scholarly journals Growth and Pubertal Development in Elite Female Rhythmic Gymnasts

1999 ◽  
Vol 84 (12) ◽  
pp. 4525-4530 ◽  
Author(s):  
N. Georgopoulos ◽  
K. Markou ◽  
A. Theodoropoulou ◽  
P. Paraskevopoulou ◽  
L. Varaki ◽  
...  

Optimal growth depends upon both environmental and genetic factors. Among environmental factors that could alter growth and sexual maturation are stress and intensive physical training. The influence of these factors has been documented in a variety of sports, but there is limited information on rhythmic gymnasts, who have entirely different training and performance requirements. The study was conducted during the 13th European Championships in Patras, Greece, and included 255 female rhythmic gymnasts, aged 11–23 yr. The study included measurement of height and weight, assessment of breast and pubic hair development, estimation of body fat and skeletal maturation, and registration of menarcheal age and parental height. Gymnasts were taller than average height for age, with mean height above and mean weight below the 50th percentile. Actual height sd score was positively correlated to weight sd score (P < 0.001), number of competitions (P = 0.01), and body mass index (BMI; P < 0.001). Predicted adult height sd score was positively correlated to weight sd score (P < 0.001) and negatively to body fat (P = 0.004). There was a delay in skeletal maturation of 1.3 yr (P < 0.001). Pubertal development was following bone age rather than chronological age. The mean age of menarche was significantly delayed from that of their mothers and sisters (P = 0.008 and P = 0.05, respectively), was positively correlated to the intensity of training and to the difference between chronological age and bone age (P < 0.001 and P = 0.002, respectively), and was negatively correlated to body fat (P < 0.001). In the elite female rhythmic gymnasts, psychological and somatic efforts have profound effects on growth and sexual development. Despite these aberrations, adult height is not expected to be affected.

Author(s):  
Marcela Vargas Trujillo ◽  
Sanja Dragnic ◽  
Petra Aldridge ◽  
Karen O. Klein

Abstract Objectives Gonadotropin-releasing hormone agonist treatment is important for optimal growth in girls with central precocious puberty (CPP). Data are lacking regarding benefit to height outcome when treatment is started after chronological age (CA) of 7 years, and if continued beyond CA of 10 years or bone age (BA) of 12 years. Methods Forty-eight girls with CPP were treated with monthly leuprolide depot. Change in predicted adult height (PAH) during treatment was assessed. Changes in PAH and growth velocity were compared between girls initiating treatment at CA <7 vs. ≥7 years, and BA ≥12 vs. BA <12 years. Results Mean baseline CA was 6.8 years, BA, 10.2 years; and PAH, 156.4 cm. BA/CA ratio decreased from pretreatment values, averaging 1.5 to 1.2 at the end of treatment. Proportion of girls with >5 cm PAH change during treatment was similar, and PAH increased throughout treatment in most girls, regardless of age at treatment initiation. PAH continued to increase in 16/19 girls who continued treatment after BA of 12 years, and also in 16/22 girls who continued treatment after CA of 10 years. Conclusions PAH improved in most girls who initiated treatment after CA of 7 years. It continued to improve in most girls with longer treatment, even past BA of 12 years or CA of 10 years, which suggests that no absolute CA or BA limit should define initiation or end of treatment. Treatment plans need to be individualized, and neither treatment initiation nor cessation should be based on BA or CA alone.


1981 ◽  
Vol 15 (2) ◽  
pp. 183-192 ◽  
Author(s):  
J. L. PENFOLD ◽  
T. C. SMEATON ◽  
J. M. GILLILAND ◽  
T. J. C. BOULTON ◽  
M. J. THOMSETT ◽  
...  

