Growth In Girls Research Articles

Turner’s syndrome: A growing concern

Turner’s syndrome: A growing concern

Relation of childhood diet and body size to menarche and adolescent growth in girls.

Adolescent growth and development may be affected by factors such as dietary intake and body size from much earlier in childhood. In a longitudinal study of 67 Caucasian girls in Boston, Massachusetts, data were collected prospectively from birth during the 1930s and 1940s. Heights and weights were measured semiannually, and dietary history interviews were conducted with mothers. Stepwise linear regression methods were used to seek factors which best predicted age at menarche, adolescent peak height growth velocity, and the age at which peak growth velocity occurred. Girls who consumed more (energy-adjusted) animal protein and less vegetable protein at ages 3-5 years had earlier menarche, and girls aged 1-2 years with higher dietary fat intakes and girls aged 6-8 years with higher animal protein intakes became adolescents with earlier peak growth. Controlling for body size, girls who consumed more calories and animal protein 2 years before peak growth had higher peak growth velocity. These findings may have implications regarding adult diseases whose risks are associated with adolescent growth and development factors.

Hormonal changes during the first year of oestrogen treatment in constitutionally tall girls.

Oestrogens are used to inhibit growth in girls with constitutionally tall stature. We studied the changes in different hormones that accompany such therapy. In this longitudinal study we examined the levels of total insulin-like growth factor-I (IGF-I), free thyroxine (FT(4)), thyrotrophin (TSH), testosterone, dehydroepiandrosterone sulphate (DHEA-S), cortisol and prolactin in two groups of girls receiving ethinyloestradiol at a dose of either 0.1mg daily (group A, n=22) or 0.2mg daily (group B, n=36). Hormonal measurements were performed at start of therapy and after 3, 6 and 12 months. In both groups the levels of IGF-I, testosterone and DHEA-S were reduced while the concentrations of cortisol and prolactin were increased. The pituitary-thyroid axis was not significantly affected by this therapy. The girls receiving 0.2mg ethinyloestradiol daily had lower IGF-I levels after 12 months of therapy and had higher serum prolactin concentrations than the girls treated with 0.1mg daily. The reduction in predicted height and the advancement in bone age were similar in both groups. Therapy with pharmacological doses of ethinyloestradiol changes the levels of several hormones including IGF-I, testosterone, DHEA-S, prolactin and cortisol but the role of the respective changes in the inhibition of growth is not clear. The suppression of DHEA-S levels by 40% suggests that the ovaries contribute significantly to the production of this hormone in pubertal girls.

Turner syndrome: a pattern of early growth failure.

The purpose of this study was to determine the pattern of early growth in girls with Turner syndrome. Analysis was performed on a total of 464 longitudinal measurements of height, obtained from birth to 8 years of age from 37 girls with Turner syndrome who did not have significant cardiac disease or autosomal abnormalities. All data were obtained prior to the initiation of any hormonal therapy. Mean height SDS fell from -0.5 at birth to -1.5 at age 1 year and -1.8 at age 1.5 years. Growth curves fitted using the first two components of the infancy-childhood-puberty model of growth revealed that growth failure was due to (a) mild growth retardation in utero, (b) slow growth during infancy, (c) delayed onset of the childhood component of growth and (d) slow growth during childhood. Physicians should consider the diagnosis of Turner syndrome in any girl with an unexplained failure to thrive or with short stature, even during the first 2 years of life.

Early dexamethasone therapy in preterm infants: a follow-up study.

