Pubertal Height Gain Research Articles

Longitudinal analysis of growth and puberty in 21-hydroxylase deficiency patients

Aims: To evaluate growth from diagnosis until final height (FH) in 21-hydroxylase deficiency patients. Methods: A retrospective longitudinal study was performed. Only patients treated with hydrocortisone and fludrocortisone (in case...

Age of pubertal onset affects the intensity and duration of pubertal growth peak but not final height.

This paper analyzed the intensity and duration of height growth during puberty in boys and girls in relation to rhythm of maturation. A longitudinal clinical follow-up between ages of 10 and 20 years, was carried out in a sample of 251 children grouped according to age at pubertal onset: boys (genital stage 2) at the ages of 11 (n = 28), 12 (n = 38), 13 (n = 42), and 14 (n = 27); and girls (breast stage 2) at the ages of 10 (n = 37), 11 (n = 47), 12 (n = 19), and 13 (n = 13). Height was measured annually. Testicular volume and genital development were assessed in boys, and breast development was assessed in girls. There were significant differences (P < 0.001) in height at the age of pubertal onset among maturity groups. Late maturers were taller than early maturers (r = 0.49, P < 0.001 for girls; r = 0.38, P < 0.001 for boys). However, final heights did not differ according to age of onset in either sex. In boys, later onset of puberty was associated with a smaller pubertal height gain (r = -0.60, P < 0.001) and a shorter period of pubertal growth (r = -0.61, P < 0.001). Equally in girls, earlier onset of puberty was associated with a greater pubertal height gain (r = -0.68, P < 0.001) and a longer period of pubertal growth (r = -0.59, P < 0.001). In conclusion, age of pubertal onset does not affect final height attained in both sexes, since there is an inverse compensatory phenomenon in both sexes between height at pubertal onset and the intensity and duration of pubertal growth.

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.

Combined GH and LHRH Analog Treatment Can Increase Pubertal Growth in Short Children

To improve the final height of short children who enter puberty at short stature, twenty-one boys who entered puberty shorter than 130 cm and twelve girls who entered puberty shorter than 125 cm were treated with a combination of GH and LHRH analog. Combined GST and GH treatment was started in boys and girls at a mean age of 11.78 (±0.82) years and 10.54 (±1.08) years, mean height of 130.0 (±4.4) cm and 122.6 (±3.2) cm, and mean height SD of -2.34 (±0.61) SD and -2.78 (±0.99) SD respectively. During the combination treatment, bone age decelerated after a bone age of 11.5 years in boys and 10 years in girls, and height velocity did not decelerate but remained at from 3 cm/year to 5 cm/year for a longer period. As a consequence of the treatment, the height SD score for bone age increased significantly. Seven boys and six girls discontinued LHRH analog treatment when the mean age was 17.11 (±1.15) years after a mean treatment period of 4.96 (±1.37) years for boys and when the mean age was 13.89 (±1.79) years after a mean treatment period of 3.21 (±1.52) years for girls. The mean height was 155.1 (±3.1) cm for boys and 143.3 (±3.0) cm for girls and their predicted adult height was 169.8 (±2.5) cm for boys and 155.8 (±3.1) cm for girls at the cessation of the combination treatment. All except one girl in our study will have achieved greater than the standard height gain during puberty. Although combined GH and LHRH analog treatment can improve the final height of short children by increasing pubertal height gain, the combination treatment seems more effective in boys than in girls.

Final height and hormonal function after bone marrow transplantation in children

AIM: To analyze final height and hormonal function in long-term survivors of bone marrow transplantation (BMT). PATIENTS: Group 1 consisted of 16 patients (10 boys) with a hematologic malignancy, mostly leukemia, conditioned for BMT with total body irradiation (TBI), 7.5 to 12 Gy, and cyclophosphamide. Group 2 consisted of 14 patients (9 boys) with severe aplastic anemia, conditioned with chemotherapy only. RESULTS: In group 1, patients achieved a reduced final height after BMT. The difference between the height standard deviation score (SDS) at BMT and the height SDS at final height was -1.96 (0.82) SDS in boys and -0.92 (0.71) SDS in girls ( p = 0.0001, and p = 0.02 respectively). Final height was also lower than target height (boys, p = 0.01; girls, p = 0.03). Prepubertal growth in the first 3 years after BMT was normal but pubertal height gain was decreased. The patients in group 2 achieved normal height. Thyroid function and adrenal function were normal in all patients, and no growth hormone deficiency was detected. Serum follicle-stimulating hormone values after BMT were increased in all group 1 patients, with return to normal in two patients. Serum luteinizing hormone values were increased in all group 1 girls, with recovery in one girl. Normal serum luteinizing hormone values and spontaneous puberty were found in all group 1 boys. In group 2, disturbances in gonadotropins were seen only in three boys and two girls. CONCLUSION: In patients treated in childhood with BMT after chemotherapy and TBI with 7.5 Gy or more, final height is compromised because of blunted growth in puberty. Patients who had not received TBI suffered no height loss. In the majority of patients, the combination of chemotherapy and TBI also resulted in irreversible disturbances of gonadal function. (J P EDIATR 1996;129:544-50)

Combined GH and LHRH analog treatment in short children.

