Standards for Children's Height at Ages 2-9 Years Allowing for Height of Parents

Tanner, J. M.; Goldstein, Harvey; Whitehouse, R. H.

doi:10.1136/adc.45.244.755

Cited by 744 publications

(417 citation statements)

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“…In order to have a strict classification, those patients who could not be differentiated as FSS or CDGP were not included in the study. Target heights of the subjects (which are calculated from heights of their parents) [21] were similar to their predicted heights (which are calculated by using bone ages according to the Greulich and Pyle atlas) [5,22,23].…”

Section: Methodsmentioning

confidence: 99%

Serum Ghrelin, IGF-I and IGFBP-3 Levels In Children with Normal Variant Short Stature

et al. 2006

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Abstract. This study is planned to investigate the role of ghrelin in normal variant short stature. Serum ghrelin, IGF-I and IGFBP-3 levels were measured in 17 children with constitutional delay of growth, 19 children with familial short stature and 11 age matched healthy children. Mean bone age of the constitutional delay of growth group was lower compared to other groups. Constitutional delay of growth group had lower mean weight compared to the controls. Serum IGF-I values were lower in the constitutional delay of growth group compared to the familial short stature and control groups. IGFBP-3 levels of the groups were similar. Ghrelin levels were higher in the short stature groups compared to the controls. In the multiple regression analyses, weight (β = -.54, p<0.0001) and height SDS (β = -.33, p = 0.01) were the independent determinants of ghrelin. The results of this study, the first one in which ghrelin levels are investigated in normal variant short stature, suggest that ghrelin does not play a role as a cause, but as a consequence in these patients because it is negatively correlated with weight and height standard deviation score. These negative correlations can be attributed to the compensatory response of ghrelin, which deserves further attention in future studies.

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Section: Methodsmentioning

confidence: 99%

Serum Ghrelin, IGF-I and IGFBP-3 Levels In Children with Normal Variant Short Stature

et al. 2006

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“…5 Patients' target heights were calculated from mid-parental heights. 6 Adult height was considered to be reached when growth during the preceding year was less than 1 cm, with a bone age of 15 years in girls and 16 in boys. GH secretion was stimulated by a sequential arginine insulin test, and by an ornithine test at a second evaluation.…”

Section: Methodsmentioning

confidence: 99%

Changes in height, weight and plasma leptin after bone marrow transplantation

Couto-Silva

Trivin

Esperou

et al. 2000

Bone Marrow Transplant

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Summary:Short stature can be a severe side-effect of bone marrow transplantation (BMT). Because of the effect of weight changes on growth rate and on plasma insulin-like growth factor (IGF I), we analyzed changes in height and body mass index (BMI) in 53 patients given BMT. Group 1 (n = 22) was given 12 Gy total body irradiation (TBI) as six fractions, group 2 (n = 14) 10 Gy TBI (one dose), group 3 (n = 8) 6 Gy total lymphoid irradiation (one dose), and group 4 (n = 9) chemotherapy alone. At the first evaluation, 13/36 patients in groups 1 and 2 had low growth hormone (GH) peaks after stimulation. The mean plasma IGF I concentrations (z score) were similar in groups 1 (−2.9 ± 0.3) and 2 (−2.5 ± 0.3), and in groups 3 (−1.4 ± 0.3) and 4 (−1.4 ± 0.7), but those of group 1 were lower than those of groups 3 (P Ͻ 0.01) and 4 (P Ͻ 0.05), and those of group 2 than those of group 3 (P Ͻ 0.05). BMI during the 5 years after BMT did not change in groups 1 and 2, decreased in group 3, and increased in group 4. However, these changes were not significant. Most of the patients given TBI had BMI below the mean at 2 (66%) and 5 (57%) years later. Their BMI and leptin concentrations correlated positively with each other (P = 0.005), and negatively with GH peak (P = 0.02 for BMI and 0.007 for leptin). In conclusion, this study suggests that TBI actually decreases GH secretion and is followed by a persistent low BMI. The negative relationship between GH peak and leptin may indicate that both are markers of a TBIinduced hypothalamic-pituitary lesion. Bone Marrow Transplantation (2000) 26, 1205-1210. Keywords: bone marrow transplantation; body irradiation; body mass index; growth; growth hormone; leptin Short stature can be a severe side-effect of bone marrow transplantation (BMT). It may be caused by the initial disease and its treatment before BMT, by the conditioning protocol used for BMT, particularly the irradiation, by the complications of the BMT, and/or by the long-term corticosteroid therapy required to treat these complications. The irradiation may cause short stature in two ways: in patients given total body irradiation (TBI), hypothalamic-pituitary irradiation may decrease the secretion of growth hormone (GH); patients given TBI or total lymphoid irradiation (TLI) may suffer from bone lesions. 1 These lesions may be responsible for resistance to insulin-like growth factor I (IGF I), the secretion of which depends on GH and nutritional state, and a poor growth response to GH therapy. 2 The fall in weight following TBI in some patients, the effect of weight changes on growth rate and plasma IGF I, 3 and the very short adult height in many patients given TBI have prompted us to analyze the factors influencing changes in height and body mass index (BMI). We have done this by comparing patients given different conditioning protocols for BMT. Our aims were to determine if TBI actually decreases GH secretion, and if there is any relationship between the conditioning protocol and changes in BMI and plasma leptin concentrations. M...