To study the outcome at 2-year corrected age of infants who participated in a double-blind controlled trial of early (<12 hours) dexamethasone therapy for the prevention of chronic lung disease (CLD). A total of 133 children (70 in the control group, 63 in the dexamethasone-treated group) who survived the initial study period and lived to 2 years of age were studied. All infants had birth weights of 500 to 1999 g and had severe respiratory distress syndrome requiring mechanical ventilation within 6 hours after birth. For infants in the treatment group, dexamethasone was started at a mean age of 8.1 hours and given 0.25 mg/kg every 12 hours for 1 week and then tapered off gradually over a 3-week period. The following variables were evaluated: interim medical history, socioeconomic background, physical growth, neurologic examinations, mental and psychomotor development index score (MDI and PDI), pulmonary function, electroencephalogram, and auditory and visual evoked potential. Infants in the control group tended to have a higher incidence of upper respiratory infection and rehospitalization than did the dexamethasone-treated group because of respiratory problems. Although there was no difference between the groups in somatic growth in girls, the dexamethasone-treated boys had significantly lower body weight and shorter height than the control boys (10.7 +/- 3.0 vs 11.9 +/- 2.0 kg; 84.9 +/- 5.7 vs 87.5 +/- 4.8 cm). The dexamethasone-treated group had a significantly higher incidence of neuromotor dysfunction (25/63 vs 12/70) than did the control group. The dexamethasone-treated infants also had a lower PDI score (79 +/- 26) than did the control group (87 +/- 23), but the difference was not statistically significant. Both groups were comparable in MDI, incidence of vision impairment, and auditory and visual evoked potential. Significant handicap, defined as severe neurologic defect and/or intellectual defect (MDI and/or PDI </= 69), was seen in 22 children (31.4%) in the control group and 26 (41.2%) in the dexamethasone-treated group. Although early postnatal dexamethasone therapy for 4 weeks significantly reduces the incidence of CLD, this therapeutic regimen cannot be recommended at present because of its adverse effects on neuromotor function and somatic growth in male infants, detected at 2 years of age. A longer follow-up is needed. If early dexamethasone therapy is to be used for the prevention of CLD, the therapeutic regimen should be modified. The proper route of administration, the critical time to initiate the therapy, and the dosage and duration of therapy remain to be defined further.

Effect of Oxandrolone on Growth of Girls With Turner's Syndrome

Turner's syndrome (T.S.) is characterized for by a short stature, this becoming more evident during puberty and attainning a final height (FH) of aproximately 140 cm shorter than that predicted from analysis of mid-parental height for normal girls. A better FH increases life quality and self-esteem. Previous studies indicate that growth velocity (GV) is increased by Oxandrolone (O), growth hormone (GH) or both. O, increases GV and FH. 0.1 mg/kg/day of this drug rarely accelerates bone maturation. We investigated the effect of O on growth and bone maturation in patients with TS, by a double-blind study in 14 patients randomized into experimental (G1) and placebo (G2) groups. Enrollment criterias were kariotipic confirmation of TS; bone age>7 years; chronological age 8-14 years; normal TSH and T4; average intellectual skills no previous therapy with O, estrogens, anabolic agents or GH. G1 received O (0.1 mg/kg/day;Oxandrin. Gynex Pharm.) and G2 a placebo. They were controlled every 3 months, evaluating: height, weight, breast development, pubic hair and adverse effects. In months 0.6 and 12:BA, FSH, LH, E2, TSH, T4, IGF-1 (RIA), CBC, biochemical and lipid profiles were evaluated, G1 included 7 girls with a mean age of 11.05±1.68 years. height Z score=-3.8±1.2 and BA=9.9±0.97 years. without secondary sexual characters. G2 had CA=11.6±0.8 years, height Z score=-3.3±0.6 and BA=11.2±1.5 years; three patients with breast Tanner stage III. At baseline. G1: FSH=80.7±73 IU/L; LH=21.0±21.4 mIU/mL; E2<1.4 pg/mL; TSH=2.44±1.06 uUI/mL: T4=7.84=1.23 ug/dL; IGF-1=27.51±7.98 nmol/L. G2:FSH=89.14±109.5 IU/L;LH=29.4±47.8 mIU/mL: E2=3.0±3.2 pg/m/L;TSH=2.0+0.92 uUI/mL. T4=9.04±1.07 ug/dL;IGF. I=28.95±8.27 nmol/L. After 1 year of treatment GV was significative higher in G1 (6.97±1 cm) than in G2(4.74±0.96 cm): a BA/CA ratio changed significatively in G1(0.90±0.08 to 0.96±0.09± while no change occurred in G2(0.96±0.11 to 0.96±0.07). During 1 year of follow up O increases GV and BA significantly. O should be carefully evaluated as a single tnerapeutic agent in TS.

