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PubMed1988

Basal and stimulated insulin levels rise with advancing puberty.

We studied the effect of pubertal development on insulin secretion. Intravenous glucose tolerance tests were performed on 47 islet-cell antibody negative siblings of diabetic children and on 16 normal adults. Puberty was staged using Tanner's criteria and subjects were grouped as follows: I, stage 1 (n = 16); II, stages 2 and 3 (n = 15); III, stages 4 and 5 (n = 16); IV, adults (n = 16). Fasting insulin increased with advancing puberty (p = 0.59, P less than 0.001). The stimulated insulin response also rose with increasing pubertal development: for the 0-10 min insulin area, p = 0.46, P less than 0.001 and for the 10-60 min area, p = 0.68, P less than 0.001. There was a low positive correlation between insulin and age to 16 years but multiple regression analysis showed that this could be accounted for by puberty alone. Indeed prepubertal children and adults did not differ. There was no correlation between glucose (fasting and 0-60 min area) and puberty or age. These findings suggest that insulin resistance increases during puberty, and this may contribute to the frequency of presentation or worsening control of insulin dependent diabetes at this time.

Adolescent↗
PubMed1997

A comparison of patients with premature thelarche and idiopathic true precocious puberty in the initial stage of illness.

A comparative study of patients with premature thelarche and patients with idiopathic true precocious puberty was conducted. The age at the first visit tended to be lower for those with precocious puberty. In comparison with normative data for children, the frequency of low birthweight and small for date (SFD) status was greater in the 55 patients with premature thelarche, but SFD was also frequent in the 18 patients with precocious puberty. The height, weight and Kaup's index were all within the normal range for these two groups. The ratios for bone age/chronologic age and bone age/height age tended to be high in both groups. In the patients with premature thelarche, the blood luteinizing hormone (LH) level showed a normal response, and the blood follicle stimulating hormone (FSH) level a hyper-response, to stimulation with luteinizing hormone-releasing hormone (LH-RH). In contrast, both the blood LH and FSH levels showed a normal response to LH-RH stimulation in most of the patients with precocious puberty, and a hyper-response was rare among them. Although the blood estradiol (E2) level was higher in patients with precocious puberty than in those with premature thelarche, about 50% and 90% of the patients in the respective groups had normal levels. These results suggest that normal responses of blood LH and excessive responses of blood FSH to LH-RH loading may be useful in some patients for diagnosing premature thelarche at an early stage.

Age Determination by Skeleton↗
PubMed1992

Minor neurological dysfunction from birth to 12 years. II: Puberty is related to decreased dysfunction.

To determine whether puberty is related to decreased minor neurological dysfunction (MND), 174 children from the Groningen Perinatal Project who had had MND at nine years were re-examined at 12 years. No signs of MND could be demonstrated in 39 of the children, 33 of whom showed at least three signs of puberty. The presence of minor physical anomalies was associated with persisting MND. The authors hypothesise that puberty is related to a decrease in MND, and discuss the role of hormonal changes in relation to the decrease in minor signs. Re-examination at 14 years will be necessary to confirm this hypothesis, since 68 per cent of the children had not yet reached puberty. Children with MND reached puberty no later than those without.

Adolescent↗
PubMed1994

Variations in pituitary-gonadal suppression during intranasal buserelin and intramuscular depot-triptorelin therapy for central precocious puberty. Belgian Study Group for Pediatric Endocrinology.

This study evaluated pubertal development, growth and pituitary-gonadal suppression in 21 patients with central precocious puberty treated with buserelin intranasally and switched after a mean of 2.1 yr to depot-triptorelin given im for 1 year. Arrest or regression of puberty was observed in 12 patients while progression of puberty during therapy was seen in 9 patients (6 on buserelin, 2 on triptorelin and 1 on both therapies). The increment in serum LH and FSH concentrations after sc injection of short-acting triptorelin was greater on buserelin than on triptorelin therapy, particularly in patients with evidence of progression of puberty. Height velocity during therapy showed a reduction which paralleled the decelerating phase of the normal pubertal growth spurt. The rate of bone maturation during therapy was inversely related to pretreatment bone age. Predicted final height showed marked individual variations which were inversely related to predicted adult height before therapy. These data indicate that differences in the nature and route of administration of Gn-RH agonist therapy for central precocious puberty can be of importance for inhibition of pituitary gonadotropin secretion and development of secondary sex characteristics. Height velocity and bone maturation are age-related and the change in predicted adult height depends on pretreatment level.

