Bone Age Progression Research Articles

Effect of major burn injury on bone age progression

Effect of major burn injury on bone age progression

Central precocious puberty in a girl with Williams syndrome: the result of treatment with GnRH analogue

Williams syndrome (WS) is a well-known microdeletion syndrome characterized by specific facial features, retardation in growth and development, typical personality and cardiac defects. Poor growth potential is further affected by central precocious puberty (CPP) which is frequent in these patients. A WS patient with CPP is presented, whose pubertal development and bone age progression were arrested by administration of GnRH analogues. The case is reported to discuss the role of GnRH analogues for management of CPP in patients with WS.

Bone Age Progression during the First Year of Growth Hormone Therapy in Pre-Pubertal Children with Idiopathic Growth Hormone Deficiency, Turner Syndrome or Idiopathic Short Stature, and in Short Children Born Small for Gestational Age: Analysis of Data from KIGS (Pfizer International Growth Database)

Background/Aims: The beneficial effects of growth hormone (GH) therapy on statural growth in children are well established, but the effects on skeletal maturation are less clear. The progression of bone age (BA) was therefore studied during the first year of GH treatment in pre-pubertal children with idiopathic GH deficiency (GHD), Turner syndrome (TS) or idiopathic short stature (ISS), and in short pre-pubertal children born small for gestational age (SGA). Methods: Cross-sectional data on 2,209 short children with idiopathic GHD, 694 with TS, 569 with ISS and 153 with SGA were analysed. Longitudinal data were also analysed from 308 children with idiopathic GHD, 99 with TS, 57 with ISS and 29 with SGA. All patients included in the study were enrolled in KIGS (Pfizer International Growth Database) and were being treated with recombinant human GH (Genotropin^®). BA was assessed using the Greulich and Pyle method at baseline and after 1 year of GH therapy. Results: In all groups of patients the mean progression of BA was 1 year during the year of GH therapy, although there was considerable individual variation. Progression of BA was not correlated with chronological age, BA, height SD score (SDS) or body mass index SDS at the onset of GH therapy. There was also no consistent effect of the GH dose on BA progression. Conclusion: Progression of BA appears to be normal in patients receiving GH in these diagnostic groups, at least over the first year of treatment in pre-puberty.

Growth Hormone Effects on Adult Height in Idiopathic Short Stature

Growth Hormone Effects on Adult Height in Idiopathic Short Stature

The Effect of Letrozole on Bone Age Progression, Predicted Adult Height, and Adrenal Gland Function

A common problem in pediatric endocrinology is limited growth potential resulting from advancing skeletal maturation. We determined the efficacy of letrozole, an aromatase inhibitor, on delaying bone age advancement in adolescent males with limited growth potential. Twenty-four patients met the study inclusion criteria. Six patients treated with androgen were analyzed separately. Low-dose ACTH stimulation tests were performed to ascertain the effect of letrozole on adrenal gland function. In patients not on androgen, bone age progression decelerated from 1.51+/-0.57 (deltabone age/deltachronological age) before treatment to 0.68+/-0.66 on therapy (mean duration 12.4 months; p <0.0005). Predicted adult height standard deviation scores (SDS) increased from -1.41+/-0.54 to -0.64+/-0.65 on treatment (p <0.0005). Similar results were noted in androgen-treated patients. Approximately one-fourth of patients displayed subnormal responsiveness to ACTH. In summary: 1) letrozole decelerates skeletal maturation, resulting in significant increases in predicted adult height, and 2) letrozole causes mild adrenal suppression.

TW3 bone age: RUS/CB and gender differences of percentiles for score and score increments

Background: Longitudinal data on bone age progression is scarce.Aim: The study aimed to present reference values for Tanner–Whitehouse 3 (TW3) bone age score and score increments, and to provide means and standard deviations of appearance time for all TW3 stages. Gender differences and differences between radio ulna and short bones (RUS) and carpal bone (CB) scores were studied.Subjects and methods: Bone age data collected for ages 3 months to 20 years in 232 subjects during the First Zurich Longitudinal Study (1954–1976) were used. Smoothed empirical percentiles of TW3 RUS and CB scores for age, of score increments for age and of score increments for attained score are presented. Means and standard deviations of the appearance times are calculated by parametric censored regression.Results: There are clear differences between the RUS and CB scores and between the genders. Boys are delayed with respect to girls, with different delays for RUS and CB. For RUS, differences in maturation reflect the known differences of physical growth, with a later and more intense peak in boys. For CB, there is little difference in timing and intensity. However, girls reach the final score about 2 years earlier than boys. The consistently earlier mean appearance times in girls indicate that skeletal maturation is, already in childhood, more rapid in girls than in boys. There are significant gender differences in the sequence of appearance.Conclusion: Reference values for TW3 score and score increments and mean appearance times for stages add to existing knowledge and indicate important RUS/CB and gender differences, whose sources are largely unknown.