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“…The formula was developed from the simple linear regression analysis of final height and parental heights; it has been reported elsewhere and is different from the commonly applied corrected midparental height method (midparental height, Ϯ 6.5 cm), because the corrected midparental height method may underestimate target height for children with short parents, which is not the case with the new model. 13,14 The target height values were converted into SDS and CMS based on the reference mean and SD.…”

Section: Methodsmentioning

confidence: 99%

Length and Body Mass Index at Birth and Target Height Influences on Patterns of Postnatal Growth in Children Born Small for Gestational Age

1998

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ABSTRACT. Objective. Previous growth studies on children born small for gestational age (SGA) indicate that birth length, weight, and target height are important predictors for postnatal catch-up growth in SGA. Their influences on different phases of catch-up growth are still not described. The aim of this study was to clarify the influences of target height, length, and nutritional status at birth on different phases of postnatal catch-up growth (infancy, childhood, puberty) in SGA and the long-term consequences.Methods. Data were obtained from a longitudinal population-based growth study on Swedish children (N ‫؍‬ 2815). Primary outcome measurements include heights, the changes in height standard deviation scores (SDS) during various phases of growth and relative risk for adult shortness.Results. The difference in final height in children born SGA was attributable to their difference in target height and the magnitude of catch-up growth during the first 6 months of life, rather than the difference in length or body mass index (BMI) at birth. Length at birth showed negative influence on catch-up growth during infancy (0 to 2 years of age), but no significant influence thereafter. The BMI or weight for length SDS at birth showed no significant influence on catch-up growth during any growth phase. Target height showed positive influence on catch-up growth from the onset of childhood. Neither target height nor length and BMI at birth showed any significant influence on catch-up growth during puberty. The magnitude of catch-up growth during infancy, especially the first 6 months of life, is most critical in decreasing risk at adult shortness. We confirmed that the SGA group had a sevenfold greater risk for adult shortness than the non-SGA group (relative risk ‫؍‬ 7.31; 95% confidence interval: 3.96 -13.52). However, ϳ40% of children who were below ؊2 in height SDS at 2 years of age remained short at final height in both SGA and non-SGA groups. The mean height SDS of children born SGA increased by 1.65 from birth to final height, but the length deficit in centimeters at birth (؊5.4 cm) persisted into adulthood (؊5.9 cm).Conclusions. BMI at birth is not related to postnatal catch-up growth in infants born SGA, but birth length and target height are important. The genetic influence on catch-up growth appears to start from the onset of childhood. Being born short or becoming short during the first 2 years of life is similar in terms of risk for adult short stature. Pediatrics 1998;102(6). URL: http://www. pediatrics.org/cgi/content/full/102/6/e72; fetal growth retardation, body mass index, birth length, genetics, catch-up growth, short stature.

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Standards for Children's Height at Ages 2-9 Years Allowing for Height of Parents

Cited by 744 publications

References 4 publications

Serum Ghrelin, IGF-I and IGFBP-3 Levels In Children with Normal Variant Short Stature

Serum Ghrelin, IGF-I and IGFBP-3 Levels In Children with Normal Variant Short Stature

Changes in height, weight and plasma leptin after bone marrow transplantation

Length and Body Mass Index at Birth and Target Height Influences on Patterns of Postnatal Growth in Children Born Small for Gestational Age

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