Administration, Intranasal↗
PubMed1999

Effect of growth hormone (GH) during puberty in GH-deficient children: preliminary results from an ongoing randomized trial with different dose regimens.

This paper reports results from an ongoing, randomized, multicentre national trial. The aim is to elucidate whether a dose of growth hormone (GH) of 0.2 IU/kg (0.07 mg/kg), given either as once-daily or twice-daily injections during puberty, is more effective than a once-daily dose of 0.1 IU/kg/day (0.03 mg/kg/day) in improving final height in children with GH deficiency (GHD). The twice-daily regimen comes closer to the spontaneous GH secretion pattern in puberty. Ninety-two children with GHD who had been receiving GH therapy for at least 1 year, and with spontaneous puberty or who were prepubertal and due to be started on replacement therapy to induce puberty, were randomly assigned to receive GH as follows: group A, 0.1 IU/kg/day (0.03 mg/kg/day), administered once daily; group B, 0.2 IU/kg/day (0.07 mg/kg/day), administered once daily; and group C, 0.2 IU/kg/day (0.07 mg/kg/day), divided into two equal injections given at 12-hour intervals. Pubertal height gain was 0.7, 0.7 and 1.3 SDS for groups A, B and C, respectively. The gain in height during puberty was thus most marked in group C. Mean final height, when corrected for parental height, was between 0 and 1 SDS in all treatment groups. All but seven children reached a final height within +/- 2 SD of the general population. There was a wide range of final heights in all three treatment groups. This variation in response suggests the need to individualize treatment in order to achieve an appropriate final height for most individuals.

Adolescent↗
PubMed1987

Precocious and premature puberty associated with treatment of acute lymphoblastic leukaemia.

Early puberty in 28 children (23 girls, five boys) treated for acute lymphoblastic leukaemia (ALL) at a mean age of 4.0 years (range 1.4-7.8) is described. All but one had received prophylactic cranial irradiation (1800-2400 cGy) and three children had received additional cranial or craniospinal irradiation as treatment for relapse of their leukaemia. Mean age for the onset of puberty was 8.8 (SD 0.8) years in the girls and 9.3 (0.8) years in the boys; this is greater than two standard deviations from the mean for normal girls and boys. Five children (three girls, two boys) had precocious puberty. The onset of puberty occurred at greater than two standard deviations from the mean for normal girls and boys in 14(13%) girls and 4(3%) boys treated at less than eight years of age between 1970 and 1985. In a group of 55 girls treated for ALL who had survived in first remission for six years or more from diagnosis, there was a relation between young age at onset of treatment and early menarche. We suggest that premature activation of the hypothalamic-pituitary-gonadal axis occurs as a consequence of hypothalamic dysfunction due to cranial irradiation. Precocious and premature puberty in children treated for ALL may be an important factor in contributing to short stature.

Age Factors↗
PubMed1993

Spermaturia and puberty.

The pattern of spermaturia in boys at different stages of puberty was investigated. Fractionated 24 hour urine was collected for nine consecutive days from eight boys aged 13-14 years and 10 boys aged 15-17 years. Spermatozoa were detected by microscopic examination of the sediment. Sex characteristics were recorded. Fifty five per cent of all urine samples were positive for sperm and all boys showed spermaturia. A large variation in spermaturia was found between and within boys at the same stage of puberty. Spermaturia was a more common and regular event during early and mid-puberty than in more mature subjects. This indicates that the mechanism of spermaturia in early and late puberty could be different. It is suggested that spermaturia in non-virilised boys could be a result of a spontaneous, continuous flow of spermatozoa to the urethra in contrast with the peristaltic flow during ejaculation occurring at a later stage of puberty.

Adolescent↗
PubMed1995

Growth and puberty after growth hormone treatment after irradiation for brain tumours.

