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PubMed1998

Bone mineral status in prepubertal children with constitutional delay of growth and puberty.

OBJECTIVE: We wished to clarify whether the osteopenia reported in adult men with a history of constitutional delay of growth and puberty (CDGP) could be due to the delayed puberty or an independent predisposition to osteoporosis in this condition. DESIGN: Short prepubertal children with CDGP and children with familial short stature (FSS) were matched for height and other auxological variables. The FSS children served as a control group. METHODS: We measured spinal (L1-L4) bone mineral content (BMC) and bone mineral density (BMD) by dual energy X-ray absorptiometry (Hologic QDR 1000/w) in 56 children aged 5-11 years. All children had height below the 10th percentile for chronological age (CA), and bone age (BA) less than 10 years, 29 of them with clinical diagnosis of possible CDGP and 27 of them with FSS. The BMD standard deviation scores (SDS) relative to the values for normal height children were obtained. RESULTS: The mean (+/-S.D.) spinal BMD was significantly lower in the children with CDGP than in the FSS group (0.534+/-0.059 vs 0.623+/-0.060 g/cm2, P< 0.001). Both groups had negative mean lumbar BMD SDS, but in the CDGP group it was significantly lower than in the FSS group as well when the SDS was based on the CA (-1.41+/-0.61 vs -0.38+/-0.51, P< 0.001) and when it was related to BA (-0.78+/-0.64 vs -0.17+/-0.52, P< 0.01). BMC was significantly lower in the CDGP than in the FSS group, when multiple regression analysis was performed by using scanned bone area, body weight and height, sex and BA as independent variables (P = 0.0005). CONCLUSION: The finding of decreased mineralization in prepubertal children with CDGP before the age of puberty suggests that they may have an inherent predisposition to osteopenia.

Absorptiometry, Photon↗
PubMed1979

Neuroendocrine effects of haloperidol in an adolescent with Gilles de la Tourette's disease and delayed onset of puberty.

The effects of haloperidol on the release of prolactin, growth hormone, and luteinizing hormone during sleep were studied in an adolescent male who had Gilles de la Tourette's disease and delayed onset of puberty. At doses of 5 and 2 mg, haloperidol led to an increase of prolactin secretion and a suppression of luteinizing hormone release. Growth hormone was unaffected. Despite these changes, the patient had normal secondary sexual development consistent with puberty.

Adolescent↗
PubMed2005

Constitutional delay of growth and puberty: from presentation to final height.

This retrospective study evaluated clinical characteristics of patients with constitutional delay of growth and puberty (CDGP) at presentation, during puberty and at final height. The records of 151 children (105 boys, 46 girls) with CDGP were reviewed and the results were evaluated with respect to findings in healthy Turkish schoolchildren. CDGP was twice as frequent in boys as in girls. Height and weight deficit and short sitting height of the children were evident at presentation and continued up to final height. Mean age of onset of puberty was retarded by 2.5 years in girls and by 3 years in boys. The time between onset of puberty and pubertal growth spurt was shorter in both girls and boys than in the controls. Peak growth velocity was compromised in both girls and boys. Forty-one patients (30 boys, 11 girls) reached final height (FH). Mean FH was shorter than both target height and predicted adult height. The Bayley-Pinneau method was found to be a better predictor of FH than either the Tanner-Whitehouse method or target height. FH also showed correlation with the father's height. There was no effect of testosterone treatment on final height. Height deficit at onset of puberty, shorter duration between onset of puberty and pubertal growth spurt, compromised peak growth velocity and short upper segment due to delayed puberty, are findings which may explain the decreased final height of children with CDGP.

Adolescent↗
PubMed1988

A comparison of IGF-I levels measured by two commercially available radioimmunoassays.

