No abstract

This study aimed to update growth reference values for height, weight and head circumference in order to reflect the changes in body size in the Swedish population during the past two decades. The data came from a large longitudinal growth study on 3650 full‐term healthy Swedish children who were born between 1973 and 1975. All of these 1801 girls and 1849 boys had longitudinal data for height and weight from birth to final height. Comparison with previous Swedish growth reference values based on children born between 1955 and 1958 revealed that there have been secular changes in body size. For instance, at 18 y of age, the updated height and weight reference values are 180.4 cm for males and 167.7 cm for females, i.e. 1.9 cm taller and 5.7 kg heavier for males and 2.3 cm taller and 3.4kg heavier for females compared with the previous reference values. Conclusion: These new growth reference values provide current national standards for growth monitoring and evaluation since the year 2000.

A model was developed that allows physicians to individualize GH treatment in children born short for gestational age (SGA) who fail to show spontaneous catch-up growth. Data from children (n = 613) in a large pharmacoepidemiological survey, the KIGS (Pharmacia International Growth Database), or who had participated in clinical trials were used to develop the model. Another group of similar children (n = 68) from KIGS was used for validation. In the first year of GH treatment, the growth response correlated positively with GH dose, weight at the start of GH treatment, and midparental height SD score and negatively with age at treatment start. Using this model, 52% of the variability of the growth response could be explained, with a mean error SD of 1.3 cm. GH dose was the most important response predictor (35% of variability), followed by age at treatment start. The second year growth response was best predicted by a three-parameter model (height velocity in yr 1 of treatment, age at start of treatment, and GH dose), which accounted for 34% of the variability, with an error SD of 1.1 cm. The first year response to GH treatment was the most important predictor of the second year response, accounting for 29% of the variability. No statistically significant differences between the predicted and observed growth responses were found when the models were applied to the validation groups. In conclusion, using simple variables, we have developed a model that can be used in clinical practice to adjust the GH dose to achieve the desired growth response in patients born SGA. Furthermore, this model can be used to provide patients with a realistic expectation of treatment and may help to identify compliance problems or other underlying causes of treatment failure.

The aim of the study was to develop and validate models that could predict the growth responses to GH therapy of individual children. Models for prediction of the initial one and 2-y growth response were constructed from a cohort of 269 prepubertal children (Model group) with isolated GH deficiency or idiopathic short stature, using a nonlinear multivariate data fitting technique. Five sets of clinical information were used. The "Basic model" was created using auxological data from the year before the start of GH treatment and parental heights. In addition to Basic model data, the other four models included growth data from the first 2 y of life, or IGF-I, or GH secretion estimated during a provocation test (AITT) or a spontaneous GH secretion profile.The performance of the models was validated by calculating the differences between predicted and observed growth responses in 149 new GH treated children (Validation group) who fulfilled the inclusion criteria used in the original cohort. The SD of these differences (SD res ) in the validation group was compared with the SD res for the model group. For the 1st y, the SD res for the Basic model was 0.28 SDscores. The lowest SD res (0.19 SDscores), giving the most narrow prediction interval, was achieved adding the 24h GH profile and data on growth from the first 2 y of life to the Basic model. The models presented permit estimation of GH responsiveness in children over a broad range in GH secretion, and with an accuracy of the models substantially better than when using maximal GH response during an provocation test. The predicted individual growth response, calculated using a computer program, can serve as a guide for evidence-based decisions when selecting children to GH treatment. Abbreviations GHD, GH deficiency GHI, GH insensitivity ISS, idiopathic short stature IGFBP-3, IGF binding protein 3 AITT, arginin-insulin tolerance test GH max , the estimated maximal GH levelThe diagnosis of severe GH deficiency (GHD) on the one hand or complete GH insensitivity (GHI) on the other, usually is obvious in the short child in whom appropriate studies have excluded other causes for growth failure. Among children forming the continuum between these two extremes, diagnosis is more challenging; that is, children with partial GHD or those considered to have partial GHI, who may be classified as idiopathic short stature (ISS). Despite investigations and discussions aimed at attaining consensus on the diagnostic discrimination between GHD and ISS (1, 2), none of the clinical measures used to date provide a reliable means for categorizing these patients and for predicting the value of GH therapy (3). The effect of the GH axis on statural growth in an individual child depends on the interaction between GH secretion and GH responsiveness. With better understanding of conditions causing GH resistance (4 -7), the need to consider responsiveness to GH, as well as secretion of GH when interpreting the growth of a child has become more apparent.Traditionally, the diagnosis of GHD relies ...

The aim of this observational study was to assess the longterm growth responses to GH treatment of children born small for gestational age (SGA). GH treatment was begun before puberty and continued to final height (FH). Seventy-seven short (height SD score below Ϫ2) prepubertal children born SGA (below Ϫ2 SD for birth weight and/or birth length), with a broad range of GH secretory capacity, were treated with GH in a daily dose of 33 g/kg (0.1 U/kg), beginning before the onset of puberty. We observed a difference between adult and pretreatment projected height of 1.3 SD (9 cm) for the entire group. Among the children treated for Ͼ2 y before puberty, this mean gain (i.e. difference) in final height was 1.7 SD, whereas the mean gain was 0.9 SD among those in whom treatment was begun Ͻ2 y before puberty. Better catch-up growth was observed in the younger (r ϭ Ϫ0.56, p Ͻ 0.0001), shorter (r ϭ Ϫ0.49, p Ͻ 0.0001), and lighter (r ϭ Ϫ0.46, p Ͻ 0.0001) subjects. We conclude that GH treatment improves the final height of short children born SGA. The height gain attained before the onset of puberty is maintained to final height. The younger, shorter, and lighter the child at the start of GH treatment, the better the response. Moreover, most of these SGA individuals treated with GH reach their target height. There is a 5-to 7-fold higher risk of short stature among adults who were born SGA, compared with those born AGA (1,2). Children born SGA comprise one-third of children who are short during childhood (1). As short stature is present in 10 -15% of children born SGA (1-3), efforts have been made to understand the etiology of their growth restriction and to increase their FH.Birth length has been shown in population-based studies to be the single most important predictor of adult height (1,2). Short children born SGA keep their prepubertal height SDS to FH, whereas short children born AGA gain further 0.6 -0.7 SDS in height during puberty (4). French data show that adult men who were born SGA are, on average 7.5 cm, and women are 9.6 cm below their mid-parent target height (5). This is at the lower end of the range compared with other studies (1,6,7), which find a growth deficit of 0.7-0.9 SDS below the MPH.Either low GH secretion or reduced sensitivity to GH may account for some of the growth retardation of children born SGA (8 -10). Boguszewski et al. (11,12) reported that short children born SGA have both lower mean GH secretion rates and lower serum IGF-I (IGF-I) values than children born AGA. In children born SGA, there is a correlation between the GH dose and the growth response, mainly during prepubertal years (13-16). The majority of short children born SGA show improvement in growth rate during GH treatment, particularly if treatment is begun early (14,16). With the exception of one large study (17), however, no information is available on the FH achieved by short children born SGA and treated with GH from a young age to FH. We report here the observational data on the effect of GH therapy on final height of childr...