Growth in the Lower Limb Following Chemotherapy for a Malignant Primary Bone Tumour: A Straight‐Line Graph

Purpose. The aim of this paper was to assess the growth in the unaffected lower limb of children who had received chemotherapy for a malignant primary bone tumour around the knee. Subjects/methods. Following diagnosis, all children (45, of which 32 were boys and 13 were girls) were staged. If limb-salvage surgery was thought appropriate, measured radiographs of both legs was performed, the bone age was estimated and the expected growth in the femur and tibia was calculated according to Tupman. These procedures were repeated at follow-up and the data plotted. Regression and correlation coefficients were also calculated. Results. The observed regression line in boys was almost identical to Tupman's curve. However, the observed growth in girls was larger than the expected growth. Discussion. It is recommended that the regression lines presented here are used in the calculation of the expected growth in the lower limb of children who have received chemotherapy for a malignant primary bone tumour, especially in girls.

Growth hormone therapy in Turner syndrome--current uncertainties and future strategies.

The effect of growth hormone (GH) on short-to-medium-term growth in girls with Turner syndrome is well-established. However, it is only relatively recently that final height data have become available. This paper reviews 10 reports from Europe (including Sweden, Austria, France, Holland, Belgium and Scotland), Canada, USA and Japan, on final height and near-final height in girls with Turner syndrome receiving GH therapy. An improvement in final height outcome versus projected adult height was found in all the studies, except for the Scottish study, in which the median final height was only 142.6 cm, and the Canadian study, in which the projected adult height was unexpectedly high at 148.2 cm. Although the mean final height was 150 cm or greater in six studies, all 10 showed considerable individual variation in final height with minimum values ranging between 131.5 and 145 cm. These results must be interpreted cautiously since the mean age of starting treatment was relatively late at 9.1-13.1 years. However, the overall modesty and interpatient variability of response to GH in Turner syndrome, and continuing uncertainty as to the role of oxandrolone and the timing of estrogen therapy, emphasizes the need for further research. National and international collaboration in both retrospective and prospective studies are necessary to achieve sufficient data to offset the large number of variables to be analysed. In the UK, the British Society for Paediatric Endocrinology and Diabetes hopes to do a retrospective meta-analysis of final/near-final height outcome, comparing this with midparental and maternal height, as well as projected height and control data. A prospective study with GH dose standardized at 30 IU/m2 per week in the form of daily injections, with randomization to receive oxandrolone or not at 9 years, and estrogen at either 12 or 14 years, is also planned.

Seasonal height velocity variation in boys and girls 8-18 years.

This study investigated the seasonal variation in height velocity during the summer and winter months. The subjects were healthy children, 109 boys and 119 girls, 8.5-18.0 years of age who are part of an ongoing longitudinal study of bone mineral accrual. Anthropometric dimensions were taken twice a year, in the fall in conjunction with the annual bone assessment measures and 6 months later. Six-month velocities for height were calculated, which produced 982 velocities in boys and 1043 velocities in girls. Over the age range studied, summer velocities accounted for at least 67% of the total yearly growth in boys and 60% of the total yearly growth in girls. Separate two-way ANOVAs (season by age) were used to compare the summer and winter velocities over half-yearly age increments in both sexes. Season and age effects were significant (P < 0.01), but the interaction effect was not significant. The seasonal differences converged in the later years when the summer and winter velocities decreased to zero. The results demonstrate the importance of considering seasonal variation in height velocity in designing studies and in assessing and interpreting growth data. Am. J. Hum. Biol. 9:709-715, 1997. © 1997 Wiley-Liss, Inc.

Growth studies in Jena, Germany: Historical background and secular changes in stature and weight in children 7–14 years

Anthropological investigations have been performed on Jena school children since 1880. The report summarizes the background of the surveys and then considers secular changes in stature and body weight since 1880. The stature of Jena school children shows a major increase over 105 years, ranging from 9.7% to 12.8% in girls and from 9.4% to 14.6% in boys. Changes in estimated growth rates are evident, especially in the preschool ages. Corresponding secular increases in weight between 1880 and 1985 range from 20.7% to 50.4%. Data during and after times of war suggest that females appear to react to changing living conditions more quickly than boys. On the other hand, the smaller variation in the stature of girls suggests more homogeneous and perhaps better buffered growth in girls. Estimated semiannual increments in stature and weight between 1880 and 1985 indicate an increase in the intensity of growth during school age in both sexes and acceleration of the pubertal growth spurt, especially in boys. The average decrease in weight in both sexes between 1932 and 1944 should be emphasized. This is the result of the poor nutritional conditions during the Second World War. Girls show a greater reduction in mean values than boys. © 1996 Wiley-Liss, Inc.