1999 ◽  
Vol 84 (2) ◽  
pp. 449-452 ◽  
Author(s):  
Anna Maria Pasquino ◽  
Ida Pucarelli ◽  
Maria Segni ◽  
Marco Matrunola ◽  
Fabio Cerrone

GnRH analogues (GnRHa) represent the treatment of choice in central precocious puberty (CPP), because arresting pubertal development and reducing either growth velocity (GV) or bone maturation (BA) should improve adult height. However, in some patients, GV decrease is so remarkable that it impairs predicted adult height (PAH); and therefore, the addition of GH is suggested. Out of twenty subjects with idiopathic CPP (treated with GnRHa depot-triptorelin, at a dose of 100 μg/kg im every 21 days, for at least 2–3 yr), whose GV fall below the 25th percentile for chronological age, 10 received, in addition to GnRHa, GH at a dose of 0.3 mg/kg·week sc, 6 days weekly, for 2–4 yr; and 10 matched for BA, chronological age, and duration of GnRHa treatment, who showed the same growth pattern but refused GH treatment, served to evaluate the efficacy of GH addition. No patient showed classical GH deficiency. Both groups discontinued treatment at a comparable BA (mean ± sem): 13.2 ± 0.2 in GnRHa plus GH vs. 13.0 ± 0.1 yr in the control group. At the conclusion of the study, all the patients had achieved adult height. Adult height was considered to be attained when the growth during the preceding year was less than 1 cm, with a BA of over 15 yr. Patients of the group treated with GH plus GnRHa showed an adult height significantly higher (P &lt; 0.001) than pretreatment PAH (160.6 ± 1.3 vs. 152.7 ± 1.7 cm). Target height (TH) was significantly exceeded. The group treated with GnRH alone reached an adult height not significantly higher than pretreatment PAH (157.1 ± 2.5 vs. 155.5 ± 1.9 cm). TH was just reached but not significantly exceeded. The gain in centimeters obtained, calculated between pretreatment PAH and final height, was 7.9 ± 1.1 cm in patients treated with GH combined with GnRHa; whereas in patients treated with GnRHa alone, the gain was just 1.6 ± 1.2 cm (P = 0.001). Furthermore, no side effects have been observed either on bone age progression or ovarian cyst appearance and the gynecological follow-up in the GH-treated patients (in comparison with those treated with GnRHa alone). In conclusion, a gain of 7.9 cm in adult height represents a significant improvement, which justifies the addition of GH for 2–3 yr during the conventional treatment with GnRHa, especially in patients with CPP, and a decrease in GV so marked as to impair PAH, not allowing it to reach even the third centile.


2020 ◽  
Vol 26 (10) ◽  
pp. 1053-1061
Author(s):  
Miguel Klünder-Klünder ◽  
Montserrat Espinosa-Espindola ◽  
Desiree Lopez-Gonzalez ◽  
Mariana Sánchez-Curiel Loyo ◽  
Pilar Dies Suárez ◽  
...  

Objective: The most commonly used methods for bone age (BA) reading were described in the Caucasian population decades ago. However, there are secular trends in skeletal maturation and different BA patterns between ethnic groups. Automated BA reading makes updating references easier and more precise than human reading. The objective of the present study was to present automated BA reference curves according to chronological age and gender in the Mexican population and compare the maturation tempo with that of other populations. Methods: The study included 923 healthy participants aged 5 to 18 years between 2017 and 2018. A hand radio-graph was analyzed using BoneXpert software to obtain the automated BA reading according to Greulich and Pyle (G&P) and Tanner-Whitehouse 2 (TW2) references. We constructed reference curves using the average difference between the BA and chronological age according to sex and age. Results: The G&P and TW2 automated reference curves showed that Mexican boys exhibit delays in BA during middle childhood by 0.5 to 0.7 (95% confidence interval [CI], −0.9 to −0.2) years; however, they demonstrate an advanced BA of up to 1.1 (95% CI, 0.8 to 1.4) years at the end of puberty. Mexican girls exhibited a delay in BA by 0.3 to 0.6 (95% CI, −0.9 to −0.1) years before puberty and an advanced BA of up to 0.9 (95% CI, 0.7 to 1.2) years at the end of puberty. Conclusion: Mexican children aged <10 years exhibited a delay in skeletal maturity, followed by an advanced BA by approximately 1 year at the end of puberty. This may affect the estimation of growth potential in this population. Abbreviations: BA = bone age; CA = chronological age; G&P = Greulich and Pyle; TW2 = Tanner-Whitehouse 2


2004 ◽  
Vol 89 (1) ◽  
pp. 236-241 ◽  
Author(s):  
Armando Flor-Cisneros ◽  
Ellen W. Leschek ◽  
Deborah P. Merke ◽  
Kevin M. Barnes ◽  
Marilena Coco ◽  
...  

