the drastic surge of circulating testosterone that occurs 2 h after birth. At weaning, similar retardation of body growth is observed in male and female pups from mothers exposed to FR. This undernutrition induces the most drastic effects when it is performed during both gestation and lactation or during lactation alone. Drastic retardation of testicle growth with reduction of cross-sectional area and intratubular lumen of the seminiferous tubules is observed in male pups from mothers exposed to undernutrition during both gestation and lactation or during lactation alone. Maternal FR during the perinatal period reduces circulating levels of FSH in male pups without affecting LH and testosterone concentrations. Maternal FR does not affect circulating levels of LH, estradiol, and progesterone in female pups. Female pups from mothers exposed to FR during both gestation and lactation show a significant increase of plasma FSH as well as a drastic retardation of ovarian growth. The follicular population was also altered. The number of antral follicles of small size (vesicular follicles) was increased, although the number of antral follicles of large size (graafian follicles) was reduced. Maternal FR occurring during both late gestation and lactation (male and female pups), during lactation alone (male and female pups), or during late gestation (female pups) induces a drastic reduction of plasma leptin and fat mass in pups at weaning. The onset of puberty is delayed in pups of both sexes from mothers exposed to FR during lactation and during both gestation and lactation. In conclusion, these data demonstrate that a perinatal growth retardation induced by maternal FR has long-term consequences on both size and histology of the genitals, on plasma gonadotropins and leptin levels, on fat stores at weaning, and on the onset of puberty.

Animals↗
PubMed2004

Effects of gestational and lactational exposure to low doses of PCBs 126 and 153 on anterior pituitary and gonadal hormones and on puberty in female goats.

The aim of the present study was to investigate if environmental doses of PCB 153 and PCB 126 could produce effects in a controlled animal model. Possible adverse effects on the hypothalamic-pitutitary-gonadal axis were examined by measuring gonadotrophins and gonadal steroid hormone concentrations in goat kids exposed during gestation and lactation. The concentrations of PCB 153 and PCB 126 in adipose tissue in the goat kids 9 months post-partum were 5800 ng/g (fat-weight, range; 2900-12700 ng/g) and 0.49 ng/g (fat-weight, range; 0.28-0.80 ng/g), respectively. The pre- and post-pubertal plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (Prl) and progesterone (P4) were analysed. LH, FSH, Prl, and P4 were also measured during an induced oestrus cycle. The prepubertal LH concentration was significantly lower, the puberty was delayed and the P4 level during the luteal phase of an estrous cycle was higher in the group exposed to PCB 153. No significant effect of PCB 153 exposure was found on Prl and FSH. PCB 126 did not produce any effects at the exposure level tested in this study. In conclusion, perinatal exposure to PCB 153 affected the reproductive function and the puberty maturation in goats.

Administration, Oral↗
PubMed1991

Delayed spontaneous pubertal growth spurt in girls with the Ullrich-Turner syndrome.

By means of an appropriate mathematical model (Sager's 2-components-concept) a delayed spontaneous pubertal growth spurt can be demonstrated in girls with 45,X Ullrich-Turner syndrome (UTS) (n1 = 45) as well as in those with 45,X/46,XX mosaicism (n2 = 14) never treated with any growth stimulating drug. On the average, this growth spurt begins later and its extent is smaller (mean growth rate = 3.10 and 2.79 cm, respectively, in the 15th year of chronological age) than in normal girls. The delay in acute growth spurt corresponds very well to the delay of skeletal maturation in the UTS (on the average 2 to 3 years of chronological age).

Adolescent↗
PubMed1984

Mauriac's syndrome revisited.

A 22 year follow-up of a female with Mauriac syndrome is presented. Despite incomplete growth she had normal, though delayed, sexual development with two successful pregnancies. There is no clinical evidence of degenerative complications.

Adolescent↗
PubMed1988

Long-term effects of accelerated or delayed sexual maturation on reproductive output in wild female house mice (Mus musculus).

The effects of acceleration and delay of puberty in female house mice on survival and reproduction were tested using 6 experimental groups: (1) control females mated at the time of first oestrus, (2) females mated at weaning, (3) females treated with male urine starting at weaning and mated at first oestrus, (4) females housed in groups and mated at first oestrus, (5) females housed alone, treated with urine from grouped females and mated at first oestrus, and (6) females housed alone and mated at 68 days of age. Females caged with males at weaning or treated with male urine and mated at puberty had lower rates of survival to 180 days of age, but did not differ in rates of fertility from mice in the other four treatments. Those females that were housed with males from weaning or treated with male urine also had smaller total numbers of litters, fewer total young, and smaller average litter sizes than did females for which the age of mating was delayed, by grouping or treatment with urine from grouped females, or by being held until age 68 days before mating. Control females mated at first oestrus generally were intermediate or did not differ from the male treatments on these dependent variables. There were no differences in the average number of female young/litter across the 6 treatments. However, females that were delayed in age of first mating had significantly more male young/litter than did females that were accelerated in their sexual development or control females.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Menstrual characteristics of women suffering from insulin-dependent diabetes mellitus.