Vertical facial growth and statural growth in girls: a longitudinal comparison

Vertical facial growth and statural growth in girls: a longitudinal comparison

Final growth in girls with Turner syndrome treated with growth hormone. Analysis of the international database of growth monitoring of the company “Kabi Pharmacia” (KIGS)

The completion of growth, which is determined in this study by slowing down the growth rate below 1 cm per year, was observed only in 15 of 640 treated with growth hormone (GH) girls with Turner syndrome (ST), information about which is included in the KIGS database. GH was administered to patients at a dose that ranged within the group within 0.31.0 IU / kg per week, with a multiplicity of 3 to 7 injections per week. The results of the study were presented graphically for each patient. At the beginning of GR therapy, the standard deviation index (SDS) of growth ranged from -2.4 to 1.5 compared with the standards for CT patients developed by M. Ranke. At the beginning of the study, the group indices of median, maximum and minimum SDS growth were 0.3, -2.4 and 1.5, respectively, and by the time the final growth was achieved, their increase was noted to 1.1, -1.8 and 2.7 respectively. The final growth in girls with ST ranged from 132.7 to 161.1 cm. Compared with the predicted growth calculated for each patient, changes in the final growth in the treatment of GH in combination with oxandrolone and ethinyl estradiol ranged from -0.9 to 11.9 cm (median - 5.4 cm), while in the treatment of GH in combination with ethinyl estradiol, the median indicator was 1.6 cm. For the whole group as a whole, the median of final growth was 150.4 cm, in the subgroup of patients treated with GH in combination with oxandrolone and ethinyl estradiol, 152.1 cm and in girls, receiving GH and ethinyl estradiol, 149.3 cm.

Cerebral irradiation causes blunted pubertal growth in girls treated for acute leukemia.

The improved treatment of childhood leukemia is a major achievement. The late effects of the treatment need further investigation. Growth inhibition has been demonstrated in earlier studies. Growth and the timing of puberty were studied in 179 girls who had been treated for acute lymphoblastic leukemia (ALL) in Denmark, Finland, Norway, and Sweden. The patients were divided into two groups according to mode of CNS prophylaxis: with or without cerebral irradiation. Longitudinal analysis of 103 patients showed no difference in prepubertal growth in irradiated and nonirradiated girls. Growth during puberty was normal in girls without irradiation and below normal in irradiated girls. There was no difference in growth between girls after 24 Gy or 20 Gy of cerebral irradiation. Irradiated girls had a final height which was one SD less than expected before puberty and menarche occurred one year earlier than in the nonirradiated girls. Prophylactic cerebral irradiation is the most important factor for subnormal growth after treatment for ALL. There is no short-term influence on growth but the effects of irradiation become apparent several years after therapy when girls enter puberty somewhat early and have a subnormal pubertal growth. Growth and growth hormone (GH) levels should be evaluated several years after CNS irradiation, and treatment with GH and/or luteinizing hormone releasing hormone (LHRH) analogues may be considered.

Окончательный рост у дево­чек с синдромом Тернера, получавших лечение гормоном роста. Анализ международной базы данных мониторинга роста фирмы «Каби Фармация» (КИГС)

The completion of growth, which is determined in this study by slowing down the growth rate below 1 cm per year, was observed only in 15 of 640 treated with growth hormone (GH) girls with Turner syndrome (ST), information about which is included in the KIGS database. GH was administered to patients at a dose that ranged within the group within 0.3–1.0 IU / kg per week, with a multiplicity of 3 to 7 injections per week. The results of the study were presented graphically for each patient. At the beginning of GR therapy, the standard deviation index (SDS) of growth ranged from -2.4 to 1.5 compared with the standards for CT patients developed by M. Ranke. At the beginning of the study, the group indices of median, maximum and minimum SDS growth were 0.3, -2.4 and 1.5, respectively, and by the time the final growth was achieved, their increase was noted to 1.1, -1.8 and 2.7 respectively. The final growth in girls with ST ranged from 132.7 to 161.1 cm. Compared with the predicted growth calculated for each patient, changes in the final growth in the treatment of GH in combination with oxandrolone and ethinyl estradiol ranged from -0.9 to 11.9 cm (median - 5.4 cm), while in the treatment of GH in combination with ethinyl estradiol, the median indicator was 1.6 cm. For the whole group as a whole, the median of final growth was 150.4 cm, in the subgroup of patients treated with GH in combination with oxandrolone and ethinyl estradiol, 152.1 cm and in girls, receiving GH and ethinyl estradiol, 149.3 cm.