Management and outcome of central precocious puberty

Management and outcome of central precocious puberty

Combined therapy with GnRH analog plus growth hormone in central precocious puberty.

GnRH analogues (GnRHa) arrest pubertal development, and slow growth velocity (GV) and bone maturation, thus improving adult height in central precocious puberty (CPP). In some patients, however, GV decreases to such an extent that it compromises the improvement in predicted adult height (PAH) and therefore the addition of GH is suggested. Of 20 patients with idiopathic CPP (treated with GnRHa [depot-triptorelin] at a dose of 100 microg/kg every 21 days i.m. for at least 2-3 yr) whose GV fell below the 25th percentile for chronological age (CA), ten received, in addition to the GnRHa, GH at a dose of 0.3 mg/kg/wk, s.c. 6 days weekly, for 2-4 yr. Ten patients matched for BA, CA, and duration of GnRHa treatment who showed the same growth pattern but refused GH treatment, served to evaluate the efficacy of the addition of GH. No patient showed classical GH deficiency. Both groups discontinued treatment at a comparable BA (mean +/- SEM): 13.2 +/- 0.2 yr in GnRHa + 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 + GnRHa showed an adult height significantly higher (p<0.001) than pretreatment PAH (160.6 +/- 1.3 vs 152.7 +/- 1.7 cm). Height SDS for BA significantly increased from -1.5 +/- 0.2 at start of GnRHa to -0.21 +/- 0.2 at adult height (p<0.001). Target height was significantly exceeded. The GnRH alone treated group reached an adult height not significantly higher than pretreatment PAH (157.1 +/- 2.5 vs 155.5 +/- 1.9 cm). Height SDS for BA did not change (from -1.0 +/- 0.3 at start of GnRHa to -0.7 +/- 0.4 at adult height). Target height 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 GnRH analogue while in patients treated with GnRH analogue alone the gain was just 1.6 cm +/- 1.2 (p=0.001). Furthermore, no side effects, bone age progression, or ovarian cysts, were observed in GnRHa + GH treated patients. 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 to conventional treatment with GnRH analogues in patients with central precocious puberty, and with a decrease in growth velocity so marked as to impair predicted adult height to below the third percentile.

Effects of puberty on bone age maturation in a girl after medulloblastoma therapy

Background: Craniospinal radiotherapy for malignant brain tumors can result in a variety of neuroendocrine disturbances, among which are the development of growth hormone deficiency and early puberty, which can markedly reduce adult height. Methods: The authors report the case of a girl who received craniospinal radiotherapy for a medulloblastoma at the age of 3.4 years. At 9.1 years, growth hormone therapy was started, and spontaneous onset of puberty (Tanner stage B2) occurred at age 10.3 years. Interval until menarche was short, at only 0.9 years. Results: Although chronologic age at appearance of Tanner stages was within the normal range, the patient showed a rapid acceleration in skeletal maturation, resulting in adult short stature. Conclusion: Bone age seems to be a more precise parameter for biologic maturation in some patients after craniospinal irradiation than is clinical assessment of pubertal stages. Thus, if progression of bone age and decreasing final height predictions are noted, puberty should be stopped with gonadotropin-releasing hormone analogs, even if pubertal development seems to be adequate for chronologic age, because this increases the remaining time for growth hormone treatment.

Bone age progression during five years of substitutive therapy for the induction of puberty in thalassemic girls--effects on height and sitting height.