The primary mechanism that initiates puberty is unknown. One possible clue is that pubertal maturation often parallels skeletal maturation. Conditions that delay skeletal maturation also tend to delay the onset of puberty, whereas conditions that accelerate skeletal maturation tend to hasten the onset of puberty. To examine this relationship, we studied boys with congenital adrenal hyperplasia (n = 13) and familial male-limited precocious puberty (n = 22), two conditions that accelerate maturational tempo, and boys with idiopathic short stature (n = 18) in which maturational tempo is sometimes delayed. In all three conditions, the onset of central puberty generally occurred at an abnormal chronological age but a normal bone age. Boys with the greatest skeletal advancement began central puberty at the earliest age, whereas boys with the greatest skeletal delay began puberty at the latest age. Furthermore, the magnitude of the skeletal advancement or delay matched the magnitude of the pubertal advancement or delay. This synchrony between skeletal maturation and hypothalamic-pituitary-gonadal axis maturation was observed among patients within each condition and also between conditions. In contrast, the maturation of the hypothalamic-pituitary-gonadal axis did not remain synchronous with other maturational processes including weight, height, or body mass index. We conclude that in boys with abnormal developmental tempo, maturation of the skeleton and the hypothalamic-pituitary-gonadal axis remains synchronous. This synchrony is consistent with the hypothesis that in boys, skeletal maturation influences hypothalamic-pituitary-gonadal axis maturation.


PEDIATRICS ◽  
1986 ◽  
Vol 78 (1) ◽  
pp. 124-132
Author(s):  
Michael C. G. Stevens ◽  
Gillian H. Maude ◽  
Lena Cupidore ◽  
Helen Jackson ◽  
Richard J. Hayes ◽  
...  

In a longitudinal study of 298 children with homozygous sickle cell (SS) disease and 157 children with hemoglobin SC disease, between birth and 9 years of age, observations of weight and height were made. These were compared with similar data derived from an age- and sex-matched group of 231 children with a normal hemoglobin (AA) genotype. Growth in children with SC disease was not significantly different from that in normal children, but children with SS disease had statistically significant, and progressive, deficits in both weight and height before 2 years of age. The average deficit approached 1 SD below the normal mean for age by 9 years. Observations of skeletal maturity, based on radiologic assessment of bone age at the wrist, were made on a proportion of these children at 5 and 8 years of age. Children with SS disease were significantly retarded at 8 years but not 5 years, which is consistent with increasing deficit in height. These observations confirm the early impact of SS disease on physical development and provide standards from which clinical expectations of growth may be derived. The relevance of these findings and their relationship to the characteristic delay in pubertal development is discussed together with a review of possible etiologic factors. The benign nature of SC disease is endorsed by the absence of an effect on growth in the prepubertal child.


2001 ◽  
Vol 86 (10) ◽  
pp. 4711-4716 ◽  
Author(s):  
Karen Oerter Klein ◽  
Kevin M. Barnes ◽  
Janet V. Jones ◽  
Penelope P. Feuillan ◽  
Gordon B. Cutler Jr.