Slow baseline growth and a good response to growth hormone (GH) therapy are related to elevated spontaneous GH pulse frequency in girls with Turner's syndrome.

Spontaneous growth and growth responses to GH therapy vary considerably among girls with Turner's syndrome. In an attempt to clarify this variability, we assessed growth parameters, 24-h GH profiles, arginine-stimulated serum GH levels, and plasma insulin-like growth factor-I (IGF-I) concentrations in a group of 41 girls with Turner's syndrome with a mean (+/- SD) age of 13 +/- 3 yr (range, 6.7-18.9). We subsequently treated all girls with biosynthetic GH (24 IU/m2 x week) and documented the growth response after 1 yr of therapy. GH profiles were analyzed according to Pulsar and Cluster, and GH secretion rates were calculated by waveform-independent deconvolution (Pulse). Factor analysis selected the mean 24-h GH secretion rate and number of GH peaks according to Cluster and Pulse as the principal GH profile variables to be used for further analysis. The mean (+/- SD) daily pituitary GH secretion rate was 127 +/- 47 micrograms/L.24 h (range, 37-232). The GH secretion rate correlated inversely with body mass index (r = -0.45; P < 0.01; n = 41). There was no relationship between the GH secretion rate and the growth parameters before or after GH therapy. However, the number of GH peaks (Pulse) correlated negatively with baseline height velocity (r = -0.53; P = 0.03) and was a positive predictor for height velocity increment during the first year of GH therapy (r = 0.71, P = 0.001). The mean (+/- SD) IGF-I level was 217 +/- 91 ng/mL (range, 87-413). There was no relationship between GH secretion rate or growth parameters and IGF-I. However, the number of GH peaks correlated negatively with IGF-I (r = -0.49; P = 0.04; n = 17). We conclude that an elevated spontaneous GH pulse frequency pattern is associated with relatively low IGF-I levels and slow baseline growth in girls with Turner's syndrome and that girls with such a pulse pattern may benefit most from exogenous GH therapy.

The long-term effect of cyproterone acetate on growth in girls with idiopathic precocious puberty. Androcur Study Group in Japan.

To define the effect of cyproterone acetate (CPA) on statural growth, 25 girls with idiopathic precocious puberty who had been treated with CPA were studied retrospectively. The final height SDS was -1.12 +/- 1.16 (mean +/- SD). The daily CPA dose was negatively related to the final height SDS. We divided our subjects into two groups according to the daily CPA dose [low dose, 84.9 +/- 15.4 mg/m2 (n = 19) vs high dose, 135.8 +/- 17.1 mg/m2 (n = 6)]. In the low dose group, the difference of the final height SDS minus height SDS for bone age at the initiation of CPA treatment was 0.55 +/- 1.16 and final height SDS was -0.82 +/- 1.05. The final height was not significantly different from the target height in the low dose group subjects whose target heights were obtained. Since the increment of height age to the increment of bone age during the treatment was significantly less in the group needing and treated with high dose CPA, high doses of CPA may reduce growth velocity more than its suppressive effect on bone maturation. These results suggest that CPA has an effect on statural growth in girls whose clinical symptoms can be controlled with a low dose of CPA, although they have not been compared with final height in untreated Japanese girls.

Growth in girls with adolescent idiopathic scoliosis.

The height development during childhood and puberty was analyzed in 54 girls with adolescent idiopathic scoliosis by the use of the Infancy Childhood Puberty growth model, which is based on healthy Swedish children. This model adjusts adolescent reference values for height for individual age at pubertal maturation. The scoliotic girls had an above-average height 2 years before the onset of the pubertal growth spurt. However, because they displayed an early pubertal maturation as well as a low pubertal gain in height, their values were only slightly higher than the reference mean values at maturity. The results indicate an increased growth hormone activity in childhood in girls with adolescent idiopathic scoliosis.

