Long-term growth in juvenile acquired hypothyroidism: the failure to achieve normal adult stature

It has been suggested that complete catch-up growth is achieved with treatment in patients with juvenile acquired hypothyroidism. We tested this assumption by examining long-term growth in 18 girls (mean [+/- SD] age, 11.4 +/- 2.7 years; bone age, 6.2 +/- 3.1 years) and 6 boys (age, 10.6 +/- 4.7 years; bone age, 6.4 +/- 2.7 years) with severe primary hypothyroidism (serum thyroxine level 1.1 +/- 0.3 micrograms per deciliter [13 +/- 4 nmol per liter]). At diagnosis, heights were 4.04 +/- 0.5 and 3.15 +/- 0.4 SD below the mean heights for age of normal girls and boys, respectively. The patients were treated with levothyroxine (3.4 +/- 0.3 micrograms per kilogram of body weight per day) to maintain normal thyroid function. During the first 18 months of therapy, the children's skeletal maturation exceeded the maturation expected for their statural growth, regardless of whether or not they were undergoing pubertal development. Predictions of decreased adult height were based on these observations. At maturity, girls and boys stood approximately 2 SD below normal adult stature, at 149 +/- 5.0 cm and 168 +/- 5.1 cm, respectively. Heights at maturity were also lower than midparental heights (P less than 0.01) and lower than pre-illness standard-deviation scores for height (P less than 0.01). The deficit in adult stature was significantly related to the duration of hypothyroidism before treatment (P less than 0.01). We conclude that despite treatment, prolonged juvenile acquired hypothyroidism results in a permanent height deficit related to the duration of thyroxine deficiency before treatment.     

CNP在GH促进GnRHa治疗中大骨龄、青春中后期CPP/EFP女孩线性生长机制中的作用

 目的:探讨生长激素（growth hormone,GH）改善促性腺激素释放激素类似物（gonadotropin-releasing hormone analogue,GnRHa）治疗中大骨龄、青春中后期中枢性性早熟（central precocious puberty,CPP）或快速进展型早发育（early and fast puberty,EFP）女孩线性生长的近期疗效,以及C型利钠肽（C-type natriuretic peptide,CNP）在GH促线性生长机制中的作用。方法:22例骨龄≥11.5岁、预测成年身高（predicted adult height,PAH）严重受损、青春中后期的特发性CPP或EFP女孩分为2组各11例：（1）单用GnRHa组:仅用GnRHa（每4周缓释型曲普瑞林60～80 μg/kg,im）治疗;（2）联用GH组:联用GnRHa和GH（每周1 U/kg,分6~7次睡前sc）治疗。每3个月测量身高和体重,检查性征;治疗开始和治疗6个月末行骨龄检查,并检测血清CNP氨基端前体（amino-terminal pro-C-type natriuretic peptide,NTproCNP）、胰岛素样生长因子1（insulin-like growth factor 1,IGF-1）及1型前胶原氨基端伸展肽（procollagen type 1 amino-terminal propeptide,P1NP）的浓度。比较治疗前及治疗后6个月的身高增长速度（height velocity,HV)、按骨龄身高的标准差分值（height SD score for bone age,HtSDSBA）、PAH及上述血清指标的变化。结果:（1）联用GH组治疗6个月的HV、HtSDSBA增值（ΔHtSDSBA）和PAH增值（ΔPAH）均显著高于单用GnRHa组(P<0.01)。（2）联用GH组治疗6个月末与治疗开始时比较,血清NTproCNP、P1NP浓度和IGF-1浓度均无显著性差异。（3）单用GnRHa组治疗6个月末的血清NTproCNP和P1NP浓度则均较治疗开始时显著下降（P<0.05),IGF-1浓度则无显著差异。结论: 对于大骨龄、青春中后期的特发性CPP或EFP女孩,GnRHa联用GH能促进线性生长,有效改善预测成年身高。GH的促生长作用不依赖于血清IGF-1水平的变化,而可能部分与CNP介导的长骨生长加速有关。     

