Background:The exact nature of the relationship between the age of onset of puberty and final height in normally maturing children is controversial. Some authors have claimed that the age of pubertal onset does not affect final height, and others have claimed the opposite. We hypothesized that both height and the age of onset of the pubertal growth spurt (PGS) are correlated to final height. Methods: The height measurements of 335 children (162 girls) were analyzed in an observational retrospective study. The age and height at the onset of the PGS were computed from the equations of the Karlberg's infancy-childhood-puberty model. results: A very low correlation was found between the age of onset of the PGS and final height. However, the correlation became very high when the parameter "height at onset of the PGS" was included in the regression analysis. The model was found reliable when tested on growth data of 60 Israeli children. conclusions: Final height is influenced by both height and the age of onset of the PGS in normal maturing children. A normal but early puberty exerts a negative effect on final height. A delayed PGS exerts a positive effect on final height. P ediatricians and pediatric endocrinologists are well aware that precocious puberty exerts a negative influence on statural growth and final height. However, the exact nature of the relationship between the age of onset of puberty, statural growth, and final height in normally maturing children is controversial. Some authors have claimed that age of pubertal onset does not affect final height (Marshall and Tanner (1), Vizmanos et al. (2)), and others have claimed the opposite (Bourguignon (3), Karlberg (4), and Tanaka (5)).It is against this background that we hypothesized that both height and the age of onset of the pubertal growth spurt (PGS) are correlated to final height. Since the pattern of statural growth in childhood is nonlinear, we also hypothesized that a nonlinear equation would be more appropriate than a linear equation to describe the influence of age and height at the age of onset of the PGS on final height. Hence, the purpose of our study was to test the hypothesis that final height correlates to both age and height at the onset of the PGS and to mathematically describe this correlation. This report informs on the results of our testing of these hypotheses and provides a mathematical description of the relationship between final height and the age and height at the onset of the PGS. RESULTSThe mean age of the onset of the PGS for boys was 11.9 y ± 1.1 (SD) and 10.0 ± 0.7 y for girls. Specifically, the age of onset of the PGS was between (i) 8.5 and 9.4 y in 2 boys, (ii) 9.5 and 10.4 y in 16 boys, (iii) 10.5 and 11.4 y in 48 boys, (iv) 11.5 and 12.4 y in 60 boys, (v) 12.5 and 13.4 y in 33 boys, (vi) 13.5 and 14.4 y in 16 boys, and (vii) 14.5 and 15.5 y in 3 boys. For girls, the age of onset of the PGS was between (i) 7.5 and 8.4 y in 2 girls, (ii) 8.5 and 9.4 y in 47 girls, (iii) 9.5 and 10.4 y in 71 girls, (iv) 10.5 and 11.4 y in 43...

Hypoparathyroidism, retardation, and dysmorphism (HRD) syndrome is the first reported disease caused by a defect in the tubulin folding and assembly pathway. We aimed to summarize our experience with a cohort of patients with HRD, analyze their growth, and evaluate patients' polymorphonuclear cell (PMN) functions. The records of 22 HRD patients in a single medical center were reviewed. Growth during infancy and early childhood were analyzed by the Infancy-Childhood-Puberty (ICP) growth model. PMN functions were compared with healthy controls. Twelve patients died and many hospitalizations due to infections and convulsions were recorded. Growth measurements, expressed as weight and height SD scores in boys at a mean age of 4 y were -13.1 Ϯ 3.8 and -8.7 Ϯ 1 and -16.6 Ϯ 4.4 and -9.5 Ϯ 2.4, respectively, in girls at a mean age of 6.4 y. Chemotactic migration, random migration, and phagocytosis of PMN from HRD patients were significantly lower than that of PMN from healthy controls. No significant differences were found in superoxide production of PMN from patients compared with controls. Functional hyposplenism has been demonstrated in most of the studied patients. The defect in the tubulin folding and assembly pathway, previously described in HRD, has grave consequences on growth and PMN functions. (Pediatr Res 62: 505-509, 2007)

Serum Lp(a) concentrations remained above pretreatment values during a 1-year period of GH treatment in short children without GH deficiency and declined shortly after cessation of therapy. Since GH therapy for short children without GH deficiency usually continues for several years, we suggest that serum Lp(a) levels should be determined and followed regularly in such children under prolonged GH therapy.

Aims: To examine ethnicity and gender differences in the evaluation of referred children with short stature and to investigate adherence of the primary care evaluation to published guidelines. Methods: Cross-sectional study in a referral center. 371 short patients aged 2–18 years were included. Outcome measures were patient’s growth characteristics, final diagnosis, and prevalence of pre-referral patient data. Results: The study population was composed of 239 Bedouin children and 132 Jewish children (p < 0.0001). More males (61%) than females were evaluated (p < 0.0001). There were no significant differences between males and females in age and growth parameters at the time of referral. Bedouins, males and females, were significantly shorter than their Jewish counterparts at the time of referral: height SD –2.44 ± 0.73 and –2.62 ± 1.05 versus –2.13 ± 0.55 and –2.21 ± 0.57, respectively (p < 0.05). There were no significant ethnic or gender differences in the final diagnosis. Significant deficiencies in the primary care evaluation of referred short children were found. Conclusions: We demonstrated novel ethnic- and gender-based inequities in the evaluation of referred short children. We found that the current evaluation of short stature in our area does not comply with existing guidelines.

Several methods for adult height prediction are currently in use. All are subject to a wide range of error which is thought to result, at least in part, from the use of bone age estimation. Following the suggestion made by Karlberg to predict adult height of pubertal children by the use of the ‘Infancy-Childhood-Puberty model’ (ICP), growth data of 39 normal boys who were followed from infancy until adult height was attained were reviewed. Use of the ICP model alone and without bone age resulted in more accurate predictions of adult height than those made by the methods which require bone age determination, the Bayley-Pinneu (BP) and the Tanner-Whitehouse methods (TW). The absolute error of prediction was. 3.4 cm as compared to 5.3 (BP) and 4.9 cm (TW) (p < 0.05) and maximal range of error was 10 cm as compared to 22 (BP) and 21 cm (TW) (p < 0.05). Finally, based on the ICP model, a new equation which incorporates paternal height was been derived. This equation, termed ICP-New (ICPN), resulted in even better accuracy: absolute error of prediction was 2.3 cm as compared to 3.4 cm (ICP) and maximal range of error was 6 cm as compared to 10 cm (ICP) (p < 0.05). It is concluded that the ICP model and the ICPN equation may predict the adult height of pubertal boys more accurately than the methods which use bone age.