It is known that in thalassemic patients there is a disproportion between lower and upper segments whose causes have not yet been identified. We evaluated whether the administration of estrogens to induce puberty in hypogonadic thalassemic girls caused an inappropriate acceleration of bone maturation and whether this had a negative influence on final and sitting height. Twelve thalassemic patients with spontaneous puberty (Group A) and seven patients with hypogonadism (Group B) were studied. The mutations of the beta gene were identified by DNA analysis. We took into account four observations, ranging from the onset of spontaneous puberty in group A or the start of substitutive therapy in group B, to 5 years later. At each observation we considered: chronological age (CA), bone age (BA), height (Ht) expressed in cm and as standard deviation score (HtSDS) calculated with respect to CA (HtSDSCA) and BA (HtSDSBA), growth spurt, sitting height, expressed as SDS (SH-SDS), and height gain (HG). The delta BA and delta CA were calculated between the first and the final observation values to evaluate the bone age acceleration (delta BA/delta CA). No acceleration of BA was noted. delta BA/delta CA was 0.98 +/- 0.1 in group A and 0.89 +/- 0.1 in group B (p > 0.05). All patients in group B had the most severe form (beta degree/beta degree) of thalassemia. During the final observation, SH-SDS was -1.43 +/- 1.2 and -2.9 +/- 0.6 in group A and B respectively (p < 0.002), while no difference between the two groups for HtSDSCA and HtSDSBA was observed. HG was greater in group A than in group B (17.7 +/- 5.4 cm vs 10.8 +/- 5.2 cm) (p < 0.002), such as the spurt 8.6 +/- 1.4 cm (group A) and 6.1 +/- 2.6 cm (group B) (p < 0.05). Girls with hypogonadism did not show an inappropriate acceleration of BA, as they reached near final height similar to girls with spontaneous puberty. The auxological parameters showed a more severe body disproportion with the prevalence of the lower segment in the hypogonadic girls. This could be explained by a higher degree of bone marrow hyperplasia related to the most severe form of thalassemia and a higher blood consumption. As a consequence, damage at the vertebral level might determine an inability of the bone tissue to respond to estrogens. We suggest beginning estrogen therapy earlier in order to obtain better truncal growth.

Central Precocious Puberty in A 20-week Old Female Born Prematurely: A Case Report (and Clinical Clue?)

<h3>Background</h3> Over the past decade. newer gonadotropin assays have enhanced our understanding of the "GnRH pulse generator" and GnRH analogues have revolutionized the treatment of central precocious puberty. If allowed to progress, precocious puberty can have serious consequences both physically and psychosocially. Premature birth has been recognized as a risk tactor for early sexual maturation in the temale child but to our knowledge there have been no prior reports of this condition manifesting as early as infancy. <h3>Case</h3> T.D. was born at 26 weeks gestation and had suffered many expected complications of premannity including: sepsis, retinopathy and bronchopulmonary dysplasia. At 20 weeks of age. (6 weeks corrected age), while still in hospital, she was referred to paediatric gynaecology because of blood in her diaper. At the time of this initial assessment, she had Tanner II breast buds and a protruding estrogenized hymen with physiologic leukorrhea. The blood was telt to be secondary to local irritation of the prominent and exposed hymen but the features of estrogenization were Surprising. Her only medications were iron and vitamins, but a brief course of Aldactazide had been discontinued one month prior. During the month prior to presentation there was an apparent acceleralion in the rate of growth involving body length and head circwnterence. Investigations revealed a markedly elevated estradiol of 250pmol/L, an FSH of 7U/L, and a normal TSH. Abdominopelvic imaging showed bilaterally enlarged ovaries (2.4cm) with multiple tollicles, but the uterus was not well seen and the adrenal glands were nonnal. Bone age was not advanced. CT and MRI of the head showed diffuse atrophy and bilateral retinal detachment, but no localized lesion otherwise. An LHRH stimulation test demonstrated a positive response yielding an LH level of 16U/L (prepubertal <8). Three months later there had been neither regression nor progression of the tindings on examination. A repeat work up is scheduled for April/98 - stay tuned! <h3>Conclusion</h3> As no focal cause has been identitied for the apparenl central activation of the hypothalamic pituitary ovarian (HPO) axis, we have generated two possible explanations. # 1) This is a rare case of true precocious puberty, whether idiopathic or brain injury related, and it will self-resolve or progress or, #2) the patient is manifesting physiological events that have not yet succumbed to "central restraint" She was old enough that maternal and placental estrogen effects should have regressed but the HPO axis can remain active and pulsatile for several years before undergoing the mid-childhood nadir. In the former scenario, treatment (LHRH analogue) will be withheld unless bone age advancement and/or progression are detected. In other scenario, this case may provide more insight into control mechanisms of the HPO axis, the GnRH pulse generator after birth and the onset of puberty.