Precocious puberty and statural growth

Precocious puberty results mostly from the precocious activation of the gonadotropic axis. Although the age limits have recently been discussed, most physicians consider that onset of pubertal development before the age of 8 years in a girl or 9 years in a boy warrants at least a clinical and bone age evaluation by a paediatric endocrinologist. The major concern in precocious puberty is the underlying condition, and central nervous system or gonadal neoplasm have to be formally excluded as a first step in the diagnosis. A secondary concern is height, since precocious puberty leads to accelerated growth, accelerated bone maturation and ultimately reduced stature. Precocious puberty is heterogeneous and strict criteria should be used to define it, both in terms of age and in terms of potential for progression. Depot forms of GnRH agonists are now the standard treatment for progressive central precocious puberty and aim at alleviating the clinical symptoms of early pubertal development, their psychological consequences and the effects on growth. Here, we review the consequences of both central and gonadotropin-independent precocious puberty on adult stature and the information available on outcomes using the therapeutic regimens currently available. In girls with progressive precocious puberty, all published evidence indicates a gain of adult height over height predicted before treatment or over untreated historical controls. However, the apparent height gain (derived from the comparison of predicted and actual heights) is very variable, in large part due to the inaccuracy of height prediction methods. In girls with onset of puberty at the lower half of the normal age (8-10 years) distribution, trials using GnRH agonists have given negative results (no benefit of treatment). In boys, precocious puberty is rare and fewer results are available but point in the same direction. The most appropriate time for interrupting the treatment is still controversial. In conclusion, GnRH agonists restore adult height in children when it is compromised by precocious puberty.     

Effect of growth hormone treatment on adult height of children with idiopathic short stature. Genentech Collaborative Group

BACKGROUND: Short-term administration of growth hormone to children with idiopathic short stature results in increases in growth rate and standard-deviation scores for height. However, the effect of long-term growth hormone therapy on adult height in these children is unknown. METHODS: We studied 121 children with idiopathic short stature, all of whom had an initial height below the third percentile, low growth rates, and maximal stimulated serum concentrations of growth hormone of at least 10 microg per liter. The children were treated with growth hormone (0.3 mg per kilogram of body weight per week) for 2 to 10 years. Eighty of these children have reached adult height, with a bone age of at least 16 years in the boys and at least 14 years in the girls, and pubertal stage 4 or 5. The difference between the predicted adult height before treatment and achieved adult height was compared with the corresponding difference in three untreated normal or short-statured control groups. RESULTS: In the 80 children who have reached adult height, growth hormone treatment increased the mean standard-deviation score for height (number of standard deviations from the mean height for chronologic age) from -2.7 to -1.4. The mean (+/-SD) difference between predicted adult height before treatment and achieved adult height was +5.0+/-5.1 cm for boys and +5.9+/-5.2 cm for girls. The difference between predicted and achieved adult height among treated boys was 9.2 cm greater than the corresponding difference among untreated boys with initial standard-deviation scores of less than -2, and the difference among treated girls was 5.7 cm greater than the difference among untreated girls. CONCLUSION: Long-term administration of growth hormone to children with idiopathic short stature can increase adult height to a level above the predicted adult height and above the adult height of untreated historical control children.     

雌激素与C型利尿钠肽介导的青春期线性生长的关系

 目的：探讨青春期女孩雌激素与C型利尿钠肽（C-type natriuretic peptide, CNP）介导的长骨生长的关系,及两者在中枢性性早熟女孩GnRHa治疗相关身高增长减速中的作用。方法：（1）检测56例正常不同青春发育期女孩空腹血清雌二醇（E2）、CNP的N端前肽（N-terminal propeptide of CNP, NT-proCNP）、胰岛素样生长因子1（insulin-like growth factor 1, IGF-1）以及骨形成生化标志物N端中段骨钙素（N-terminal mid-fragment of osteocalcin, N-MID OC）的浓度。（2）检测13例特发性中枢性性早熟（idiopathic central precocious puberty, ICPP）女孩在促性腺激素释放激素类似物（gonadotropin-releasing hormone analogue, GnRHa）治疗开始、治疗6个月末及12个月末时血清E2、NT-proCNP、IGF-1和N-MID OC水平,并计算身高增长速度（height velocity, HV）。结果：(1) 在56例正常不同青春发育期女孩中,与青春前期相比,血清NT-proCNP、IGF-1、E2和N-MID OC浓度均自青春早期开始升高（P<005或P<0.01）;血清NT-proCNP在青春中期维持高水平,至青春后期达峰值（P<005）;血清IGF-1和E2浓度于青春中期继续升高（P<0.01）,亦至青春后期达峰值（P<0.01）;血清N-MID OC浓度于青春中期达到峰值（P<0.05）,青春后期则开始下降（P<0.05）。(2) ICPP女孩GnRHa治疗6个月末HV、血清NT-proCNP和血清N-MID OC均较治疗开始时显著下降（P<0.05）,但与12个月末相比无显著差异;GnRHa治疗开始、治疗6个月末和12个月末后血清IGF-1浓度无显著差异;治疗后血清E2显著下降并回复至青春前期水平（P<0.05）。结论：女孩血清NT-proCNP水平随青春发育进程升高,与血清E2和IGF-1浓度平行,提示女孩青春期升高的雌激素在一定程度上可诱导CNP介导的青春期生长加速。ICPP女孩经GnRHa治疗后,随着雌激素受抑,生长速度减慢,血清NT-proCNP浓度下降,并与生长速度和骨形成平行,提示GnRHa致ICPP女孩生长减速部分缘于雌激素被抑制后CNP介导的长骨生长减慢。     