OBJECTIVE: To assess the frequency of menarche and menstrual disturbances among women suffering from insulin-dependent diabetes mellitus, and to evaluate their correlation to the onset of diabetes, its duration, and complications. RESEARCH DESIGN AND METHODS: Retrospective analysis of the menstrual regularity and gynecologic and fertility history of 100 women suffering from insulin-dependent diabetes mellitus. These data were compared with information obtained from the patients' medical records regarding the age at onset of diabetes, its management, control, and complications. RESULTS: The average age at menarche was 13.5 years. Delayed menarche tended to appear in girls whose diabetes was diagnosed before the age of menarche, and before the age of 10 years. Menstrual disturbances, such as oligomenorrhea, amenorrhea, and polymenorrhea, occurred in 32% of the women. A significant correlation was found between late menarche and menstrual disturbances. Furthermore, patients with diabetic complications had a higher incidence of menstrual disorders compared with uncomplicated diabetic patients. CONCLUSIONS: It appears that women with insulin-dependent diabetes mellitus who had been diagnosed prior to menarche had a higher probability of delayed menarche, and were at higher risk for development of menstrual disturbances, including amenorrhea with subsequent fertility disorders.

Adolescent↗
PubMed1981

The reproductive endocrine system in cystic fibrosis. I. Basal gonadotropin and sex steroid levels.

Serum gonadotropin and sex steroid levels were measured in 106 patients with cystic fibrosis (CF), 46 males and 60 females, aged 8 to 24 years. The finding of delayed pubertal increments of serum gonadotropin and sex steroid levels in CF patients suggests late maturation of the reproductive endocrine system. Although pubertal changes in reproductive endocrine hormones in patients with CF appear to be temporally delayed, generally appropriate levels of these hormones are finally attained in most patients by the late teenage years. Delayed maturation of the reproductive endocrine system probably is secondary to hypothalamic-pituitary dysfunction, the result of chronic inanition.

Adolescent↗
PubMed2003

Bone mineral density, biochemical and hormonal profiles in suboptimally treated children and adolescents with beta-thalassaemia disease.

OBJECTIVE: Thalassaemia/haemoglobinopathy is a hereditary disease causing increased erythropoiesis and expansion of the bone marrow cavity. As a consequence, there is a reduction in trabecular bone tissue resulting in osteopenia/osteoporosis. The present study was performed to assess bone mineral density (BMD) in children and adolescents with beta-thalassaemia disease and to determine biochemical and hormonal changes that may affect BMD. METHODS: Forty-eight children and adolescents with beta-thalassaemia were divided into two groups, transfusion-dependent (TD) (n = 16) and transfusion-independent (TI) (n = 32). All patients were treated suboptimally. BMD was determined by dual-energy X-ray absorptiometry. Bone maturation was assessed by radiographic bone age (BA). Blood and urine samples were obtained for the determination of biochemical and hormonal profiles, which included PTH, 25-hydroxyvitamin D (25-OHD), osteocalcin, bone-specific alkaline phosphatase, IGF-1, fT4, TSH and urine deoxypyridinoline. RESULTS: Most of the patients were short and underweight, and they had delayed BA with mean Z-scores of -2.77 in the TD and -2.04 in TI groups. The mean Z-scores of BMD in the TD vs. TI groups of total body, radius, femoral neck and lumbar spine were -2.09 vs.-1.49, -0.73 vs. -0.54, -1.93 vs.-1.17 and -3.45 vs.-2.43, respectively. Although the means BMD values in the TD group were lower than those in the TI group, they were not significantly different. Mean serum IGF-1 levels were lower in the TD than the TI groups, 11.6 and 24.9 nmol/l, respectively (P < 0.05). Other biochemical and hormonal profiles did not differ between these two groups. CONCLUSIONS: Patients with undertransfused severe beta-thalassaemia had more bone marrow expansion, lower serum IGF-1 levels and more delayed bone age than did patients with untransfused moderately severe beta-thalassaemia. Therefore, the severity of the disease appeared to be a primary factor for low bone mineral density in undertransfused patients in association with bone age delay and low serum IGF-1.

25-Hydroxyvitamin D 2↗
PubMed1994

Delayed adolescent growth in homozygous sickle cell disease.