Variation of bone age progression in healthy children.

Bone age assessments were related to auxological variables in 407 Italian boys, between 7 and 12 years of age, in order to elucidate the factors that affect the rate of skeletal maturation and to examine the possibility of using measures of skeletal maturation of evaluate individual patients. Using the radius-ulna-short bones (RUS) method of assessment, bone age velocity was greater in the Italian boys than for the UK reference standards, although there was considerable interindividual dispersion around the mean. Bone age velocity and height velocity were poorly correlated, and there was little correlation between skeletal and pubertal maturation. There was a slight positive correlation between bone age velocity and height SDS and between bone age velocity and body mass index. Bone age estimations using RUS were greater than those obtained using the carpus. In conclusion, the marked interindividual deviation in measured bone ages makes it difficult to relate data on an individual basis to other measures of growth and maturation

Gonadotropin-releasing hormone agonist treatment of girls with constitutional short stature and normal pubertal development.

GnRH agonists have been proposed to improve final height in patients with constitutional short stature. We treated 31 girls, aged 11.9 +/- 1 yr (mean +/- SD), with short stature, recent pubertal onset and predicted final height of 155 cm or less with depot triptorelin. During the 23 +/- 4 months of treatment, bone age progression was 0.6 +/- 0.3 bone age yr/yr, and growth velocity declined from 7 +/- 2 to 4 +/- 0.8 cm/yr (P < 0.0001). Height prognosis, calculated by the Bayley-Pinneau method, progressed from 149.6 +/- 3.4 to 151.8 +/- 4 cm at the end of treatment (+2.2 +/- 2.6 cm; P < 0.0001). When treatment was interrupted, growth velocity slightly increased to 4.6 +/- 1.6 cm/yr, and bone age maturation was accelerated: 1.3 +/- 0.4 bone age yr/yr during the first posttreatment year. At the last visit, 26 +/- 9 months after interruption of treatment, bone age was 14.9 +/- 1.3 yr (> or = 13.5 yr in all patients), height was 149.1 +/- 4 cm, and final height prognosis was 150.6 +/- 3.6 cm. Final height prognosis was 1 +/- 2.3 cm greater than pretreatment height prognosis (P < 0.02) and 1.2 +/- 2.2 cm below the height predicted at the end of the treatment (P < 0.01). No major side-effect was observed. Height SD score decreased during treatment with GnRH agonist from -2.3 +/- 0.9 to -2.7 +/- 0.7 SD score (P < 0.0001). We conclude that 2 yr of depot triptorelin-induced pubertal delay has a limited effect on near-final height in girls with constitutional short stature and that the growth benefit observed does not currently justify the use of GnRH agonists, given their cost and potential side-effects.

Growth promotion by oxandrolone in a girl with short stature and early pubertal development treated with growth hormone and gonadotropin‐releasing hormone‐analogue. A case study

Gonadotropin-releasing hormone (GnRH)-analogues are widely used for treating precocious puberty, and occasionally in short patients and patients with growth-hormone deficiency, in order to delay pubertal development and increase final height. Yet, many of these children only decelerate growth velocity and neither improve in final height nor even in height prediction. As GnRH-analogue treatment dramatically reduces sexual steroid levels, I hypothesized the need for steroid hormone substitution during this treatment. Growth promotion was tried in a healthy girl, with a very unsatisfying height prediction of only 144 cm, using a combination of GnRH-analogue (75 micrograms/kg/4 weeks), plus growth hormone (4 IU/m2/d), plus oxandrolone (1 mg/d). Knemometric measurements of lower leg growth velocity demonstrated that GnRH-analogue alone depresses growth. Additional GH administration only sporadically increases growth velocity, and not until the additional substitution of oxandrolone does growth velocity catch up and return to near pretreatment level. In spite of a 10.3 cm increase in body height during the 15-month period of observation, little bone age progression took place, and height prediction improved from 144 cm to over 149 cm after 9 months, and to 152 cm after 15 months of observation.