Pubertal height gain: male-female and interpopulation comparisons

Data are not available as to the exact age of the start of the pubertal growth spurt (or age at its conclusion) in various populations. As an initial approach, contribution of the pubertal gain to overall height was examined, using age 9 as the start of puberty in girls and age 11 in boys. Data were analyzed from 11 reports (single assays on five populations, two studies on a group analyzed 30 years apart, and four studies of a population spread over 31 years. Using the percent contribution to overall height, pubertal growth showed a close agreement between the populations as well as between male and female values (overall p < 0.003). Results for both sexes clustered around a narrow range. Pubertal growth for the 50th percentile, expressed as a percent contribution to overall height, may approach a biologic invariant. The value of percent contribution of pubertal growth to final height, did not show a secular trend.     

Pathogenesis and epidemiology of precocious puberty. Effects of exogenous oestrogens

Precocious puberty is generally defined as the appearance of secondary sex characteristics before age 8 years in girls (or menarche before age 9 years) and before 9 years in boys. The overall incidence of sexual precocity is estimated to be 1:5,000 to 1:10,000 children. The female-to-male ratio is approximately 10:1. In addition to the psychosocial disturbances associated with precocious puberty, the premature pubertal growth spurt (with less time for prepubertal growth) and the accelerated bone maturation result in reduced adult height. Precocious puberty may be gonadotrophin-dependent [i.e. of central origin with premature activation of the gonadotrophin-releasing hormone (GnRH) pulse generator] or gonadotrophin-independent (i.e. peripheral where the GnRH pulse generator is suppressed). This can be determined by GnRH testing. The pathophysiology is the basis for different diagnostic and therapeutic strategies, i.e. in the first case a stimulated LH/FSH ratio >1 and suppressive treatment with GnRH agonists (e.g. in hypothalamic hamartoma), and in the second decreased gonadotrophins and removal or suppression of the endogenous or exogenous sex steroid source (e.g. congenital adrenal hyperplasia). While several cases of gonadotrophin-independent precocious puberty due to oestrogen exposure via the transdermal, oral, or inhalative route have been reported, no case is known with the development of subsequent secondary central precocious puberty. Food contamination with oestrogens is theoretically possible, but would most probably be sporadic and, thus, would not lead to precocious puberty. As steroid hormones in meat production are banned in the European Union, no data on the impact of environmental oestrogenic substances on human maturation are currently available. In conclusion, the risk for children to develop precocious puberty through exposure to oestrogens (or androgens) in the environment or in food is very low. Nevertheless, studies of the effects of defined environmental oestrogenic substances on the human reproductive system and on pubertal development are warranted.     

Genetic and environmental influences on pubertal timing assessed by height growth

Secular trends towards earlier puberty, possibly caused by new environmental triggers, provide a basis for periodic evaluation of the influence and interaction of genetic and environmental effects on pubertal timing. In such studies, a practical marker that reflects timing of puberty in both genders needs to be used. We investigated genetic and environmental influences on pubertal timing by using change in the relative height between early and late adolescence (HD:SDS, height difference in standard deviations) as a new marker of pubertal timing. HD:SDS correlated well with age at peak height velocity in a population of men and women with longitudinal growth data. In 2,309 twin girls and 1,828 twin boys, HD:SDS was calculated between height SDs at age 11.5 and 17.5, and 14.0 and 17.5 years, respectively. Quantitative genetic models for twin data were fitted to estimate the genetic contribution to HD:SDS. We also investigated whether the same genetic factors influenced individual differences between HD:SDS and development of secondary sex characteristics prospectively collected by pubertal development scale (PDS). Genetic effects contributed to 86 and 82% of the variance in HD:SDS in girls and boys, respectively, when using the same model including additive genetic and specific environmental factors. In girls, 30% and in boys, 49% of the genetic factors affecting PDS and HD:SDS were the same. Future comparison of the results of periodic evaluations allows estimation of possible changes in the effects of environment on timing of puberty. In such studies, HD:SDS can be used as a practical marker of pubertal timing. Am. J. Hum. Biol., 2008. © 2008 Wiley‐Liss, Inc.     