It has been reported that the final height in short children is strongly related to the height at the onset of pubertal development, and pubertal height gain in GH-treated children is not exceed the gain in normal children. Therefore, it is now the consensus that insufficient height at the onset of puberty leads to short final height. We have already demonstrated that the final height in GH-deficient children with spontaneous puberty with gonadal suppression therapy by medroxyprogesterone or cyproterone acetate was significantly taller than GHD with spontaneous puberty without gonadal suppression therapy. In this study, we treated short boys who started puberty at height shorter than 130 cm with combined GH and LHRH analog. Final height was predicted by the height SD score for bone age. Although pubertal growth spurt was not recognized in short children on combination treatment, bone age maturation over 11.5 years decelerated significantly to the rate of one year in three or four years. Even during this slow bone maturation period, growth velocity remained at 4 cm/year due to GH treatment. Therefore, height SDS for bone age was improved in combination with the elongation of treatment period by the slow bone maturation. Some investigators recommend not to delay induction if puberty much beyond the normal age to avoid psychological problems and ennuchoid proportion in these children. When we explained to our Japanese patients the chance of increasing the final height with gonadal suppression treatment and the risk of delaying the pubertal development, almost all children preferred taller final height to pubertal development and they did not experience much psychological trouble. The differences in social and cultural circumstances do, however, influence patients' preferences.

Longitudinal data on growth and final height in diabetic children.

The available data on growth in children with insulin-dependent diabetes mellitus are conflicting and are mainly derived from cross-sectional studies. In this longitudinal study, height, weight, skeletal age, and pubertal development were recorded until final height was attained in 46 children (22 girls and 24 boys) with onset of diabetes before the age of 10 y. At the onset of diabetes, height SD score (SDS) averaged 0.41 in girls and 0.56 in boys, which was normal when corrected for the secular trend. Prepubertal growth was unaffected in both sexes. Diabetic boys had a marked delay in onset of puberty (mean age at genitalia stage 2: 13.7 y) but attained a normal final height (final height SDS: 0.48 +/- 0.89). In girls final height was slightly reduced (height SDS 0.27 +/- 0.97) due to a suboptimal pubertal growth spurt. Mean pubertal height gain in girls was 16.6 cm and mean age at breast stage 2 was 11.6 y. Diabetic girls also tended to become obese during puberty. Skeletal maturation was normal at all ages. These data suggest that conventional therapy does not guarantee optimal growth, especially in girls.

Growth in stature in fragile X families: a mixed longitudinal study.

The effect of fragile X on growth in stature was estimated in individuals aged 5-20 years from 50 fragile X families. The multivariate normal model for pedigree analysis was applied to the mixed longitudinal data, which varied with regard to intervals between the measurements and their number in individual subjects, totalling 349 measurement data points from fragile X families, and 292 data points from unrelated normal subjects. The results of genetic and regression analysis showed that, in fragile X boys and girls, total pubertal height gain is impaired, whereas the rate of growth during the preadolescent period is increased, compared with the growth rate of nonfragile X subjects. Moreover, the growth parameters in fragile X males were found to be correlated with the size of CGG trinucleotide expansion. The hypothesis of premature activation of the hypothalamo-pituitary gonadal axis is postulated as the cause of growth impairment in fragile X boys and girls, which should be verified by data on the timing of pubertal stages, hormone levels, and bone maturation.

Bone Age at Onset of Pubertal Growth Spurt and Final Height in Normal Children

The purpose of this study was to examine the influence of the variation in bone age at the onset of the pubertal growth spurt (PGS) on pubertal height gain and on final height. The subjects were 26 boys and 28 girls who had been treated at the Department of Orthodontics, School of Dentistry, Tohoku University, and had reached their final heights. Each child had longitudinal growth record and several hand and wrist X-ray films.A significant positive correlation between the bone age and height at the onset of PGS was recognized in boys (r=0.734, P<0.01, n=26) and girls (r=0.655, P<0.01, n=28). A significant negative correlation between the bone age at the onset of PGS and the pubertal height gain was recognized in boys (r=-0.732, P<0.01) and girls (r=-0.775, P<0.01). However, there was no significant correlation between final height and bone age at the onset of PGS.We found that the rate of bone maturation during puberty negatively correlated with the bone age at the onset of PGS and although bone age at the onset of PGS was distributed over a wide range, bone age at PHV was concentrated around 13 years in boys and 11 years in girls.