We report 98 children who have reached final adult height in a long-term trial of LHRH agonist treatment. These children were 5.3± 2.1 yr old at the start of treatment and were treated with either deslorelin (4 μg/kg·d sc) or histrelin (4–10 μg/kg·d) for an average of 6.1 ± 2.5 yr. Final height averaged 159.8 ± 7.6 cm in the 80 girls, which was significantly greater than pretreatment predicted height (149.3 ± 9.6 cm) but still significantly less than midparental height (MPH) (163.7 ± 5.6). Final height averaged 171.1 ± 8.7 cm in the 18 boys, which was significantly greater than pretreatment predicted height (156.1 ± 14.2 cm) but still significantly less than MPH (178.3 ± 5.2 cm). However, the average adult height of the 54 children who had less than a 2-yr delay in the onset of treatment was not significantly different from their MPH, and 21 children exceeded MPH. Final height sd score correlated positively with duration of treatment (P &lt; 0.01), midparental height (P &lt; 0.001), predicted height at the start of treatment (P &lt; 0.001), and growth velocity during the last year of treatment (P &lt; 0.001) and correlated inversely with delay in the onset of treatment (P &lt; 0.001), age at the start of treatment (P &lt; 0.001), bone age at the start of treatment (P &lt; 0.001), bone age at the end of treatment (P &lt; 0.001), breast stage at the start of treatment (P = 0.02), and bone age minus chronological age at the start of treatment (P = 0.001). We conclude that LHRH agonist treatment improves the final height for children with rapidly progressing precocious puberty treated before the age of 8 yr for girls or 9 yr for boys. Less delay in the onset of treatment, longer duration of treatment, and lower chronological and bone age at the onset of treatment all lead to greater final height. All children with onset of pubertal symptoms before age 8 in girls and age 9 in boys should be evaluated for possible treatment. Treatment is appropriate in children with rapidly progressing puberty, accelerated bone maturation, and compromise of adult height prediction, regardless of bone age or chronological age at time of evaluation. However, once treatment is considered appropriate, it should be initiated quickly, because longer delays lead to shorter final height. In addition, the longer the treatment is continued, the greater is the final height outcome.


2017 ◽  
Vol 2017 ◽  
pp. 1-6
Author(s):  
Serife Uysal ◽  
Juanita K. Hodax ◽  
Lisa Swartz Topor ◽  
Jose Bernardo Quintos

Background. Data on adult height outcomes of the use of Anastrozole and Growth Hormone (GH) in pubertal males with Growth hormone deficiency (GHD) and Idiopathic short stature (ISS) are limited. Objective. We examined the effect of Anastrozole and GH therapy on near adult height (NAH) with pubertal males with GHD or ISS. Methods. Retrospective review of 419 charts from 2008 to 2015. The primary outcomes are NAH compared to mid-parental target height (MPTH) and predicted adult height (PAH). Results. We identified 23 patients (5 SGA/IUGR, 1 Noonan syndrome, 6 GHD, and 11 ISS). Six patients (4 GHD; 2 ISS) achieved NAH. Prior to Anastrozole treatment, the mean chronological age was 13.9±0.2 years (range 13.7–14.4), bone age was 13.6±0.6 years (range 12.5–14), mean height SDS was -1.5±0.5 (range −0.8 to −2.3), and mean PAH was 162.6±5.9 cm (range 153.5–168.6). MPTH was 173.6 cm ± 7 (range 161.8–181.6). Patients received Anastrozole for an average of 30.5 months (range 19–36 months). At NAH, the mean chronological age was 16.7±0.8 years (range 15.9–18.1 years) and height was 170±1.8 cm (range 168.5–173.4 cm). The mean height SDS improved to +0.81±0.6 (range +0.08 to +1.92, p=0.002). Net height gain was 7.3 cm compared to pretreatment PAH (p<0.01) and overall the mean adult height remained 3.5 cm below MPTH. Conclusion. Anastrozole and GH therapy can be effective in augmenting adult height without significant side effects. However, the long-term safety and efficacy of aromatase inhibitor use in pediatrics remain limited.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A679-A679
Author(s):  
Benjamin Udoka Nwosu ◽  
Sadichchha Parajuli ◽  
Gabrielle Jasmin ◽  
Austin F Lee