Sex dimorphism in growth

While there is agreement that sex differences in height are small up to the onset of the pubertal spurt in girls, there has been some debate about the question of which, and to what extent, various growth phases contribute to the average adult sex difference of about 13 cm. There has been no consistent agreement between authors as to what extent this difference is due to the late onset of the pubertal spurt (PS) for boys and to what extent it is due to their more intense PS. In this paper, we investigate this question for the variables height, sitting and leg height, arm length, bihumeral and biiliac width. Biiliac width is a special case since both sexes have roughly the same adult size, but girls still have a shorter growing period. The gains for boys, when compared to girls, show a very different pattern across variables: for the legs, the additional growth due to the later spurt is responsible for most of the adult sex difference (64%). On the other hand, for bihumeral width and sitting height, the more intense PS contributes almost 50% to the adult sex difference. An analysis across variables indicates that increments from 1.5 to 6 years largely compensate for deviations in infant morphology from adult morphology.     

Serum dehydroepiandrosterone sulphate and pubertal development in Chinese girls

Serum dehydroepiandrosterone sulphate (DHEAS), estradiol (E2), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured by radioimmunoassay in 170 healthy school girls from 7-16 years old. Blood samples from postmenarcheal girls were taken on days 6-10 of the menstrual cycle. Bone age, height, weight, breast and pubic hair development were also investigated. Of the four hormones measured, serum DHEAS displayed the earliest elevation, at 7 years and upwards. A significant DHEAS increment at chronological age 13 years was observed. Girls with earlier menarche had higher DHEAS level than girls having later menarche. Serum DHEAS levels also correlated with bone age, height, weight, subcutaneous fat and pubertal stages. The results suggest that adrenal androgen might be involved in the initiation of puberty and female maturation.     

Serum dehydroepiandrosterone sulphate and pubertal development in Chinese girls

Serum dehydroepiandrosterone sulphate (DHEAS), estradiol (E2), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured by radioimmunoassay in 170 healthy school girls from 7–16 years old. Blood samples from postmenarcheal girls were taken on days 6–10 of the menstrual cycle. Bone age, height, weight, breast and pubic hair development were also investigated. Of the four hormones measured, serum DHEAS displayed the earliest elevation, at 7 years and upwards. A significant DHEAS increment at chronological age 13 years was observed. Girls with earlier menarche had higher DHEAS level than girls having later menarche. Serum DHEAS levels also correlated with bone age, height, weight, subcutaneous fat and pubertal stages. The results suggest that adrenal androgen might be involved in the initiation of puberty and female maturation.     

Effect of growth hormone treatment on the adult height of children with chronic renal failure. German Study Group for Growth Hormone Treatment in Chronic Renal Failure

BACKGROUND: Growth hormone treatment stimulates growth in short children with chronic renal failure. However, the extent to which this therapy increases final adult height is not known. METHODS: We followed 38 initially prepubertal children with chronic renal failure treated with growth hormone for a mean of 5.3 years until they reached their final adult height. The mean (+/-SD) age at the start of treatment was 10.4+/-2.2 years, the mean bone age was 7.1+/-2.3 years, and the mean height was 3.1+/-1.2 SD below normal. Fifty matched children with chronic renal failure who were not treated with growth hormone served as controls. RESULTS: The children treated with growth hormone had sustained catch-up growth, whereas the control children had progressive growth failure. The mean final height of the growth hormone-treated children was 165 cm for boys and 156 cm for girls. The mean final adult height of the growth hormone-treated children was 1.6+/-1.2 SD below normal, which was 1.4 SD above their standardized height at base line (P< 0.001). In contrast, the final height of the untreated children (2.1+/-1.2 SD below normal) was 0.6 SD below their standardized height at base line (P<0.001). Although prepubertal bone maturation was accelerated in growth hormone-treated children, treatment was not associated with a shortening of the pubertal growth spurt. The total height gain was positively associated with the initial target-height deficit and the duration of growth hormone therapy and was negatively associated with the percentage of the observation period spent receiving dialysis treatment. CONCLUSIONS: Long-term growth hormone treatment of children with chronic renal failure induces persistent catch-up growth, and the majority of patients achieve normal adult height.     