Insulin-like growth factor I levels were measured in a parallel fashion in 77 extracted sera using the INCSTAR RIA (radioimmunoassay) and in the EDTA plasma of the same subjects by the NICHOLS RIA. The subjects suffered from untreated hGH deficiency, short stature, delayed and precocious puberty and acromegaly. Significant differences (P less than 0.05) were found between the mean IGF-I levels of all groups using both RIA systems. However, using the INCSTAR RIA, 85% of IGF-I values in untreated hGH deficiency were below normal, and a rise in IGF-I detected in the sera of all 5 patients who were treated with hGH. Using NICHOLS RIA, 55% of basal IGF-I values were below normal and a hGH-stimulated rise in IGF-I was found in only two of the treated patients. The INCSTAR RIA seems more precise and reproducible than the NICHOLS RIA and enables better discrimination of hGH-deficient patients from age-matched controls.

Acromegaly↗
PubMed1985

Oxandrolone in low dose for constitutional delay of growth and puberty in boys.

Twenty four boys with delayed pubertal growth spurt were treated with oxandrolone (2.5 mg daily) for 0.21 to 0.65 years. The mean increment of growth velocity was 4.4 cm/year during treatment, which was maintained at 3.7 cm/year after treatment. There was no significant change in height for bone age standard deviation scores.

Adolescent↗
PubMed1995

Predictive factors in the determination of final height in boys with constitutional delay of growth and puberty.

Seventy-eight patients who had constitutional delay of growth and puberty were included in a retrospective study to determine whether, at the time of first evaluation, any predictive features could suggest final height outcome. Mean chronologic age was 14.3 years (range, 12 to 18 years), and all were either prepubertal or in an early stage of pubertal maturation (4 ml testicular volume). Initial mean (+/- SD) height standard deviation score was -2.74 (+/- 0.71); 85% had a relatively short spine compared with subischial leg length. Mean (+/- SD) growth rate was 4.8 (+/- 1.6) cm/year, and epiphyseal maturation was delayed by 2.4 (+/- 1) years. Sixteen boys were treated with a sustained-action preparation of testosterone (50 mg monthly for 3 to 4 months), six with oxandrolone (1.25 mg daily for a mean of 4 months), and one with both drugs in sequence. At final height attainment, 58% of the boys failed to achieve their full genetic potential; among the remaining 42%, only 0.7% attained a final height above corrected mid-parental height. The relative disproportion between the segments had no significant change at final height attainment. Regression analysis showed that final height impairment (the difference between mid-parental height and final height) was negatively influenced by standing height and growth velocity when initially evaluated and positively by the degree of segmental body proportion; that is, patients who were taller, were growing at a faster rate, and who had a major degree of segmental body disproportion with a short spine and long leg length attained a final height closer to their mid-parental height, irrespective of the degree of delayed epiphyseal maturation. Neither testosterone nor oxandrolone administered during early puberty modified final height attainment or segmental proportion. We conclude that a late onset in the timing of puberty seems to be deleterious to spinal growth and consequently to final height attainment. An alternative diagnosis should be sought among patients with features of constitutional delay of growth and puberty who do not have a significant degree of body disproportion. In these patients, as well as in those who are extremely short, who have a poor growth rate, or who have an unfavorable genetic potential, an alternative therapeutic approach may be required.

Adolescent↗
PubMed1995

Degree of activation of the pituitary-testicular axis in early pubertal boys with constitutional delay of growth and puberty determines the growth response to treatment with testosterone or oxandrolone.

Early pubertal boys (testicular volume, 4-6 mL) with constitutionally delayed growth and puberty were randomized to 3 months of treatment after a baseline 12-h overnight hormone profile: group 1 (n = 5), daily placebo; group 2 (n = 5), 2.5 mg oxandrolone daily; or group 3 (n = 6), 50-mg testosterone monthly im injections. LH and GH profiles (15-min samples) were analyzed by peak detection (Pulsar), Fourier transformation, and autocorrelation. FSH and testosterone levels were measured hourly, and insulin, sex hormone-binding globulin, insulin-like growth factor-I, and insulin-like growth factor-binding protein-3 levels were determined at 0800 h. Multiple regression was used to analyze the response to treatment (growth) with respect to baseline features. Endocrine variability was marked. Profiles ranged from unreactive to well established LH pulsatility and adult testosterone levels. The areas under the curve (AUC) for LH, FSH, and testosterone ranged 10-fold (4.4-46.3 IU/L.h), 8-fold (7.9-63.4 IU/L.h), and 45-fold (3.6-161.7 nmol/L.h), respectively. The growth response was individually varied, but significantly increased 0-6 months in the active treatment groups. Age, testicular volume, and LH AUC interacted significantly (r2 = 0.95; P < 0.05). Allowance for these produced a highly significant treatment effect (P = 0.006). Age, testicular volume, LH AUC, and testosterone AUC, but not treatment, significantly increased growth by 0-12 months (r2 = 0.88; P < 0.05). We demonstrate a spectrum of activation of the reproductive axis despite tight clinical staging. This, and not GH status at treatment commencement, influenced the growth response.

