Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PUBERTY”

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 811 records · Page 45Linked to original sources

Female precocious puberty, obesity and polycystic-like ovaries.

OBJECTIVE: To evaluate the characteristics of obese girls with gonadotropin releasing hormone-dependent precocious puberty with and without polycystic-like ovaries. METHODS: Forty-seven overweight (> 75(th) centile of the Italian reference data) girls with a diagnosis of isosexual precocious puberty underwent auxological analysis, hormonal assay and utero-ovarian sonographic and Doppler evaluation. On the basis of sonography the patients were subdivided into two groups, girls presenting normal ovaries (Group I; n = 31) and those with polycystic-like ovaries (Group II; n = 16). RESULTS: The mean body weight was significantly higher (P = 0.003) in Group II than it was in Group I. In addition, the patients with polycystic-like ovaries fell within our definition of superobese (> or = 97(th) centile of the Italian reference data) in 44% of cases. The uterine and ovarian volumes were significantly greater in Group II compared with Group I patients. The Doppler evaluation showed intraparenchymal ovarian vascularization and low downstream impedance to flow in all patients in Group II. CONCLUSIONS: Girls with precocious puberty and polycystic ovaries, compared with those without polycystic ovaries, have a higher incidence of body weight exceeding the 85(th) centile of the Italian reference data (obesity).

Child↗

The measurement of puberty: a review.

This paper has two main objectives. Firstly, to review the feasibility and validity of the various methods that have been used to measure puberty. With an appreciation of these measurement issues, the second objective is to summarize the evidence-base as to whether the age at menarche and the age at onset of puberty has decreased in recent years. In consideration of these methodologies, all of which report different levels of reliability and validity, it is only possible at present to draw inferences about possible changes in pubertal age and onset. Moreover, the wide variations in sample size, selection of participants (usually non-random), and study design reported in the reviewed studies have compounded this situation further. The paper closes by providing a summary of the findings which will be of relevance to those intending to critically review the current evidence surrounding age of puberty, as well as those set on carrying out future research into this area.

Adolescent↗

Changes in the characteristics of anaerobic exercise in the upper limb during puberty in boys.

The aim of this study was to examine the relationships between the characteristics of anaerobic exercise in the upper limb and important indicators of growth and developmental age such as height (h), body mass (mb), skeletal age (SA), plasma testosterone (T) and pubertal stage (PS). We used the force-velocity (F-v) relationship test in a population of 66 healthy adolescent male junior jockeys, with considerable variation in these indicators but of the same physical fitness level (training effect). The mean values of the maximal anaerobic power (Wan,max) were 391 (SD 93) W. The values of the variables in the F-v relationship for the upper limb were only slightly or uncorrelated with the chronological age, but highly correlated with h, mb and SA (P < 0.001). The correlation with T was less significant. Using ANOVA a highly significant effect of PS on the variables in the F-v relationship was found (P < 0.001). The absolute or relative (normalized to mb) increase in Wan,max during puberty was greater from PS P2 and P3 than at other stages. Therefore PS would appear to be a significant factor for developmental changes in anaerobic characteristics during puberty in the adolescent. The PS P3 determined only by public hair might be an easy and accurate indicator for sports category classification of adolescents during puberty.

Adolescent↗

Plasma concentrations of vitamin D metabolites during puberty of diabetic children.

Plasma concentrations of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D and vitamin D binding protein were determined in 87 serum samples from 46 Type 1 (insulin-dependent) diabetic children and adolescents at the various stages of puberty. The results were compared with data similarly obtained from healthy pubertal children. The diabetic patients had lower mean 1,25-dihydroxyvitamin D concentrations (p less than 0.05) and higher molar ratios of 24,25-dihydroxyvitamin D to 25-hydroxyvitamin D (p less than 0.05) than their healthy counter parts. In contrast to the reference group, the diabetic patients failed to attain the increase in 1,25-dihydroxyvitamin D normally seen during the pubertal stages of maximal growth velocity. The mean plasma levels of vitamin-D binding protein did not differ between the two groups, and a calculated 'free' 1,25-dihydroxyvitamin D value followed a pattern similar to that of total 1,25-dihydroxyvitamin D throughout puberty for both groups. The results suggest that the regulatory mechanisms of the vitamin D endocrine system are altered in diabetic children at puberty, resulting in a relative decrease in 1,25-dihydroxyvitamin D plasma concentration and increased 24,25-dihydroxyvitamin D levels.