The impact of treatment with either cranial or craniospinal irradiation with or without cytotoxic chemotherapy for a brain tumour distant from the hypothalamic-pituitary axis was assessed in 29 children who had reached final height. All had received growth hormone treatment for radiation induced growth hormone deficiency. Final height, segmental growth during puberty, and duration of puberty were studied. Both craniospinal irradiation and the use of chemotherapy resulted in a significant and equal reduction in final height; this effect in those children who received both craniospinal irradiation and chemotherapy was additive. The degree of height loss was related to the age at irradiation, the most profound effect on final height occurring in the youngest at irradiation. The mean duration of puberty from G2-G4/B2-B4 (1.97 years) was not significantly different from the duration of puberty in normal children. Growth hormone increases growth velocity in children with radiation induced growth hormone deficiency but their final height is significantly less than their mid-parental height. The use of spinal irradiation and chemotherapy in the original treatment of brain tumours has a marked effect on growth which is not overcome with the use of growth hormone treatment in current doses. Early puberty of normal duration contributes to poor growth.

Adolescent↗
PubMed1996

Increased perinatal intracranial pressure and prediction of early puberty in girls with myelomeningocele.

An increased risk of developing precocious puberty has been reported in children with myelomeningocele. In order to evaluate this further and to study factors associated with early or precocious puberty the medical records of all girls with myelomeningocele, born from 1970 onwards (n = 64), who were admitted to our unit were reviewed. Early/precocious puberty (E/PP) was defined as breast development or pubic hair corresponding to Tanner stage 2 before the age of 9.2 years. In 32 out of 62 cases data were sufficient for evaluation of the timing of puberty. Twenty girls had E/PP and 12 girls normal timing of puberty. In the girls who had reached the age of 9.2 years the incidence of E/PP was at least 52%. Girls with E/PP had a higher incidence of hydrocephalus, were treated with intraventricular shunts more often, and had significantly higher frequency of increased intracranial pressure during the perinatal period (p < 0.05, p < 0.01, and p < 0.001, respectively). The group of girls developing E/PP was also more severely disabled with respect to motor and urological function and had more shunt revisions. In conclusion, E/PP in girls with myelomeningocele is strongly associated with increased intracranial pressure particularly during the perinatal period.

Child↗
PubMed1998

Management of recombinant human growth hormone therapy at puberty.

Treatment modalities for growth hormone (GH) substitution in GH-deficient children at puberty is still a matter of debate. Although circulating GH levels increase during puberty, it has not been proven that the increase of exogenous GH is necessary for a normal pubertal growth spurt. Increasing GH levels may thus well be the consequence and not the cause of the pubertal growth spurt. A permissive role of GH for pubertal growth has been hypothesized. Some effects of exogenous GH may even be detrimental to pubertal growth; specifically, puberty seems to be shortened by GH administration. Further aspects of the physiology of GH secretion and the poor imitation by current replacement schemes are discussed. Only randomized, prospective studies will allow to define the optimal dose of GH at puberty. As long as these studies are missing, a pragmatic approach is an individualized, minimalistic GH substitution scheme under close surveillance. GH dose at puberty should be kept at prepubertal levels, but must be increased once height velocity drops below the 50th percentile. This widely used approach ensures unnecessary, costly and potentially harmful overdosages of GH.

Animals↗
PubMed2003

Dose effects of growth hormone during puberty.

During puberty, the production rate of growth hormone (GH) doubles and is associated with an increase in growth velocity. A significant percentage of the final adult height is attained during puberty, then after puberty, the production rate of GH decreases with age. In children with GH deficiency, it is known that the dosage of GH, in addition to the duration of treatment, can greatly influence the final adult height. At present, the dosage of GH given to children of short stature is kept at a constant rate throughout puberty. Thus, a study was conducted to investigate the effects of a higher dose of GH given to GH-deficient children during puberty. In this article, the design and results of the investigation and the importance of the findings will be discussed.

Adolescent↗
PubMed2003

Ascertainment and treatment of delayed puberty.