Longitudinal growth of stature in boys according to age and puberty: Prediction of adult stature from the age of 13 years

Background

The purpose of this study was to cross-validate and demonstrate how adult stature can be predicted in 13-year-old teenager's boys by using a new reference specific growth curve obtained from chronological age and maturity.

Methods

Stature measurements of 125 boys aged from 12 to 17.5 years were obtained over a period of five consecutive years. The maturity was based on the age of peak height velocity (APHV). An assessment of secondary pubertal stages using a simplification of the Tanner stages was also carried out. We found a connection between the secondary pubertal stage and the APHV. We carried out a prediction of the adult stature of 67 teenagers aged from 160 and 164 months.

Results

Significant differences between APHV enabled us to classify the adolescents into three categories according to their biological maturity: 19% of adolescents with advanced puberty, 62% with standard puberty and 19% with delayed puberty. The mean growth curves were used to predict the adult stature of 67 individuals with a good accuracy (±3 cm). The mean differences between predicted and real adult stature are −0.11 cm with 95% limits of agreement of [−3.2; + 2.8 cm].

Conclusions

The new stature growth curves developed from age and maturation enables us to accurately track individual growth kinetics.     

Changes in serum inhibin, activin and follistatin concentrations during puberty in girls

Serum concentrations of inhibin A, inhibin B, activin A and follistatin were determined using two-site enzyme-linked immunosorbent assays (ELISA) during pubertal ovarian development in 28 girls and five follicular phase women. Blood obtained every 15 to 20 min overnight was pooled for peptide determination. Serum inhibin A concentrations increased in mid puberty, exhibiting positive correlations with bone age (r = 0.527, P = 0.0016) and oestradiol concentrations (r = 0.581, P = 0.0005). Inhibin B concentrations peaked in mid puberty and declined thereafter, but remained greater than concentrations seen in prepubertal girls, and correlating positively with oestradiol (r = 0.362, P = 0.046) and follicle stimulating hormone (FSH) concentrations (r = 0.369, P = 0.038). Total activin A concentrations did not vary significantly across pubertal stages. Total follistatin concentrations, determined by radioimmunoassay, decreased with advancing puberty, exhibiting negative correlations with bone age (r = -0.634, P = 0.0001) and oestradiol concentration (r = -0.687, P = 0.0001). Follistatin concentrations determined by an ELISA specific for follistatin 288 were greatest in mid-pubertal girls, but concentrations in late puberty were less than those in early puberty. The free follistatin assay indicated that all circulating follistatin was activin-bound. These results suggest that significant changes in serum concentrations of FSH-regulatory peptides accompany the onset of puberty.     

Catch‐up reproductive maturation in rural Tonga girls,Zambia?

To compare the timing of reproductive maturation among urban and rural Tonga girls in Zambia, anthropometric measures and Tanner stages of breast development were obtained. Subjects were 774 (282 rural, 492 urban) girls ages 6-18. Results indicate that rural girls are shorter and have smaller triceps and subscapular skinfolds than their urban counterparts. Median age at menarche for the entire sample, as estimated by probit analysis, was 14.8 years (95% CL = 14.34-15.40). Onset of breast development among urban girls was significantly younger than for the rural girls: 11.47 (95% CL 11.22-11.71) years vs. 13.15 (95% CL 12.40-14.15) years. In contrast, the two groups did not differ in timing of pubertal completion as assessed by median age for Tanner Breast Stage 5: 17.01 (95% CL 16.30-18.33) vs. 16.96 (95% CL 16.37-17.56) years. Predictors of pubertal onset, based on multivariate logistic regression, included dental maturation, height, and triceps skinfold. Triceps skinfold was the only significant predictor of pubertal completion. These results suggest that rural girls progress through puberty more rapidly than the urban girls despite their later start. This finding of maturational catch-up contrasts with earlier urban/rural comparisons of girls as well as previous results among Gwembe boys, for which later pubertal onset is associated with longer duration of pubertal maturation. While the mechanism remains unclear, biocultural explanations suggest preferential feeding during adolescence as a source for rural girl's maturational catch-up.     

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. Am. J. Hum. Biol. 13:409–416, 2001. © 2001 Wiley‐Liss, Inc.     