24,25-Dihydroxyvitamin D 3↗

Long-term treatment of central precocious puberty with an intranasal LHRH analogue: control of pituitary function by urinary gonadotropins.

Daily subcutaneous doses of luteinizing hormone-releasing hormone (LHRH) analogues are a well-established therapy for gonadotropin-dependent precocious puberty. Reports on intranasally administered analogues, however, are controversial. We studied the effect of intranasal D-Ser(TBU)6-LHRH(BUS) on growth rate, skeletal maturation, and urinary gonadotropins in five girls and one boy with central precocious puberty (CPP) who had been treated for 1.4-2.3 years (mean 1.9). Because of the potential antifertility effects of LHRH analogues, testicular histology was analysed in the boy. In the five children with accelerated growth, the bone age-related velocity of height gain decreased from 10.58 +/- 2.77 to 5.82 +/- 1.8 cm/year (means +/- SD, P less than 0.01), and the ratio of change in bone age to change in chronological age fell below 1. Basal luteinizing hormone (LH), and LHRH-stimulated LH and follicle stimulating-hormone, at pubertal levels before treatment, decreased significantly in all children, normalizing in four (P less than 0.04). During therapy, pituitary function was best controlled by urinary LH, which correlated with clinical data. After 13 months of therapy, testicular histology showed degenerated Sertoli cells, and absence of B- and Ap-spermatogonia and of primary spermatocytes in the boy. We conclude that: (1) Efficient long-term suppression of central precocious puberty--including accelerated growth and skeletal maturation--can be maintained by intranasal dosage of BUS. (2) Urinary LH reflects pituitary function and proves to be a reliable guide to adjustment of the LHRH-analogue dose regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗

Neuroendocrine mechanisms mediating awakening of the human gonadotropic axis in puberty.

The hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator presides over the pulsatile and feedback-regulated activities of the pituitary-gonadal axis. Awakening of synchronous activity of the GnRH neuronal ensemble in the earliest stages of puberty heralds the onset of full activation of the reproductive axis in girls and boys. Progression from prepuberty to adulthood in boys is directed by marked (30-fold) amplitude enhancement of pulsatile luteinizing hormone (LH) secretion, as assessed by an ultrasensitive immunofluorometric assay and deconvolution analysis. There is a much less apparent rise in LH secretory burst frequency (approximately 1.3-fold increase). Consequently, human puberty is an amplitude-driven neuroendocrine maturational process. However, less is known about pulsatile follicle-stimulating hormone (FSH) release in puberty. Multiple pathophysiologies that result in hypogonadotropic hypogonadism can converge on a final common mechanism of attenuated hypothalamic GnRH pulse generator output and hence reduced LH (and FSH) secretion. Disturbances may take the form of reduced GnRH pulse frequency and/or attenuated GnRH secretory burst mass. When the pathophysiology of hypogonadism originates exclusively in a failed GnRH pulse generator, then either treatment of the primary disease process where possible (e.g., by refeeding in starvation, improved metabolic control in diabetes mellitus, dopamine agonist treatment in hyperprolactinemia, etc) and/or treatment with pulsatile GnRH (e.g., in Kallmann's syndrome, isolated hypothalamic lesions, etc.) can provide relevant therapeutic options in children and adults.

Adolescent↗

Hypomelanosis of Ito and precocious puberty.