Adolescent↗
PubMed2004

Development of hip dysplasia in puberty due to delayed ossification of femoral nucleus, growth plate and triradiate cartilage.

Besides hip dysplasia diagnosed after birth, there are dysplasias that do not develop until puberty, causing subluxation of the femoral head to occur late in the skeletal growth period. These dysplasias have various causes. In the two siblings described in this study, the boy showed a conspicuous delay in the appearance of the femoral nuclei and the fusion of the triradiate cartilages. The fusion occurred at 16 years of age in the boy and at 13-14 years in the girl. This was preceded by conspicuous structural changes, especially in the posterior triradiate cartilage and acetabular roof but also affecting the lateral growth plate of the femoral neck, which was horizontal over two-thirds of the diameter. We know from animal studies that the growth of the triradiate cartilage increases the diameter of the acetabulum but not the depth. The acetabulum is deepened by pressure from the femoral head. As a result of coxa valga and a prolonged period of acetabular expansion, combined with abnormalities of the superior acetabular rim, the femoral heads in these children finally subluxate. Whenever development of the femoral ossific nucleus is delayed during the first year of life, radiographic follow-ups should be instituted at 8 years of age.

Acetabulum↗
PubMed2004

Learning problems, delayed development, and puberty.

Language-based learning disorders such as dyslexia affect millions of people, but there is little agreement as to their cause. New evidence from behavioral measures of the ability to hear tones in the presence of background noise indicates that the brains of affected individuals develop more slowly than those of their unaffected counterparts. In addition, it seems that brain changes occurring at approximately 10 years of age, presumably associated with puberty, may prematurely halt this slower-than-normal development when improvements would normally continue into adolescence. The combination of these ideas can account for a wide range of previous results, suggesting that delayed brain development, and its interaction with puberty, may be key factors contributing to learning problems.

Acoustic Stimulation↗
PubMed1994

Growth hormone secretion in children with normal variants of short stature.

Pulsatile growth hormone (GH) secretion plays a central role in human growth during the prepubertal period of life. In order to investigate whether or not short stature in prepubertal children with normal variants of short stature (NVSS) may be explained, at least in part, by the presence of abnormalities in the pulsatile pattern of GH secretion, we have studied the spontaneous secretion of GH/24 h in 139 prepubertal children with short stature (< or = -2 SD) and normal growth velocity (> -1 SD) and in 37 prepubertal children with normal height and growth velocity. All of the subjects included in this study exhibited a body mass index (BMI) lower than 1 SD. The patients with short stature were divided into three groups according to their bone age and the existence of familial antecedents of short stature. These groups were: (1) familial short stature without bone age retardation (FSS-1); (2) constitutional, nonfamilial short stature, with bone age retardation suggesting further delay of puberty (possible constitutional delay of growth and puberty), and (3) familial short stature with bone age retardation (FSS-2). Spontaneous GH secretion was analyzed by using a computerized mathematical algorithm of pulsatility (Cluster). In addition, in all of the patients with short stature, the GH secretory response to three different pharmacological stimuli was evaluated, including: clonidine, growth hormone-releasing hormone (GHRH) and hypoglycemia after insulin administration. The mean values of GH/24 h exhibited a wide range of distribution (1.4-7.8ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMedDate not supplied

Final height outcome in both untreated and testosterone-treated boys with constitutional delay of growth and puberty.