The majority of patients with pubertal delay, can be classified as having primary pubertal delay (constitutional delay of growth and puberty, CDGP), although any child with a chronic disease could present with delayed puberty. In contrast, children with hypogonadism, either hyper- or hypogonadotropic, exhibit a total absence of pubertal development. Hence, early evaluation of these patients should be performed. Delay of puberty leads to psychological problems, secondary to short stature and/or delay in the acquisition of secondary sex characteristics and the reduction of bone mass. Although the final height in patients with CDGP is usually normal, some of these patients do not reach the third percentile or remain in the lowest part of the growth chart according to familial height. The most common reason for treating CDGP patients, usually with sex steroids, is for psychological difficulties and for loss of bone mineralization. Treatment must be individualized. Therapeutic options and new drugs will be discussed. Appropriate treatment and adequate nutritional intake are indicated in patients with delayed puberty due to chronic illness. In patients with hypo- or hypergonadotropic hypogonadism, puberty must be induced or completed. Different treatments (GnRH analogues, gonadotropins and sex steroids), and the main objectives are discussed.

Adolescent↗
PubMed2005

Puberty and fertility in congenital adrenal hyperplasia.

Congenital adrenal hyperplasia (CAH) is a disorder of adrenal steroid synthesis. The symptoms and signs of CAH depend on the degree of enzyme deficiency; severe salt-wasting (SW) form, less severe simple virilizing (SV) form and mild nonclassic (NC) form. In this paper, puberty and fertility in CAH are discussed. The time of onset of puberty and progress of pubertal development is quite normal, except in NC patients (earlier). Also the age of menarche in CAH girls is normal, but it can depend on the level of therapeutic control. In prepuberty, bone age is advanced. In puberty, peak height velocity is normal but occurs at a younger age and can therefore be considered to be low (compared to healthy early maturers). In puberty there seems to be an increased sensitivity for glucocorticoids leading to growth inhibition. All three above factors can play a role in reducing adult height. Subfertility is frequently found in both female and male CAH patients. In females, the pregnancy rate depends on the severity of 21-hydroxylase deficiency (SW<SV<NC). Adrenal progestagens and androgens are the main cause of disturbed ovarian activity. In addition psychosexual problems (e.g. as a result of genital surgery) are an important factor. In males, the main cause of subfertiltiy is the presence of testicular adrenal rest tumors, which are thought to originate from aberrant adrenal tissue and respond to treatment with glucocorticoids. Although in general fertility is not a paediatric item, in CAH most fertility problems have their origins in childhood years. Therefore prevention of subfertility has to be implemented as a treatment goal in paediatric endocrinology from the start of puberty.

Adolescent↗
PubMed2006

Voice complaints, risk factors for voice problems and history of voice problems in relation to puberty in female student teachers.

The aim of the study was to estimate voice complaints, risk factors for voice complaints and history of voice problems in student teachers before they embarked on their professional teaching career. A cross-sectional questionnaire survey was performed among female student teachers. The response rate was 72% and 457 questionnaires were analyzed. Voice complaints at the moment and/or during the past year were reported by 39.6% subjects. Subjects with voice complaints had significantly higher VHI scores than subjects without voice complaints. In comparison to subjects without voice complaints, overall, subjects with voice complaints reported more frequently that vocal loading factors, physical factors, environmental factors and psychological factors had a negative influence on their voice. Subjects with voice complaints reported more frequently a history of voice complaints during puberty and before puberty in comparison to subjects without voice complaints. Voice complaints in student teachers apparently had a multifactorial genesis and with roots during puberty or before puberty. Logistic regression analysis revealed that intensive voice use, emotions and history of voice complaints during puberty were the most discriminating set of risk factors for voice complaints. Subjects with voice complaints in comparison to those without voice complaints reported more frequently that they would develop a voice problem due to future teaching and that future teaching would have a negative influence on their voice. Around three quarters of subjects with and without voice complaints reported that attention paid to their voice during their training was sufficient. However, subjects with voice complaints were observed to report the need for a refresher course on voice use more frequently than those without voice complaints. The findings call for more intensive voice training for student teachers to cope with the vocal, physical and psychological demands of the teaching profession. Authorities should take responsibility to monitor and improve working conditions of student teachers and teachers.

Adolescent↗
PubMed1986

Two possible mechanisms for precocious puberty induced in female rats by pituitary grafts.

Many reports indicate that prolactin has a role in puberty occurrence. The present study was developed to evaluate the action of pituitary grafts on puberty. Female rats grafted on day 21 with "adult' (90 days old) or "young' (21 days old) pituitaries showed precocious vaginal opening and first estrus. The puberty advancement induced by "adult' transplants was due to an increase in plasma prolactin values and can be blocked by bromocriptine treatment. The puberty advancement induced by "young' transplants was not associated with increased prolactin levels and cannot be blocked by bromocriptine. These results suggest the existence of two possible mechanisms in precocious puberty induced by pituitary grafts: a prolactin-dependent one and another one not directly related with prolactin.