Use of Combined Gn-RH Agonist and hGH Therapy for Better Attaining the Goals in Precocious Puberty Treatment

We studied 30 girls (age 6.36 +/- 1.21 years, range 4.6-8.8) affected by idiopathic precocious puberty with significant reduction of height velocity (below the 25th centile) at the end of 1 year of Gn-RHa (triptorelin intramuscular depot) treatment, to evaluate GH-IGF-I axis activity and the effects of combined Gn-RHa plus hGH therapy. After 12 months, 15 patients continued Gn-RHa and started hGH therapy for 12 months, while 15 continued treatment with Gn-RHa alone (control group). We evaluated height velocity, bone age, urinary GH, serum IGF-I and IGFBP-3 levels throughout the study; plasma GHBP levels were determined only in the first 12 months of Gn-RHa treatment. Height velocity decreased significantly during Gn-RHa treatment; it increased significantly and became higher than the control group after 12 months of Gn-RHa plus hGH treatment. During Gn-RHa therapy alone, bone age progressed less than chronological age, while in the 12 months of Gn-RHa plus hGH treatment there was a slight nonsignificant increase in bone age progression in comparison to controls. Serum IGF-I and IGFBP-3 levels decreased significantly at 12 months of Gn-RHa therapy and increased significantly after Gn-RHa plus hGH treatment. Urinary GH levels showed the same behavior. Plasma GH binding to peak II-BP, slightly lower than the prepubertal normal range before treatment, significantly increased after 12 months of Gn-RHa treatment. Therefore, in these girls, during Gn-RHa treatment alone, we have a reduction in GH-IGF-I axis activity. During Gn-RHa plus hGH therapy there was a significant increase in height velocity, in urinary GH levels, in serum IGF-I and IGFBP-3 levels. Bone age did not seem to advance faster than chronological age and this may imply a better prediction in adult height. In our opinion, only in a small percentage of patients affected by precocious puberty (with a very low predicted adult height or an important reduction of growth velocity during Gn-RHa treatment) may an association with hGH therapy be useful.

Precocious puberty in a case with probable Angelman syndrome

The authors report a 9-year-old girl with mid-facial hypoplasia, maxillary hypoplasia, prognathia, microbrachycephaly, mouth opening and protruding tongue. She also had psychomotor retardation such as mental retardation and speech delay. Frequent laughter fits and seizure disorder was also noted. Although the high resolution chromosome study failed to demonstrate any deletion of chromosome 15q, the clinical picture was compatible with Angelman syndrome. Breast development at the age of six and rapid progression of bone age was noted at follow up. After a series of examinations, the diagnosis of gonadotropin-dependent precocious puberty was made. MRI of brain revealed an intermediate cyst in the pituitary gland and slightly enlarged pineal gland. However, serum α-fetoprotein and β-HCG were undetectable and the size of the pineal gland remained the same at the 1-year follow-up. She was treated with long-acting GnRH analogue and valproic acid. The combination of precocious puberty and Angelman syndrome has not been reported before and such association needs further experience for clarification.

Diagnosis and treatment of central precocious puberty--can final height be improved? German/Dutch Central Precocious Puberty Study Group.

Central precocious puberty is characterized by premature activation of the hypothalamic gonadotrophin-releasing hormone (GnRH) pulse generator, resulting in accelerated growth and bone maturation with clinical signs of gonadarche before the age of 8 years in girls and 9 years in boys. In rapidly progressing central precocious puberty, the plasma luteinizing hormone (LH) response to exogenous GnRH exceeds the reference range for sex and stage of puberty, and the ratio of LH:follicle-stimulating hormone after GnRH is usually above 1. Short adult stature, with unfavourable body proportions, i.e. an increased upper:lower segment ratio, is probably the only handicap of idiopathic central precocious puberty that persists into adulthood. This cannot be avoided by treatment with either medroxyprogesterone or cyproterone acetate. Following the first report of pituitary-gonadal suppression in a 2-year-old girl with central precocious puberty using daily injections of the gonadotrophin-releasing hormone (GnRH) agonist deslorelin, various short-acting GnRH agonists have been studied in children with central precocious puberty. Some of the older patients treated for shorter periods have now reached adult or near-final height. By 1985, slow-release (depot) GnRH agonists, such as triptorelin and later leuprorelin, were available. These are injected only once every 4 weeks instead of daily or given by nasal spray six times daily, making long-term treatment much more acceptable to patients and their parents. Moreover, suppression of gonadarche is more complete with long-acting (e.g. triptorelin) compared with short-acting (e.g. buserelin) agonists, resulting in significantly slower bone age progression and, thus, greater improvement in predicted, and probably also in achieved, final height.(ABSTRACT TRUNCATED AT 250 WORDS)