Analysis of the growth abnormalities in sickle cell disease has been limited by the lack of longitudinal observations in individuals, and by an inability to quantitate the observed patterns. To investigate the timing and pattern of the adolescent growth spurt, longitudinal observations of height from the Jamaican cohort study were fitted to a mathematical model of growth (Preece-Baines model 1). The study included 44 children with homozygous sickle cell (SS) disease, 44 age and sex matched subjects with sickle cell haemoglobin C (SC) disease, and 44 age and sex matched controls with normal (AA) haemoglobin. Compared with AA controls, the onset of the adolescent growth spurt was delayed in SS disease by 1.4 years (95% confidence interval 0.8 to 2.0) with no significant sex difference. The age at peak height velocity was delayed by 1.6 years (0.9 to 2.3) in SS compared with AA subjects but the adolescent growth of SS children was otherwise normal and there was no difference in the attained height by age 17.9 years. The growth spurt was not delayed in SC disease. The age at menarche in girls with SS disease (mean (SD) 15.4 (1.3) years) was significantly later than girls with SC disease (13.7 (1.7) years) and those with AA haemoglobin (13.1 (1.3) years) but these genotype differences were no longer significant after controlling for the delay in the adolescent growth spurt. The normally coordinated but slightly delayed pattern of growth and normal adult heights suggests a good prognosis for adolescent growth delay in SS disease. Most children with SS disease can therefore be reassured on the outcome of retarded adolescent growth.

Adolescent↗
PubMed1996

Essentials of growth diagnosis.

There is more to growth than GH. Growth disorders can be approached expeditiously by assessing the relationships among height, weight, BA and height velocity. Undernutrition is indicated by low weight for height; diabetes mellitus, hyperthyroidism, and electrolyte disturbances are the major endocrine considerations. Short stature results from intrinsically short, delayed, or attenuated growth patterns. Excessive stature results from intrinsically tall, advanced, or accelerated growth patterns. Each of these patterns causing linear growth abnormalities has a distinct differential diagnosis that variously includes endocrine, metabolic, genetic, and systemic disorders.

Adult↗
PubMed1991

Puberty and its disorders in boys.

The secular trend toward an earlier age of puberty implicates health and nutrition as major determinants of the onset of sexual maturation. The pattern of hypothalamic stimulation of pituitary gonadotropin secretion causing gonadal steroid secretion that is active in the fetus, subdued in the child, and again awakened in the peripubertal period is well described, although the specific trigger of the initiation of puberty is unknown. Pubertal delay may have a cause in the CNS or in the gonad. Constitutional delay in pubertal development, a variant of normal, is difficult to differentiate from isolated gonadotropin deficiency, a permanent condition. However, a myriad of congenital defects, tumors, injuries, and infections can lead to hypogonadotropic hypogonadism, which may be diagnosed by associated physical findings. Gonadal abnormalities are characterized by elevated gonadotropin concentrations and often are associated with specific physical features. Early pubertal development may also be divided into etiologies based in the CNS or in other parts of the body. Idiopathic precocious puberty, in which the endocrine profile is identical to that of normal puberty, is seen in the early childhood period or as a minor variation from the normal range of the onset of pubertal development. Tumors of the CNS, however, are more often responsible for the youngest childhood cases of complete precocious puberty. Incomplete precocious puberty in boys can be caused by androgen production from the gonads or adrenal glands or can be caused by autonomous production of hCG. Variations of pubertal development are self-limited, although they may awaken parental or patient concerns. Thus, premature adrenarche is best differentiated from more serious and treatable causes of androgen production. Gynecomastia is usually treated with reassurance.

Adolescent↗
PubMed1999

Puberty in chronic renal failure.

Puberty is a period of transition characterized by a sequence of profound physical and psychological changes leading to full sexual maturity. This process is driven and orchestrated by the awakening of the gonadotropic hormone axis. Chronic renal failure and its treatment may interfere with the onset and progress of puberty by numerous mechanisms including endocrine, metabolic and neuropsychological abnormalities, and drug effects. On average, the onset of puberty is delayed by 2 years in children with chronic renal failure, even after successful transplantation. Moreover, pubertal height gain is only 50% of that observed in healthy children. In this report, we discuss the endocrine mechanisms underlying these alterations and highlight new therapeutical options for pubertal growth failure.

Female↗
PubMed2002

Osteopenia in exercise-associated amenorrhea using ballet dancers as a model: a longitudinal study.