The present retrospective study is based on a historical follow-up of 49 boys with constitutional delay of growth and puberty (CDGP) who went into puberty spontaneously (27 cases) or induced by depotestosterone treatment, 50 mg/ month for 6 months (22 cases). At the time of puberty the two groups of boys were similar in bone age, height deficiency, target height (TH) and had similar predicted final heights (FH). Their FH was measured and compared with TH calculated from measured parents' heights. FH did not significantly differ between the untreated boys and those treated. In the two groups of patients FH was similar and corresponded to both TH and height predicted at puberty onset. This study confirms that most boys with CDGP spontaneously attain a FH within the target range (24/27 cases). A short-term and low dose course of depotestosterone can be used without adverse effects on FH. The Bayley-Pinneau method can be generally considered accurate for predicting FH in CDGP, although significant discrepancies between FH and predicted height have been recorded in a fair number of both untreated and treated boys.

Adolescent↗
PubMed1987

Oxandrolone induces a sustained rise in physiological growth hormone secretion in boys with constitutional delay of growth and puberty.

We describe the treatment of 3 boys, mean age 14.9 years (range 13.8-16.1 years) with constitutional delay of growth and puberty using oxandrolone in two dose regimens, 2.5 or 1.25 mg/day for 3 months. Treatment induced an increase in mean height velocity from 5.1 to 8.5 cm/year; this was sustained at 8.8 cm/year in the period following treatment. Growth hormone (GH), luteinising hormone and testosterone secretion were assessed by overnight or 24-hour venous sampling at 15-min intervals before, during treatment and after cessation of treatment. A computer programme was used to analyse GH secretory dynamics. The 3 boys had a mean sustained increase in total GH secretion of 190%. The increase in GH secretion was associated with an increase in amplitude of GH pulses rather than an alteration in pulse frequency.

Adolescent↗
PubMed1988

Double blind placebo controlled trial of low dose oxandrolone in the treatment of boys with constitutional delay of growth and puberty.

Nineteen boys, mean age 14.4 years (range 12.9-16.3), with constitutional delay of growth and puberty were randomised into two groups in a double blind fashion for a three month period. Ten boys received oxandrolone, 2.5 mg per day (mean dose 0.072 mg/kg/day), and nine boys were treated with placebo. Mean growth velocity increased from 4.5 cm/year in the oxandrolone treated group to 9.6 cm/year in three months, and this was sustained at 8.6 cm/year after cessation of treatment. In the placebo treated group, growth rate showed no alteration from 5.1 cm/year to 5.2 cm/year; boys in this group were then treated with oxandrolone, 2.5 mg a day (mean dose 0.073 mg/kg/day) for three months and growth velocity accelerated to 8.6 cm/year. Serum concentrations of insulin-like growth factor -1/somatomedin-C (IGF-1) increased during oxandrolone treatment and continued to rise after treatment had ceased. There was no change in serum IGF-1 concentration during treatment with placebo. Oxandrolone, when used in an appropriate regimen, is an effective, safe treatment for boys with constitutional delay of growth and puberty.

Adolescent↗
PubMed1994

X-linked agammaglobulinemia, growth hormone deficiency and delay of growth and puberty.

Coinheritance of X-linked agammaglobulinemia and growth hormone deficiency (XLA/GHD) has been classified as an independent primary immune deficiency. We evaluated the pattern of growth and endocrine function in seven XLA subjects (ages 10.9-20.1 years); four belonged to two different XLA pedigrees and three represented sporadic XLA cases. Three had reached adulthood (final stature 176.0, 173.5 and 165.0 cm, respectively) and their retrospective growth showed delay in growth and puberty during adolescence. In the other four subjects, growth hormone production was measured by growth hormone pharmacological stimulation tests (clonidine, arginine): three of four patients had insufficient growth hormone responses (peak growth hormone < 10 micrograms/l); all three had delayed puberty; their growth hormone responses increased after "priming" with testosterone, reaching values > 10 micrograms/l in two of them and allowing diagnosis of "true" growth hormone deficiency in the third. The fourth was a normally growing subject who showed a normal growth hormone response both before and after testosterone priming. Six out of the seven subjects showed a growth pattern consistent with delay in growth and puberty. Our results suggest that true XLA/GHD is rarer than previously supposed and that subnormal responses to growth hormone stimulation tests may be found without sex steroid priming of the test in adolescence. The most probable growth pattern in XLA appears to be delay in growth and puberty, as has already been described for other chronic diseases.