PUBERTAL DELAY IN BOYS AS A MODEL OF THE ROLE OF GH, IGFI AND TESTOSTERONE IN THE PUBERTAL GROWTH

The respective role of the sex steroids, GH and IGFI increase in the pubertal growth acceleration is not clear. Clinical data suggest that sex steroids have a direct and preponderant effect. Girls with central precocious puberty have an early growth acceleration which is Independent of plasma IGFI level (Horm Res, 1991, p116). 72 boys were evaluated for short stature (<−2SD) and pubertal delay (P1 stage >14 yr). All had GH peak after arginine insulin stimulation >8 ng/ml. They were classified in 2 groups according to their plasma testosterone (T, ng/ml) : Group I 0-1 (0.5 ± 0.1, n=54) and II 1-2 (1.5± 0.2, n=18). The mean age and height level were similar 15 ±0.1/15± 0.2 yr and −3.0±0.1/−3.4 ± 0.2 SD in I/II respectively. m±SE, p<*0.05, ***0.001T correlated with plasma IGFI (r=0.42, p<0.001) but not with GH peak. Height gain during the preceding year did not correlate with GH peak, IGFI or T.Conclusion. The Initial Increase in testosterone secretion in boys is accompanied by a significant and important increase in GH peak and in plasma IGFI. In spite of this Increase, growth velocity remains in the prepubertal level. This is at variance with which occurs in girls : a small increase in estradiol secretion induces growth acceleration before incrasing plasma IGFI. These data suggest that the increase in GH/IGFI is not critical for the pubertal growth acceleration in boys and that plasma testosterone levels >2 ng/ml are required to induce growth acceleration and bone age progression.

Two-year Results of Sustained-Release Leuprorelin Acetate (TAP-144-SR) Treatment in Children with Central Precocious Puberty

The effect of leuprolide acetate in depot suspension (TAP-144-SR), a synthetic analog of luteinizing hormone-relasing hormone, was studied in 34 patients with central precocious puberty. The doses were adjusted according to changes in hormone levels or clinical manifestations. The treatment was terminated or prematurely discontinued within 96 weeks in seven patients but was continued for more than 96 weeks in 27 patients.Mean basal and peak gonadotropin levels in response to LH-RH test decreased to the normal range from the fourth week of treatment and were maintained at prepubertal levels till 96 weeks. Mean concentrations of plasma testosterone and estradiol were mostly maintained at low levels during the treatment with TAP-144-SR.At 96 weeks of treatment, breast development had progressed in three, regressed in 10 and remained at the same stage in the other patients. The growth velocity was significantly suppressed from the pretreatment rate of 9.83 ±5.70 cm/year to 5.81 ± 2.80cm/year at 48 weeks of treatment (32 patients) and further to 4.87 ± 2.20 cm/year at 96 weeks (27 patients). The ratio δ bone age/ δchronological age for all the patients was 0.83 ± 0.78 at 48 weeks of treatment and 0.69 ± 0.47 at 96 weeks. The progression of bone age was suppressed by the treatment, especially in those patients with an initial bone age of 12 years or older.Of the adverse effects that appeared, those presumably related directly to TAP-144-SR were only genital bleeding in the stimulatory phase following the initial dose, and redness and induration at the site of injection. The once-monthly injection is a regimen well tolerated by children, and when its reliability and efficacy are considered, TAP-144-SR will be the drug of first choice in the treatment of precocious puberty.

Spontaneous growth in turner syndrome: Evidence for a minor pubertal growth spurt

Spontaneous growth of 141 untreated girls with Turner syndrome was analysed. Of the patients 25% were born prematurely; their weight and height were normal when compared to prematurely born healthy infants. However, birth weight and height was significantly retarded in Turner patients born at term. A curve for height and growth velocity for the age range 0-16 years was constructed with a sensitive statistical method. By use of a mathematical model equations were created for calculating z-scores and the related percentiles for the height of individual patients at given age. Median height of 18 untreated patients at 18 years was 143.8 cm. Analysis of growth velocity revealed a minor but significant growth spurt at the age of 12.5 years. This growth spurt was also detectable in patients without signs of spontaneous puberty and occurred later in patients with 45,X0 karyotype. Bone age progression was linear up to the age of 7.5 years and decelerated thereafter.