Growth in Infancy and Childhood in Girls with Turner's Syndrome

We describe spontaneous longitudinal growth in girls with Turner's syndrome (TS), using the infancy-childhood-puberty (ICP) growth model. Length/height during the first 12 years of life was studied in 58 Swedish girls with TS. Their mean length at birth was 47.8 cm (SDS -1.4) and mean height at 12.0 years of age 127.3 cm (SDS -3.0). A clear age-dependent subnormality was observed in the change in length-height SDS (delta SDS). Mean delta SDS values at ages 0.0 to 0.5 and 3.0 to 6.0 years were normal. In contrast, the mean delta SDS at ages 0.5 to 3.0 and 6.0 to 12.0 years were subnormal. The onset of the childhood growth component (normally located between 0.5 and 1.0 year of age) was, on the average, delayed by 0.28 year. This accounts for the subnormality of delta SDS at 0.5 to 3.0 years of age. About 50% of the variation in height at 12.0 years of age, as determined by a multiple linear regression analysis, was significantly explained by length at 0.5 year of age, age at the onset of the childhood component, and delta SDS at 6.0 to 12.0 years of age.

Disproportionate Body Growth in Girls with Adolescent Idiopathic Scoliosis

Two thousand, one hundred and eighty-nine southern Chinese women, aged 8-21 years, were studied: 541 with adolescent idiopathic scoliosis (176 treated with posterior spinal fusion and Harrington instrumentation, 150 with brace, and 215 who did not require any treatment), and 1,648 age-matched normal controls from schools and colleges. Scoliotic girls treated at Duchess of Kent Children's Hospital were examined clinically, radiologically, and anthropometrically, including a roentgenogram of the left hand for bone age, at yearly intervals from their first visit to hospital until maturity. Leg:spine and leg:arm ratios were calculated to study the proportionate body growth. The data obtained at first visit and at maturity for each treatment group were compared within treatment groups, and also with normal controls (all age-matched comparisons). The results are summarized as follows: The comparison of leg:spine ratio between fusion, brace, and untreated groups at first visit using uncorrected spinal length showed inconsistent results, but when these ratios were calculated using spinal length corrected for scoliosis, the results were all consistent, showing no significant difference between these groups at first visit. At maturity, leg:spine ratios, using either uncorrected spinal length or corrected spinal length, were highly significantly greater for the fusion group compared to the brace and untreated groups. The leg:spine ratio comparisons of scoliosis groups against normals showed that brace and fusion groups had highly significantly greater ratios at first visit and at maturity, using uncorrected spinal length. Similar comparison using corrected spinal length showed minimum or no difference at first visit, but at maturity, only the fusion group had a significantly greater ratio than normals.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth prognosis and growth after menarche in primary hypothyroidism.

The long term growth of 20 girls and nine boys with juvenile primary hypothyroidism was studied until they reached final height. At diagnosis the girls had a mean age of 8.8 years (range 3.0-13.0); mean bone age was 5.4 years. The mean age of the boys at diagnosis was 9.5 years (range 3.7-14.2); mean bone age was 6.3 years. The patients were treated with thyroxine 100 micrograms/m2/day and serum thyroxine concentrations were maintained in the normal range. During treatment the rate of skeletal maturation exceeded the change in chronological age. Initial mean height SD score for bone age before treatment in the girls was +0.59 and after 11 years of treatment fell to -0.55 Mean height SD score for bone age in the boys decreased from +1.6 to -0.87 during treatment. In the girls the onset of puberty was 1.2 years later than the normal population but the duration of puberty was reduced. Mean age (SD) of menarche was 13.8 (1.7) years. The pattern of growth in girls with treated hypothyroidism was abnormal as growth continued after menarche, at a time when normal girls have almost stopped growing. During the second year after menarche our patients still had a mean growth velocity of 4.1 cm/year. Our data suggest that juvenile primary hypothyroidism results in a permanent height deficit. In addition, there is a loss of the normal harmony between growth and sexual maturation in girls, despite adequate treatment, in that growth continues for much longer after menarche than in normal girls.