Adrenal Glands↗
PubMed1988

Precocious or early puberty and growth failure in girls treated for acute lymphoblastic leukaemia.

We have studied 41 children with early or precocious puberty who have been treated for acute lymphoblastic leukaemia with prophylactic cranial irradiation (1,800-2,400 cGy) accompanied by intrathecal methotrexate and systemic chemotherapy. Mean age at radiotherapy was 3.9 years (range 1.7-7.7) in the girls and 4.8 years (range 2.6-7.8) in the boys. Mean age at the onset of puberty was 8.6 years (range 6.7-9.7) in the girls and 9.3 years (range 7.8-10.3) in the boys. Of the 41 children with early puberty (greater than 1.4 SD from the mean) 36 were females and 5 were males. 21 of the 36 girls had an absent or inadequate growth acceleration of puberty. 7 of 12 girls who had a pharmacological test of growth hormone (GH) secretion had GH insufficiency (peak level less than 20 mU/l). Early or precocious puberty combined with GH insufficiency may produce severe growth failure and we have used a treatment regimen of a gonadotrophin-releasing hormone analogue, in order to reduce the rate of epiphyseal maturation, combined with biosynthetic GH to increase or sustain growth rate. We have treated 4 girls in this manner. During a mean treatment period of 0.86 years, height SDS for bone age rose from a mean of -1.06 to -0.59. Longer treatment periods will be required to assess the effect on final height.

Child↗
PubMed1988

Time-related neuroendocrine manifestations of puberty: a combined clinical and experimental approach extracted from the 4th Belgian Endocrine Society lecture.

The neuroendocrine manifestations of puberty converge on changes in GnRH secretion. Their appraisal through the assay of GnRH-like material in 24-hour urine extracts shows an increased excretion of this material in the late prepubertal period. The most striking pubertal changes in GnRH secretion occur on a circadian and ultradian basis. In man, they can be evaluated only indirectly. The circadian variations in LH and FSH secretion characteristic of puberty may be observed in timed fractions of 24-hour urine with some delay when compared to the variations of plasma levels. Studies on the frequency of pulsatile LH secretion and during chronic intermittent administration of GnRH support the existence of an increased frequency of GnRH secretory episodes at puberty. LH response to synthetic GnRH is directly related to the frequency of stimulation by endogenous GnRH pulses and provides a very useful index of neuroendocrine maturation in patients with delayed or precocious puberty. A direct evaluation of pulsatile GnRH secretion is possible using the rat hypothalamus in vitro. In these experimental conditions, the frequency of pulsatile GnRH release increases during very early stages of sexual maturation in the male rat. GnRH itself and beta-endorphin are inhibitory regulators of GnRH secretion in vitro and may participate in the mechanisms restraining the pulse-generating machinery in the hypothalamus before puberty.

Circadian Rhythm↗
PubMed1994

Gonadotropin regulation during puberty in complete androgen insensitivity syndrome with testicles in situ.

This paper describes the time course of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels in two patients with the complete androgen insensitivity syndrome (AIS) during puberty and adolescence prior to gonadectomy. In early puberty, LH values were comparable to normal male as well as female standards. At the age of 17 and 18.7 years, respectively, a sudden rise in LH occurred just after the start of estradiol supplementation. These high LH concentrations in the late puberty of our patients are comparable to the values found during early puberty in castrated individuals and children with gonadal dysgenesis. In contrast, FSH concentrations continuously showed levels in the normal male or female range with no rise during adolescence. The sudden increase of LH in late puberty is most probably due to defective testosterone receptors in the pituitary/hypothalamus which apparently can no longer be suppressed by rising testosterone levels and an escape from the negative estradiol feedback. The role of estradiol supplementation might be incidental and further investigation into its role is needed. In contrast to the elevated levels of FSH in patients with defective spermatogenesis, FSH is normal in our patients with AIS and testes in situ. This indicates that FSH secretion is regulated by a combined action of estradiol and gonadal hormones like inhibin.

Adolescent↗