We describe two girls with hypomelanosis of Ito, one of whom was demonstrated to have diploid-triploid mixoploidy in skin fibroblasts. Both had precocious puberty which was probably gonadotrophin-independent. The association of precocious puberty and hypomelanosis of Ito has not been previously reported. We have speculated on the possible mechanism of gonadotrophin-independent precocious puberty.

Child↗

Reduction of bone density: an effect of gonadotropin releasing hormone analogue treatment in central precocious puberty.

Gonadal steroids drive the significant bone mineral increase that occurs at puberty. Oestrogen deprivation in women results in bone loss. We investigated bone mineralization by single photon absorptiometry in girls with central precocious puberty (n = 13, age 3.8-8.5 years) before and during 1 year of treatment with gonadotropin releasing hormone analogue (GnRH-a = long-acting D-Trp6-GnRH, 60 micrograms i.m. every 28 days). Before GnRH-a therapy, bone mineral density (BMD) was significantly higher in patients than in ten control girls matched for chronological age (patients 0.575 +/- 0.097 g/cm2, controls 0.433 +/- 0.049 g/cm2, P < 0.001). Patient BMD was not significantly different from that of ten control girls matched according to patient bone, age (0.550 +/- 0.046 g/cm2, P = NS). During GnRH-a treatment, pituitary-gonadal axis was suppressed and patient BMD significantly decreased (6 months: -6.0%, P < 0.002 vs baseline; 12 months: -8.0%, P < 0.001 vs baseline). We conclude that in girls with precocious puberty the activation of gonadal steroid secretion induces an increase in bone mineralization and that oestrogen deprivation by GnRH-a treatment caused a significant decrease in BMD.

Absorptiometry, Photon↗

Final height in girls with untreated constitutional delay in growth and puberty.

During a 10-year period, 23 girls compared to 118 boys presented with constitutional delay in growth and puberty. Of these girls, 15 were followed to final height to determine the outcome of the untreated condition in terms of both growth and psychological well-being. At presentation chronological age was 13.2 (1.7) years [mean (S.D.)], bone age delay 2.7 (0.9) years, standing height standard deviation score (SDS) -3.4 (0.9), and predicted adult height (PAH) SDS -1.3 (0.7) (Tanner-Whitehouse II method). Final height SDS was -1.5 (0.8) measured at 18.9 (2.6) years of age. Mean age at menarche was 15.6 (0.9) years. There was no significant difference between final adult height (FH) and PAH but there was a significant difference between FH and target height (P less than 0.001). Psychological questionnaires revealed no significant difference in self-esteem, marital or employment status between the patient and control groups. There was no significant correlation between self-esteem and FH but 80% felt their growth delay had affected success either at school, work or socially. Of the patients, 50% would have preferred treatment to advance their growth spurt. This study demonstrates that girls with constitutional delay in growth and puberty reached their PAH, although this was lower than the midparental heights. The girls also experienced significant distress due to delayed growth and puberty and treatment to advance growth should be considered more frequently.

Adolescent↗

Growth and puberty in a fostered kindred.

A kindred of four children of different ages was at the same time adopted and transferred from a very poor to a fairly good environment. A rapid catch-up growth was observed in all four during the first 2 years after adoption. Beyond the 2nd year, physical development varied according to age, sex, and the rhythm of sexual maturation. Puberty was not advanced. Final height depended mainly on the height at the onset of puberty. The homogeneity of this familial story can contribute to a better understanding of the age-related interactions between the nutritional and environmental conditions and the genetic factors in human development. The growth and puberty of children coming from poor areas of the world to be fostered in families living in industrialized countries may shed some light on the role of nutritional and environmental factors in human development.

Adoption↗

Bone turnover in male puberty: a longitudinal study.

