Comparison of bone age in small-for-gestationalage children vs appropriate-for-getational-age children

BackgroundAbout 10-15% small-for-gestational-age children are in higher risk for having linear growth retardation due to growth hormone-insulin like growth factor 1 axis defect (GH-IGF 1) which causes bone age delay.ObjectivesTo compare bone age in 24-36 month old children born small-for-gestational-age (SGA) to that in children born appropriate-for-gestational-age (AGA).MethodsA cross-sectional study was conducted in Hasan Sadikin General Hospital, Bandung, from January to April 2009.Subjects consisted of50 healthy children of 24-36 months old (25 children born at term, SGA, 25 children born at term, AGA). We compared the appropriateness and delay of bone age between the two groups. ResultsMean bone age in the SGA group was 20.8 (SD 7.7) months, and in the AGA group was 25.7 (SD 7.1) months (P=0.022). Mean bone age deficit was -10.5 (6.5) months in the SGA group and -5.5 (SD 5.7) months in the AGA group (P=0.009). The prevalence ratio was 1.77 (95% CI: 1.19–2.62). Bone age delay was found to be higher in children born SGA than that in children of the other group (23 vs 13). On the contrary, appropriate bone age was found more in children born AGA (12 vs 2) (P=0.002).Conclusion Bone age delay in 24-36 months old children born small-for-gestational-age was found to be higher than in those born appropriate-for-gestational-age.

Phenotypic variation in constitutional delay of growth and puberty: relationship to specific leptin and leptin receptor gene polymorphisms

Objectives: Constitutional delay of growth and puberty (CDGP) is a variant of normal pubertal timing and progress, often with dominant inheritance. It is likely that one or more genes will be associated with CDGP. Possible candidates are the leptin (L) and the leptin receptor (LR) genes, as the leptin axis links nutritional status to pubertal development. This study has assessed whether a) L or LR gene polymorphisms were associated with CDGP and b) the CDGP phenotype was influenced by these polymorphisms. Design: Case–control and transmission disequilibrium tests were used to test genetic association of L and LR polymorphisms with CDGP. Methods: We genotyped L (3′CTTT repeat) and LR polymorphisms (Gln>Arg substitution, exon 6) in 81 CDGP children and 94 controls in the UK and 88 CDGP children from the US and assessed the effect of genotype on their anthropometric characteristics. Results: There was no association of these L or LR gene polymorphisms with CDGP. There was no difference in height or bone age delay within L or LR genotypes. However, UK CDGP children homozygous for the L short allele were heavier than heterozygotes and long allele homozygotes, with a similar trend in the US cohort. UK CDGP children with severe pubertal delay, who were thin, had significantly greater bone age delay and an increased frequency of parental pubertal delay than other groups and were less likely to be L short allele homozygotes. Conclusions: There was no association of specific L or LR polymorphisms with CDGP, but L short allele carriage influenced the phenotype within CDGP.