Adult↗
PubMedDate not supplied

Vitamin A and beta carotene levels in constitutional delay of growth and puberty.

The objective of this study was to investigate the vitamin A (vit A) status and beta carotene levels of children with constitutional delay of growth and puberty (CDGP). Serum vit A and beta-carotene levels of 26 children with CDGP were measured. 20 age-matched healthy children with normal pubertal development served as controls. Except for the height SDS, which was significantly lower in the CDGP group (p < 0.05), no significant differences were found between chronological ages, weight for height indices and beta-carotene levels of the two groups (p > 0.05). Although serum vit A levels of children in both groups were within normal limits according to WHO criteria, serum vit A levels were significantly lower in the CDGP group than in controls (44.13 +/- 12.25 and 59.60 +/- 19.75 micrograms/dl respectively, p < 0.05). It was concluded that vit A deficiency may play a role in CDGP in developing countries.

Adolescent↗
PubMed1991

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↗
PubMed1993

The effects of oxandrolone on the growth hormone and gonadal axes in boys with constitutional delay of growth and puberty.

OBJECTIVE: We studied the effects of oxandrolone on serum concentrations of LH, FSH, testosterone, GH, SHBG, DHEAS, IGF-I and insulin in boys with constitutional delay of growth and puberty. DESIGN: Ten boys with constitutional delay of growth and puberty, mean age 13.8 years (range 12.4-15.5) were studied. Twenty-four-hour serum concentration profiles of GH, LH and FSH were constructed by drawing blood samples at 20-minute intervals. Three study occasions over a period of 6 months were chosen to assess hormone concentrations before, during and 6 weeks after a 3-month course of oxandrolone (2.5 mg once daily) therapy. RESULTS: Growth velocity increased during oxandrolone treatment and stayed higher after therapy (pre 3.9 +/- 0.5; on 6.3 +/- 0.8; post 6.4 +/- 0.9 cm/year (mean +/- SEM) two way ANOVA, F = 5.3, P = 0.02). Oxandrolone had androgenic effects, suppressing mean serum LH concentrations from 1.7 +/- 0.3 to 1.1 +/- 0.2 U/I and serum testosterone concentrations from 1.9 +/- 0.6 to 0.8 +/- 0.1 nmol/l. SHBG concentrations were also reduced from 130.9 +/- 14.6 to 30.7 +/- 7.3 nmol/l. Serum GH concentration fell slightly from 5.9 +/- 0.6 to 4.8 +/- 0.5 mU/l. After cessation of treatment, there was a significant 'rebound' in mean 24-hour serum LH (2.6 U/l +/- 0.4) and testosterone concentrations (3.2 +/- 0.9 nmol/l) but no change in serum GH concentrations. SHBG values also rose but not to the same extent as those observed before therapy (82.0 +/- 8.4 nmol/l). There were no statistically significant differences in serum concentrations of FSH, DHEAS, IGF-I and insulin over the study period. In a stepwise multiple regression analysis of factors that might influence the growth rate observed, the 24-hour mean serum testosterone concentration and the treatment (on or off) with oxandrolone were the main influences. The relationship was described by the equation Height velocity = 0.69 (24-hour mean serum testosterone concentration)+1.70 (treatment regimen)+3.37 (adjusted R2 = 0.35, F = 8.39, P = 0.001). CONCLUSIONS: Oxandrolone has an androgenic action as shown by changes in serum LH, testosterone and SHBG concentrations and by the lack of effect on FSH. No effect of oxandrolone on the GH axis was documented. We suggest that the growth promoting effects of oxandrolone are related in part to the mild androgenic effects of the steroid and the growth acceleration following oxandrolone withdrawal may reflect increasing total serum testosterone concentrations and decreasing levels of SHBG and progress in puberty.

Adolescent↗