In a longitudinal study of male puberty, 18 boys were examined every 3 months for at least 2 years. Serum bone Gla protein (BGP), a biochemical marker of bone formation, was determined and related to changes in serum testosterone (T), serum alkaline phosphatase (AP), serum calcitonin, and bone mineral content (BMC). The data demonstrate a steep increase in serum T during puberty (P less than 0.001), with an almost concomitant increase in serum BGP (P less than 0.001) and serum AP (P less than 0.001). Ten months after the maximal increase in serum T, the increase in BMC reached its maximum, whereas there was no significant change in the serum calcitonin. The data demonstrate that the steep increase in serum T during puberty, directly or indirectly, produces acute stimulation of bone formation (estimated from BGP and AP) followed by a highly significant increase in the integrated measurement of bone apposition (BMC).

Alkaline Phosphatase↗

Precocious puberty.

Puberty occurring before the age of 8 years in girls and 9 years in boys in considered precocious. The numerous causes of precocity can be classified as central or peripheral. Central or true precocious puberty (CPP) is due to premature activation of the hypothalamopituitary-gonadal axis and is isosexual. Peripheral or pseudoprecocious puberty (PPP) results from the production of sex steroids independent of the H-P-G axis and may be isosexual or heterosexual. CPP is the most common form of precocity involving more than 50% of children and is much more common in girls than boys. CPP is more common between 4 and 8 years. A peak serum LH levels > 10 iu/l following GnRH stimulation is the absolute evidence of CPP. Serum IGF-I levels are predictive of the outcome. Availability of CT and MRI has helped to determine the cause of CPP in most cases. Hypothalamic hamartoma is the most common tumour causing CPP especially in boys. Adrenal causes, particularly CAH, are the commonest cause of PPP in boys whereas ovarian causes are more likely in girls. Long acting GnRH analogues provide a safe and effective form of treatment of CPP.

Child↗

Final height in a patient with Laron syndrome after long-term therapy with rhlGF-I and short-term therapy with LHRH-analogue and oxandrolone during puberty.

OBJECTIVE: To report our experience on long-term treatment with recombinant-human-IGF-I (rhIGF-I) of a female patient with Laron syndrome (mutation G223G in the GH receptor gene), who received short-term treatment (1 yr) with LHRH analogue at the start of puberty and subsequently with oxandrolone. CASE REPORT: The patient started IGF-I therapy (dose 40 microg/kg bid for 9 months, 80 microg/kg bid until 13.7 yr of age and 120 microg/kg bid thereafter) when she was 7.6 yr old (height -6 sds), and was treated for 9.4 yr until final height (cm 129.7; -5.5 sds). At first signs of puberty (age 12.7 yr; height 116.3; -5.3 sds), LHRH analogue was started (3.75 mg/28 days) and bone age progressed by 6 months in the 12-month period. Growth velocity decreased in the 6-12th month of combined treatment (0.9 cm/6 months), and treatment was suspended. At age 14.8 (height 124.5; -6.6 sds), oxandrolone was added (0.1 mg/kg/day), but after 12 months (height 128 cm; -5.7 sds) bone age increased from 11.5 to 13.5 yr and the drug was stopped. No side effects occurred during the various treatments. Body segments progressed harmonically: there was a tendency towards improvement in the upper to lower body segment ratio and in cranial growth. Only biiliac diameter did not increase during LHRH treatment. During the 9-yr period, body mass index (BMI), subscapular and triceps skinfold centiles did not show any significant variations. CONCLUSIONS: Our patient with Laron syndrome after long-term treatment showed a final result below the initial expectations, confirming that IGF-I used with the present schedule is less effective than GH in GH-deficient patients. LHRH analogue therapy at puberty was associated with a slower bone age maturation but with an almost complete arrest of growth. On the contrary, oxandrolone sustained growth but caused an excessive maturation of bone age. Other strategies are necessary to improve final height in these patients.

Age Determination by Skeleton↗

Spontaneous growth hormone and somatomedin-C/insulin-like growth factor-I secretion in obese subjects during puberty.