Pubertal linear growth of Indian girls adopted in Sweden

Pubertal linear growth in 66 adopted Indian girls was studied. The infancy-childhood-puberty standard was used, since it is applicable to Indian girls, and enables determination of the onset and height gain of the pubertal growth phase in an individual. At arrival in Sweden, mean height was -2.8 SDS. Despite rapid catch-up growth, the girls were still below the reference mean (-0.8 SDS) at the onset of the pubertal growth spurt, which occurred approximately 1.5 years earlier than in Swedish girls and also earlier than in Indian girls. The pubertal height gain, however, was equivalent to that in Swedish girls with similar timing of puberty. The short final height found in some of these girls appears to be related to shortness prior to puberty and to very early onset of an otherwise normal pubertal growth component.

Pubertal Growth in Short Children

Pubertal growth is analysed in 41 normal short boys and 31 normal short girls, whose height SDS at 7 years was below-1.5 SD, among 450 normal healthy boys and 483 normal healthy girls. Fourteen of 41 (34%) normal short boys and 15 of 31 (48%) normal short girls had a height SDS at 17 years above -1.5 SD (Group A), while the height SDS at 17 years of the rest of the normal short boys (27 boys) and girls (17 girls) remained below -1.5 SD (Group B).The mechanism of height gain during puberty differs between normal short boys and girls. In normal short boys, height and percent overweight at 7 years, and pubertal height gain correlated closely with height at 17 years. In normal short girls, the age and height at onset of PGS are the important factors influencing height at 17 years.

Pubertal Growth in Chronic Renal Failure

We evaluated the growth records of 15 boys and 14 girls who developed end-stage renal failure before or during puberty and who were regularly followed from the onset to the end of their pubertal growth spurt. Height data were smoothed by using the kernel estimation method. Mean values for age, height, and height velocity at defined points of the pubertal growth period were compared with those of normal children entering puberty both at an average and late age. The start of the pubertal growth spurt was delayed by 2.5 y in both sexes. Its duration and intensity were significantly reduced. Mean pubertal height gain was 17.3 cm in boys and 13.9 cm in girls, i.e. 58 and 48% of that observed in the late maturing control group. Mean height at the onset of the pubertal spurt in the patients was the same as that in the late maturing healthy girls and 1.0 SD below that of corresponding boys. During the pubertal growth spurt, mean height declined to -2.9 SD in boys and -2.3 SD in girls. Although skeletal maturation was increasingly retarded, we did not observe accelerated growth velocity during late puberty. Our data indicate that most patients reaching end-stage renal failure before or during puberty irreversibly lose growth potential during this period. Renal transplantation did not consistently improve pubertal growth.

Relationships between Puberty and Growth at Adolescence in Growth-Hormone-Deficient Males: Effect of Growth Hormone and of Associated Gonadal Suppression Therapy

125 boys with idiopathic GH deficiency who received GH treatment were followed until they reached their final height. In 85 patients who had spontaneous puberty (group I), the mean final height was 151.5 +/- 6.6 cm. In 23 patients with combined GH and gonadotropin deficiency (group II) whose pubertal development was induced artificially at age 19.4 +/- 2.1 years, the mean final height was 163.7 +/- 3.9 cm (p less than 0.01 vs. group I). Final height was strongly related to height at the onset of pubertal development in combined groups I and II when the time of gonadal replacement treatment was taken as the onset of pubertal development in group II. In 17 patients (group III) who developed spontaneous puberty, gonadal suppression treatment was started at their early stage of puberty and was continued for a mean duration of 4.3 +/- 1.1 years. The mean final height in group III was 157.9 +/- 3.0 cm (p less than 0.01 vs. group I, group II). Longitudinal growth pattern analysis demonstrated that this beneficial effect on final height by gonadal suppression treatment was attributed to the elongation of pubertal growth spurt and pubertal height gain.