Abstract Context: There is no consensus on the effect of recombinant human growth hormone (rhGH) therapy on skeletal maturation in children despite the current practice of annual monitoring of skeletal maturation with bone age in children on rhGH therapy. Aims: To investigate the effects of long-term rhGH therapy on skeletal age in children and explore the accuracy of bone age predicted adult height (BAPAH) at different ages based on 13 years of longitudinal data. Methods: A retrospective longitudinal study of 71 subjects aged 2-18 years, mean 9.9 ± 3.8y, treated with rhGH for non-syndromic short stature for a duration of 2-14y, mean, 5.5 ± 2.6y. Subjects with syndromic short stature and systemic illnesses such as renal failure were excluded. Results: Bone age minus chronological age (BA-CA) did not differ significantly between baseline and the end of rhGH therapy (-1.05 ± 1.42 vs -0.69 ± 1.63, p=0.09). Piece-wise regression however showed a quantifiable catch-up phenomenon in BA of 1.6 months per year of rhGH therapy in the first 6.5y, 95%CI 0.023 - 0.229, p=0.017, that plateaued thereafter, β=0.015, 95% CI -0.191-0.221, p=0.88. There was no relationship between BAPAH z score – height z score and the duration of rhGH therapy, p=0.68. BAPAH overestimated final adult height in younger subjects but became more precise in older subjects (p&lt;0.0001). Conclusion: Long-term rhGH therapy demonstrated an initial catch-up phenomenon in skeletal maturation in the first 6.5y that plateaued thereafter with no overall significant advancement in bone age. These findings are reassuring and do not support the practice of yearly monitoring of skeletal maturation with bone age in children on rhGH therapy, especially in younger subjects where BAPAH is imprecise.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1022-1022 ◽  
Author(s):  
Sharyne M. Donfield ◽  
Alice Lail ◽  
Edward D. Gomperts ◽  
W. Keith Hoots ◽  
Erik Berntorp ◽  
...  

Abstract The development of inhibitory antibodies to factor VIII or factor IX is the most serious complication of replacement therapy for people with hemophilia. Inhibitors decrease effectiveness of treatment, increasing risk of morbidity including bleeding frequency and arthropathy, and mortality. The current study examined the association between history of inhibitors and physical growth measured by skeletal maturation (bone age, BA) in participants enrolled in the longitudinal Hemophilia Growth and Development Study (HGDS). The HGDS is a population-based multicenter study of children and adolescents enrolled between 1989 and 1990. Participants not skeletally mature (n=306) were included in this investigation. Their mean age was 12, range 7–18 years. Seventy-five percent had severe hemophilia, 19% moderate, and 6% mild. Eighteen percent (n=54) had a history of inhibitors, with maximum lifetime Bethesda titers ranging from 1 to 2048. In general, HGDS participants received on-demand therapy prior to and during study follow-up. Skeletal maturation was determined centrally from x-rays of the hand-wrist according to the Fels method. Readers were masked to the clinical status of participants. Growth delay was defined as chronological age (age) minus BA and modelled using a longitudinal mixed effects polynomial model including age, race, HIV and inhibitor status, and their interactions. P-values were adjusted for multiple comparisons using Scheffe’s method. At every year evaluated (10 through 16), growth delay was greater among HIV-negative subjects with a history of inhibitors compared to HIV-negative subjects without inhibitors (p-values ranged from 0.042 to 0.12). The greatest differences, 9 to 10 months, were observed during the period of expected maximum growth velocity, 12 through 14 years of age (all p&lt;0.05). At ages 15 and 16, subjects with inhibitors lagged approximately 9 months behind those without inhibitors in their skeletal maturation (p=0.067 and 0.12). The predicted BA of HIV-negative adolescents without inhibitors was quite similar to age during this period. At 12, 13, 14, 15 and 16 years, they were 11.9, 13.1, 14.3, 15.4, and 16.4 respectively. Previous investigations from the HGDS have reported delays in skeletal maturation associated with HIV. In this study, delays were greater among HIV-positive subjects with an inhibitor compared to HIV-positive subjects without an inhibitor at every age, but perhaps due to intervening effects of HIV, the differences were generally small (1 to 2 months) and not statistically significant. In conclusion, the differences in bone age relative to chronological age between the HIV-negative groups suggest that a history of inhibitors is associated with delays in onset of puberty. Further investigation of this association and other growth parameters is a priority. If confirmed, the observation has important clinical, epidemiologic and therapeutic implications for the children and adolescents most severely impacted by hemophilia.


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