Few longitudinal studies have investigated the effects of amenorrhea and amenorrhea plus exercise on bone mineral density (BMD) of young women. We carried out a 2-yr comparison of dancers and nondancers, both amenorrheic and normal, that investigated the role of hypothalamic amenorrhea on bone in this context. We studied 111 subjects (mean age, 22.4 +/- 4.6 yr; age of menarche, 14.1 +/- 2.2 yr), including 54 dancers, 22 with hypothalamic amenorrhea, and 57 nondancers, 22 with hypothalamic amenorrhea. Detailed hormonal and nutritional data were obtained in all groups to determine possible causal relationship to osteoporosis. The amenorrheic groups, dancers and nondancers, both showed reduced BMD in the spine, wrist, and foot, which remained below controls throughout the 2 yr. Only amenorrheic dancers showed significant changes in spine BMD (12.1%; P < 0.05) but still remained below controls, and within this subgroup, only those with delayed menarche showed a significant increase. The seven amenorrheic subjects (three dancers and four nondancers) who resumed menses during the study showed an increase in spine and wrist BMD (17%; P < 0.001) without achieving normalization. Delayed menarche was the only variable that predicted stress fractures (P < 0.005), which we used as a measure of bone functional strength. Analysis of dieting and nutritional patterns showed higher incidence of dieting behavior in this group, as manifested by higher Eating Attitudes Test scores (16.3 +/- 2.00 vs. 11.5 +/- 1.45; P < 0.05) and higher fiber intakes (30.7 +/- 3.00 vs. 17.5 +/- 2.01 g/24 h; P < 0.001). We concluded that low bone mass occurs in young women with amenorrhea and delayed menarche, both exercisers and nonexercisers. Crucial bone mass accretion may be compromised by their reproductive and nutritional health.

Adult↗
PubMed1986

Effects of urine from females in oestrus on puberty in female mice.

A series of 9 experiments was conducted to examine various characteristics of the urinary chemosignal found in the urine of oestrous female mice that accelerates the sexual development of conspecific females. This urinary chemosignal was effective in doses as small as 0.001 ml/day, was present in excreted and bladder urine, required 3 days of treatment starting before Day 29 of age to effect an acceleration of puberty, required a minimum daily exposure of 2 h, and was relatively nonvolatile. In addition the chemosignal from oestrous females was effective in summer but not in winter months, was significantly more effective when collected at the middle or end of the dark portion of the daily cycle than at the beginning of the dark phase or middle of the light phase, and was not affected by food deprivation or shortened photoperiod. Simultaneous treatment of test subjects with urine from oestrous females and grouped females resulted in delays in puberty and simultaneous treatment with urine from oestrous females and urine from males or pregnant or lactating females did not result in any enhanced acceleration of puberty.

Age Factors↗
PubMed1987

Constitutional delay of growth and pubertal development: growth hormone secretory pattern and possible therapy.

Constitutional delay of growth and pubertal development is a frequent cause of short stature. These children have a significant retardation of skeletal age and delayed sexual development. They generally maintain a normal growth curve and tend to attain normal adult height. Although children with constitutional delay of growth are believed to have no medical or endocrine abnormality to explain their short stature, some controversy regarding their growth hormone secretory status has recently surfaced; some authors have reported low growth hormone levels to provocative stimuli and decreased growth hormone secretion during sleep, as well as low somatomedin C values in some children with constitutional delay of growth. Others, however, have found the growth hormone secretory status to be normal and similar to that of a control population. The implications of these findings, particularly in regard to possible forms of therapy, are discussed in some detail.

Adolescent↗
PubMed1974

Long-term chelation therapy in thalassaemia major: effect on liver iron concentration, liver histology, and clinical progress.

A prospective trial of continuous chelation therapy in children with homozygous thalassaemia on a high transfusion regimen was started in April 1966. The effect of treatment on iron concentration in the liver and on hepatic histology was examined in 49 biopsy specimens obtained from nine chelator-treated patients and nine control patients between April 1966 and April 1973.Chelation therapy was associated with a significant reduction in liver iron concentration, and by the end of the trial the values for the two groups showed no overlap. A similar difference was seen in the amount of hepatic fibrosis, which showed little or no change in the chelator-treated patients but was progressive in the controls.No major clinical differences were seen, probably because both groups included several older children who were heavily loaded with iron at the start of the trial. Among the younger patients, however, puberty was delayed in four of five controls but in only one of four chelator-treated children. Prepubertal growth rate was significantly greater in the chelator-treated patients than in the controls.

Biopsy↗
PubMed1999

Physiological perspectives on leptin as a regulator of reproduction: role in timing puberty.

How nutrition regulates reproductive activity remains a major unsolved question of reproductive biology. Reducing the level of nutrition during adulthood can lead to infertility, primarily through reduction of GnRH secretion. Inquiry about such a mechanism has its roots in the search for cues timing the onset of fertility, because the tempo of sexual maturation is much more closely associated with body growth than with chronological age. Growth depends on the quantity and quality of food intake. When food availability is low, small, short-lived species with high metabolism and reduced growth may not even attain puberty before they die. In longer-lived species, puberty is delayed for months or even years until more food becomes available. To appreciate fully how the pubertal progression is timed will require understanding how peripheral signals relating information about energy metabolism are sensed by the brain and how such information is routed through pathways controlling GnRH secretion. Here, we provide some background and physiologic perspective on the question of whether the fat-derived hormone leptin is the unique peripheral signal, is an important signal, is but one of a constellation of signals, or is not a signal timing puberty.

Aging↗