It has been reported that adult obese subjects present a reduced growth hormone secretion. As no data are available in the pubertal period, which is characterized in lean subjects by an increased spontaneous growth hormone secretion, the growth hormone circadian concentration was studied in a group of 18 obese male subjects in different pubertal stages, and compared to 26 age-matched control subjects. The data observed evidenced no statistically relevant differences regarding LH and FSH circadian secretion and morning testosterone concentration. On the contrary a statistically significant (p less than 0.02) difference in growth hormone 24 h integrated concentration was evident, particularly in prepubertal subjects; the sleep-related peak was evident in 28% of obese subjects and in 85% of controls. Sm-C/IGF-I concentration was similar to the concentration observed in controls in the prepubertal stage, but did not show the expected increase in the late puberty. Auxological data, performed on a sample of 80 subjects, showed both advanced height and bone age at beginning of puberty, and a trend toward a reduction of percentile for height in parallel with the pubertal maturation, suggesting that pubertal growth spurt in obese subjects is at least less pronounced than in lean subjects. It is concluded that GH and Sm-C/IGF-I secretion is impaired during puberty in obese subjects, leading to a reduced growth rate, while in the prepubertal period factors other than GH may replace or even potentiate its action.

Adolescent↗

Gender differences in the ratio between humerus width and length are established prior to puberty.

SUMMARY: On a sample of 1,317 children aged 9.9 years we developed a novel method of measuring humeral dimensions from total body dual-energy X-ray absorptiometry (DXA) scans and showed that gender differences in the ratio between humeral width and length are established prior to puberty. INTRODUCTION: It is recognised that long bone cross-sectional area is greater in males compared to females, which is thought to reflect more rapid periosteal bone growth in boys. However, it is currently unclear whether these findings reflect gender differences in bone size or shape. In the present study, we investigated whether gender differences exist in the balance between longitudinal and periosteal long bone growth in children, leading to gender differences in bone shape, based on a novel method for evaluating shape of the humerus. We also examined whether these differences are established prior to puberty. METHODS: Length, area and width of the humerus were estimated from total body DXA scans in 1,317 children aged 9.9 +/- 0.33 years, who had participated in a nested case-control study of fractures within the Avon Longitudinal Study of Parents and Children (ALSPAC) (a geographically based birth cohort based in South West England). No differences were observed with respect to parameters of humeral geometry according to fracture history, and so both groups were pooled for further analysis. Aspect ratio (AR) of the humerus was calculated as humeral width divided by length. Total body height and weight were measured at the same time as the DXA scan. Puberty was assessed using self-completion questionnaires. RESULTS: Humeral width and length were positively associated with age and height in boys and girls combined (P<0.001), and with Tanner stage in girls (P<0.002). In contrast, age, height and Tanner stage were not related to humeral AR. We then examined gender differences in humeral shape according to pubertal stage. In prepubertal children (i.e. Tanner stage 1), humeral length was similar in boys and girls, but width (1.92 vs 1.88 cm, P<0.001) and area (47.7 vs 46.9 cm(2), P<0.001) were greater in boys, resulting in a greater AR (7.78 vs 7.53, P<0.001). Similar gender differences were observed in early pubertal children (i.e. Tanner stage 2). CONCLUSION: We conclude that the greater periosteal diameter of boys compared to girls reflects differences in the balance between longitudinal and periosteal bone growth. Interestingly, resulting gender differences in humeral AR are established in prepubertal children.

Absorptiometry, Photon↗

Quantitative calcaneal ultrasound parameters and bone mineral density at final height in girls treated with depot gonadotrophin-releasing hormone agonist for central precocious puberty or idiopathic short stature.