The Influence of Gonadal Function and the Effect of Gonadal Suppression Treatment on Final Height in Growth Hormone (GH)-Treated GH-Deficient Children*

One hundred and sixty-one children with idiopathic GH deficiency who received GH treatment were followed until they reached their final height. Final height was found to be influenced by gonadal function. In 108 patients who had spontaneous puberty (91 boys and 17 girls; group A), the mean final height was 151.8 +/- 6.6 (+/- SD) cm in boys and 141.7 +/- 7.4 cm in girls. In 29 patients with combined GH and gonadotropin deficiency (23 boys and 6 girls; group C), whose pubertal development was induced artificially at age 19.5 +/- 2.1 yr in the boys and 18.6 +/- 1.8 yr in the girls, the mean final height was 163.7 +/- 3.9 cm in boys and 151.0 +/- 5.1 cm in girls. The differences in final height between groups A and C were significant in both boys and girls. The shorter final height in group A was caused by the shorter pubertal duration and smaller pubertal height gain than those in normal children. In 24 patients (17 boys and 7 girls; group B) who developed early signs of puberty, gonadal suppression therapy with cyproterone acetate and/or medroxyprogesterone acetate was given. The mean SD score of the final height in these 24 patients was -2.1 +/- 0.6, significantly higher than that in group A. This beneficial effect of gonadal suppression treatment on final height was caused by increases in the duration of puberty and the pubertal height gain.

2 FACTORS CONTRIBUTING TO IMPAIRMENT OF GROWTH IN CHILDREN WITH ACUTE LYMPHOBLASTIC LEUKEMIA (ALL)

In 88 ALL pat. (43 ♂ 45 ♀) studied retrospectively, mean chronological age(CA)at diagnosis was 6.0 yrs, mean SDS of height for CA(+0.40SD), height for bone age(BA)(+0.44 SD) and weight (-0.06SD). In 48 pat. now in puberty, mean height for CA has decreased to -0.73SD and mean height for BA is -1.71SD. In 8 pat.final height is -0.68SD when adult height predicted at diagnosis was +0.32SD. Growth impairment was determined by the following: 1)duration of chemotherapy: 5 yrs after diagnosis, mean height SDS for CA was reduced by -0.65 SD and by -1.01 SD respectively in patients treated for 2 and for 5 yrs. 2)Radiation doses: 5 yrs after diagnosis mean height SDS for CA was reduced by -0.34 SD and by -1.14 SD in those receiving 18 Gy and 24 Gy respectively 3) Lack of catch-up growth after therapy : between end of therapy and onset of puberty, height SDS for CA did not change (-0.06 SD). In 16/33 euthyroid pat. evaluated at least 2 yrs after irradiation GH response was blunted (<10 ng/ml) in 2 pharmacological tests. In 11/30 Sm-C was low for CA. No hGH treatment was given. 4)Early puberty in relation to age at diagnosis:in girls diagnosed before or after age 7, M2 started respectively at mean CA of 10.6 yrs (n=16) and 11.4(n=15), accounting for a difference of -0.4 SD in height for CA at puberty. 5) Reduction of pubertal growth spurt : compared to average normal girls, mean pubertal height gain was reduced by 3,8 cm. Pituitary-gonadal function(GnRH-test, n=30) was normal. Conclusion : In ALL pat. growth impairment has several components, differing by time of occurrence and mechanism.

Pubertal growth and final height in hypopituitary boys: a minor role of bone age at onset of puberty.

Twenty-two hypopituitary boys treated with human GH were studied longitudinally before and during puberty. Eight patients entered spontaneous puberty at a mean bone age of 12.4 +/- 1.0 (+/- SD) yr. Height velocity reached a mean peak of 6.8 cm/yr during the second year of spontaneous puberty. In these patients, the mean total height gain throughout puberty was 22.8 +/- 5.2 cm, and the mean final height was 158.6 +/- 7.2 cm. Fourteen patients received testosterone enanthate (100 mg/month, im) starting at a mean bone age of 13.6 +/- 1.1 yr. Height velocity was maximal (7.5 cm/yr) during the first year of therapy. The mean final height was 162.9 +/- 5.0 cm, with a mean pubertal gain of 15.9 +/- 3.8 cm. Genital development, peak height velocity, and increase in plasma testosterone levels occurred earlier during testosterone therapy than during spontaneous puberty. In both groups of patients, there was a positive correlation between the bone age at onset of puberty and the height at onset of puberty (r = 0.65). There was also a negative correlation between bone age and total pubertal height gain (r = -0.73). This reduction in pubertal height increase was less than expected for bone age at onset of puberty, which can be explained by a decrease in bone age velocity in relation to bone age at onset of puberty (r = -0.81). Therefore, advancement in bone age at the onset of testosterone therapy did not impair final height, whereas it may increase height at onset of puberty, which is the major factor in final height. We conclude that in GH- and gonadotropin-deficient boys 1) a reduced dosage of testosterone enanthate (25 mg twice a month, im) should be used to induce pubertal development, and 2) the major criterion to decide when to give testosterone is height reached at that time regardless of bone age.