Estrogen-induced weight gain cannot be predicted in individuals

Summary The effect of high estrogen doses on weight was studied in 36 adolescent girls with familial tall stature treated to reduce adult height. Mean weight gain during the first year was 9.03.6 kg. Thereafter, there was no or minimal gain on continued treatment. The largest weight velocity occurred during the first 6 months. Within that period, it was most marked during the first 5 weeks, probably due to early water retention. The gain (total, in different groups of patients and in treatment periods of different duration) did not correlate with height and weight before treatment expressed in absolute values or standard deviation scores. It is concluded that the weight gain induced by long-term estrogen treatment cannot be predicted quantitatively before treatment in individuals, and that heavy or fat girls do not necessarily gain more weight than light and lean girls.Abbreviations BA bone age - CA chronologic age - SDS standard deviation score     

Analysis of the adolescent growth spurt using smoothing spline functions

Height growth velocity curves between 4·5 and 17·75 years were estimated, using smoothing spline functions, for 112 boys and 110 girls from the Zurich Longitudinal Study (1955–1976). Parameters characterizing the growth process, such as peak height velocity and age at peak height velocity, were calculated directly from the estimated curves.

The variability of parameters describing the adolescent growth spurt is large, both between and within sexes. Peak height, defined as increase of height velocity during the growth spurt, and age at peak height velocity both characterize the sex difference in growth in a highly significant manner. Peak height of at least 4 cm/year is found in 70% of the boys, but in only 11% of the girls. The age at peak height velocity averages 12·2 years in girls and 13·9 years in boys and has a wide range of 5·7 years and 3·8 years respectively.

The sex difference in adult height of 12·6 cm is composed of the following 4 factors: +1·6 cm caused by more prepubertal growth in boys, +6·4 cm by the boys' delay in spurt, +6·0 cm by the more extensive spurt in boys and ?1·4 cm by more post-spurt growth in girls.

Correlations between parameters indicate that the adult height depends neither on the duration of growth, nor on the duration and height of the peak. Minimal pre-spurt height velocity and peak height velocity, but not peak height, are age- and height-dependent.

Partial correlations given adult height reveal two compensating mechanisms between growth in the prepubertal and in the pubertal period. Small prepubertal height and low height velocity with respect to adult height are followed by a late adolescent spurt and vice versa. Small height at the onset of the spurt with respect to adult height is followed by a longer lasting, but not higher spurt and vice versa.     

Growth processes leading to a large or small adult size

BACKGROUND: The way in which a large size in anthropometric variables is achieved is a longstanding problem, since the pubertal spurt shows statistically and clinically little association with adult size (mostly studied for height). By analysing longitudinal growth of groups of subjects with a large or a small adult size separately for height, leg and sitting height, and bihumeral and biiliac width, we studied this problem in some detail. Of interest are growth patterns specific for these variables and for boys or girls. METHODS: The data consist of 120 boys and 112 girls followed longitudinally from 4 weeks until adulthood. Statistically, structural average velocity curves were computed for each variable and each subgroup separately for comparison. This velocity curve represents the average intensity and the average tempo of growth. Since the area under the velocity curve is adult size, differences in the growth process can be visualized. RESULTS: Both sexes show similar patterns in reaching a small or large adult size. The different variables, however, show marked differences. Only for legs is the pubertal spurt delayed for the large groups (with additional gains in prepubertal years). For sitting height and biiliac width, a slightly elevated velocity all along development (after 2 years) leads to a larger size and for bihumeral width the size of the pubertal peak is decisive. CONCLUSIONS: The steering of growth to a certain target size is qualitatively similar for boys and girls, but quite different for different anthropometric variables. This leads to questions about endocrinological control for various parts of the body and differential bone growth in development.     

The application of new height-prediction equations (Tanner-Whitehouse mark 2) to a sample of Canadian boys

The adult statures of a sample of 71 Canadian boys from the Saskatchewan Longitudinal Growth Study were predicted using the original TW Mark 1 and the new TW Mark 2 prediction equations. The subjects had a mean chronological age of 11.59 years (SD = 0.30), a mean RUS bone age of 11.62 'years' (SD = 1.18), a mean height of 145.0 cm (SD = 6.98) and a mean measured adult height of 177.2 cm (SD = 6.65). The Mark 2 equations improved the predictions over Mark 1 by an average of 0.2-0.6 cm and slightly reduced the range of errors. No improvement in the prediction of boys above the 75th centile of British standards was noted but 60-70% of boys below the 25th centile predicted better with the Mark 2 equations. This pattern may well be repeated in more extreme subjects. About 80% of individuals who predicted badly with the Mark 1 equations, i.e. with errors equal to or greater than 5 cm, improved their predictions when Mark 2 equations were used.