UNLABELLED: To evaluate the effect of gonadotrophin-releasing hormone (GnRH) agonist treatment on bone quality at final height, we studied girls with central precocious puberty (CPP) and with idiopathic short stature (ISS). A total of 25 Caucasian girls were included: group A (n=14) with idiopathic CPP (mean age at start 7.4 years) and group B (n=11) with ISS (mean age at start 11.7 years). Treatment duration was 3.8 and 1.7 years respectively. The quantitative ultrasound parameters (QUS) broadband ultrasound attenuation (BUA) and speed of sound (SOS) were measured at the calcaneus (UBIS 3000 device). Lumbar spine bone mineral density (BMD; L2-L4) was measured by dual energy X-ray absorptiometry (DXA) (Hologic QDR1000). Measurements were performed at final height and expressed as Z-scores corrected for bone age. Mean Z-scores of QUS parameters, areal BMD and volumetric BMD (BMDvol) were above -1 in both groups (group A: BUA Z-score -0.21, SOS Z-score -0.29, BMD Z-score 0.02, BMDvol Z-score 0.05, group B: BUA Z-score -0.93, SOS Z-score -0.40, BMD Z-score -0.86, BMDvol Z-score -0.68), although mean Z-scores of BUA and areal BMD in group B were significantly different from zero (P=0.03 and P=0.02 respectively). Mean Z-score BMDvol was not significantly different from zero (P=0.05), we found no significant difference between the groups for BMDvol (P=0.13). CONCLUSION: Although quantitative ultrasound parameters parameters and bone mineral density were normal in girls with central precocious puberty at final height after gonadotrophin-releasing hormone agonist treatment, mean Z-score for broadband ultrasound attenuation and areal bone mineral density were significantly different from zero and mean Z-score for volumetric bone mineral density was (just) not significantly different from zero in idiopathic short stature girls with normal puberty treated with gonadotrophin-releasing hormone agonists. Therefore we cannot say that this treatment is safe in these girls with regard to bone health.

Absorptiometry, Photon↗

Obese Japanese children have low bone mineral density after puberty.

The purpose of this study was to determine the relationship between BMD and childhood obesity. We examined 1070 obese children (722 boys and 348 girls) aged 7 to 15 years. Their mean relative weight, as a percentage of the standard weight for age, height, and sex, was 152.9 +/- 14%. BMD was assessed, by a digital image processing method, in the second metacarpal bone of the left hand. We compared our results with those of healthy nonobese Japanese children based on both chronological and bone age. Mean BMD values for bone age in the obese children were significantly higher than those in control groups in boys aged 11 years and under and girls 9 years and under. On the other hand, in boys over 12 years old, BMD values for bone age were lower than those in the control groups. In girls over 11 years old, BMD values tended to be lower than those in the control groups. In conclusion, we studied the BMD of obese children from the point of view of advanced bone age. Our results showed that BMD was higher than in prepubertal obese children, but a low BMD value was found after puberty, due to poor gain of BMD during puberty. It is important to prevent obesity in childhood in order to prevent the low BMD after puberty.

Adolescent↗

Early psychopathological signs in bulimia nervosa. A retrospective comparison of the period of puberty in bulimic and control girls.

While bulimia nervosa (BN) typically begins in girls during late adolescence, puberty and associated developmental changes have been linked to negative body image and onset of a variety of psychological problems. This study aimed to identify early psychopathological signs, which could have marked the period of puberty in subjects whom later developed BN. In a case control study, we compared 49 girls with BN according to DSM-IV, aged between 18 and 20 years, to 49 girls of the same age, who were free of any past or current psychiatric diagnosis. Psychiatrists or clinical psychologists, using a semi-structured clinical interview including retrospective assessment of the emotional and behavioural changes that had occurred in puberty evaluated both groups. Before the onset of a clinical eating disorder, the subjects with BN presented significantly more often than controls weight related concerns, attitudes of withdrawal and social isolation, and negative changes in their body image and self-image, as well as in their relationships with siblings and peers. The results suggest that early psychological distress precedes the onset of an eating disorder in many cases, and that prevention efforts should be directed towards peripubertal psychopathology.

Adolescent↗